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February 3, 2017:

Does detecting heart failure in MVD-affected cavaliers
matter anymore?

More vets are prescribing heart failure drugs before heart failure

Their new threshold is called “enlargement”

The slippery slope of drug tolerance is ignored

Peer-reviewed research be damned!

Anecdotal reports are meaningless,
unless the cardiologists want to believe them

Heart FailureFor decades, hundreds of veterinary cardiologists have been researching dozens of ways to determine if and/or when dogs, especially our cavalier King Charles spaniels (CKCS), affected with mitral valve disease (MVD) are at risk to enter into congestive heart failure (CHF).

They have taken x-rays to measured heart enlargement and lung congestion.

They have counted breaths.

They have counted heart beats.

They have devised complicated calculations of measurements of the heart’s left ventricle and left atrium, using several different types of echocardiograph devices, including one-dimension (M-mode, or 1-D), two-dimension (2-D), and three-dimension (3-D) echocardiographic devices, color-flow Doppler, tissue Doppler imaging, the Tei Index, left ventricular torsion, and speckle-tracking.

They have used cardiac magnetic resonance imaging (cMRI).

They have used computed tomography (CT).

They have used advanced electrocardiography (ECG or EKG).

They have measured natriuretic peptides.

They have measured these other cardiac biomarkers: cardiac troponin I (cTnI), and high-sensitivity cardiac troponin I (hscTnI), C-reactive protein (CRP), sodium-calcium exchanger (NCX-1), aldosterone concentration (UAC), serum serotonin (serum 5HT), antidiuretic hormone (ADH), histamine concentration, enzymes and growth factors, Galectin-3 (Gal-3), vitamin D, microRNAs (miRNAs), serum cystatin-C (Cys-C) and symmetric, dimethylarginine (SDMA), oxidative stress, serum fatty acids, serum leptin and adipokines, anemia, desmin, vimentin, periostin,  caspase-3, complement factor H isoform 2, calpain-3 isoform X2, dystrobrevin beta isoform X7, CD5 molecule-like and l-2-hydroxyglutarate dehydrogenase.

They have studied DNA and cell transitions.

All for what? To determine when the dog’s MVD progresses to heart failure.

But why has it been so important to pinpoint the moment of heart failure? Because the commencement of heart failure traditionally has been the threshold for medicating the MVD, based upon peer-reviewed scientific research.

But the operative words seem to be “has been”. Because, no longer is the start of heart failure the balance-tipper for plying pills into the MVD patient. Peer ReviewIt seems that now, even otherwise cautious cardiologists have jumped the gun and started the pill-plying before heart failure. Now, instead of heart failure, the operative word is “enlargement”. If the left atrium or left ventricle is the least bit enlarged, that seems to be the latest excuse for these canine heart specialists to start writing their prescriptions for their cocktails of pimobendan, diuretics, ACE-inhibitors, and spironolactone.

And, they are prematurely pushing these pills without any peer-reviewed veterinary cardiology research to support their multitude of medicinal scripts. The one possible exception is the EPIC Study, which, when its troubling flaws are ignored, arguably justifies prescribing pimobendan to MVD-affected dogs with enlarged hearts but no CHF if two echocardiograph measurements and one radiograph measurement exceed precise minimum dimensions. But even the EPIC Study tested only one medicine – pimobendan – without any other medications combined with it.

No excuse for starting diuretics, ACE-inhibitors, or spironolactone before CHF

Peer-review cartoonThere is no excuse for prescribing diuretics before CHF because no unwanted fluids are being retained in the dog’s heart or lungs until heart failure starts. And, there is no excuse for prescribing ACE-inhibitors to cavaliers prior to heart failure because the SVEP Trial of 229 CKCSs conclusively showed that they do not extend the time in which cavaliers reach heart failure. And, there is no excuse for prescribing spironolactone prior to heart failure because there is no peer-reviewed research showing that it would have any benefit to pre-CHF dogs.

But, despite the lack of veterinary research justifying the pre-CHF dosing of these drugs, it unquestionably has become the mainstream way to treat mitral valve disease these days. No longer are many cardiologists following the principle of “do no harm”.

That means, in the context of prescribing diuretics, they should wait until the MVD-affected dogs are retaining fluids which need to be removed. It does not mean giving the diuretic in advance of fluid retention, in the blind hope of preventing or delaying it. We say, “blind hope” because there is no peer-reviewed research which shows that giving a diuretic to a dog which is not retaining fluids will prevent the dog from retaining fluids and otherwise do no harm to that dog.

It means, in the context of prescribing ACE-inhibitors to cavaliers, they should wait until the MVD-affected dog is in heart failure. It does not mean giving the ACE-inhibitor in the blind hope of preventing or delaying it. We say, “blind hope” because there is no peer-reviewed research which shows that giving an ACE-inhibitor to an MVD-affected CKCS before heart failure will prevent or delay the onset of heart failure and otherwise do no harm to that dog. In fact, the research, the SVEP Study, concluded the opposite – that ACE-inhibitors prior to heart failure does not delay the onset of MVD in the 229 cavaliers in that study. ACE-inhibitors have documented side effects which could be avoided if the drugs are not prescribed prematurely.

And it means, in the context of prescribing spironolactone, they should wait until the MVD-affected cavalier is in heart failure. It does not mean giving the spironolactone in the blind hope of preventing or delaying it. We say, “blind hope” because there is no peer-reviewed research which shows that giving spironolactone to an MVD-affected dog before heart failure will prevent or delay the onset of heart failure and otherwise do no harm to that dog. In addition, spironolactone has been approved within the European Union only for use in dogs with clinical signs of heart failure.

The slippery slope of drug tolerance is ignored

Cavalier with Prescription BottleAnother hazard to the premature administration of these drugs is that the patients may develop a tolerance to the drugs, thereby decreasing their effectiveness. Drug tolerance is a pharmacological concept describing the patient's reduced affinity to a drug after sustained exposure to that drug. This means that starting the drug earlier than necessary can result in having to increase the dosage later on to achieve the same beneficial effect. Even worse, at some point the drug may become totally ineffective.

Drug tolerance is a known factor in treating MVD-affected dogs with diuretics, since in nearly all cases, the dosage of the diuretic must be increased over time. In the case of furosemide, it eventually can become so ineffective that it must be replaced with the ten-times more powerful torsemide.

Also, in the EPIC Study, an un-acknowledged (by its authors) but obvious consequence of the pre-CHF administration of pimobendan is the evidence that the time between heart failure and death appeared to be shorter than for dogs in the placebo group. In the placebo group, the dogs did not receive pimobendan until they reached CHF, while in the pimobendan group, the dogs were started on the pimobendan from day one. A most plausible hypothesis for this evidence is a pharmacological tolerance to the drug, but the authors of the EPIC Study have ignored that data which their study produced, much as they have chosen to overlook other apparent downsides to their study, replete as their report is with cherry-picked good news.

Anecdotal reports are meaningless, unless the cardiologists want to believe them

So, why do these cardiologists ignore the peer-reviewed research and prescribe these drugs to MVD-affected dogs before heart failure? Anecdotes are not dataWe have asked some cardiologists that very question, and their answers have been consistent and also troubling. They respond that they do not agree with the research. In some cases, they argue that the parameters of the research were not appropriate; in others, that the doses of the drugs in the studies were too low. In still others, they claim the early dosing has worked for their patients -- in other words, their own anecdotal evidence. But in no case have they cited any alternative research to justify their decisions to blindly prescribe these drugs to our cavaliers before they really need them. They do not cite any alternative research, because there is none!

All too often, cardiologists will tell cavalier owners that ancedotal reports about the effectiveness of supplements (e.g., CoQ10, Vitamins C and E, fish oils) are meaningless, and therefore the cardiologists do not recommend the supplements. However, it appears that when the anecdotal reports -- or even worse, just gut feelings -- come from those cardiologists themselves, they not only are meaningful, but they are more reliable than the peer-reviewed studies which contradict them. In short, these cardiologists are following the basic tenet of hypocrisy. The problem is that they are applying that tenet to our dogs and putting them at risk.

January 20, 2017:

All that cavalier owners need to know
about spironolactone

A mild, potassium-sparing diuretic treatment for mitral valve disease

SpironolactoneSpironolactone (Aldactone, Prilactone) is both an aldosterone antagonist and a potassium-sparing diuretic. It has been approved within the European Union for use in dogs with clinical signs of heart failure secondary to MVD (meaning, the ACVIM Consensus Statement’s Stage C), as adjunctive therapy. It typically acts as a comparatively weak diuretic, when administered alone, but has synergistic effects when combined with other diuretics.

The main reason for prescribing spironolactone is to protect the dog against the harmful effects of aldosterone on the heart and blood vessels. It reportedly is rapidly absorbed through the dog’s gastrointestinal tract into the bloodstream and then converted to active metabolites. Its value level is highest when it is administered with food.

Approved for cavaliers in Stages C and D – congestive heart failure

Spironolactone is a drug often prescribed by veterinary cardiologists to cavalier King Charles spaniels in congestive heart failure (CHF) resulting from our breed’s worst nemesis, mitral valve disease (MVD). It usually is not in the first wave* of medications prescribed for CHF, but typically is added as the heart failure worsens.

* That “first wave” – called “conventional therapy” – consists of pimobendan, a loop diuretic such as furosemide, and an ACE-inhibitor such as enalapril. (Spironolactone is not a loop diuretic.)

In this 2010 European study, spironolactone, when added to the conventional CHF therapies, was found to significantly decrease the risk of reaching the primary endpoint (i.e., cardiac-related death, euthanasia, or severe worsening) in dogs with MVD. However, this 2011 report indicated that spironolactone did not extend survival times of dogs with advanced heart failure.

ACVIM Stages of MVDIn a 2013 study of the possible increased risk of adverse events for dogs taking spironolactone in addition to conventional therapies, the researchers concluded that dogs with heart failure receiving spironolactone in addition to conventional treatment are not at a higher risk for any adverse events, such as death caused by cardiac disease, renal disease, or both. This study was funded by the manufacturer of Prilactone, a spironolactone trade name.

The guidelines of the American College of Veterinary Internal Medicine (ACVIM) 2009 Consensus Statement on MVD (chart at right) recommend spironolactone as an additional therapy in dogs with Stage D MVD. A majority of panelists recommended the use of spironolactone to treat Stage C MVD, although a 100% consensus agreement was not reached. Oddly, a minority of the ACVIM panelists recommended the use of spironolactone in dogs Stage B2 MVD. (See below.)

Cardalis is a tablet which combines spironolactone with the ACE-inhibitor benazepril. Aldactazide is a combination of spironolactone and hydrochlorothiazide, which inhibits the activity of the hormone aldosterone.

Spironolactone is NOT approved for cavaliers in Stage B2

ACVIM Stages B1 & B2There are no veterinary studies recommending beginning spironolactone in Stage B2.* To repeat that: There are NO veterinary studies recommending beginning spironolactone in Stage B2! The emphasis is necessary because that fact is inexplicably ignored by many veterinarians and even several cardiologists.

* Stage B2 of MVD consists of an MVD murmur and heart enlargement but no symptoms of heart failure.

In 2010, a team of Italian cardiologists, led by Dr. Michele Borgarelli (now at VA-MD Regional College of Veterinary Medicine in Virginia, USA), began the DELAY Study of 240 dogs to determine if giving combined doses of spironolactone and benazipril can delay the onset of symptoms of heart failure in dogs with MVD. The results of the study are expected to be reported in 2018.

Dr. Borgarelli reiterated in a December 2016 email that, “About your question on prescribing spironolactone to cavaliers prior to heart failure at this moment there is no scientific background for this recommendation.”

In conclusion, spironolactone may extend the lives of cavaliers in heart failure (Stages C and D) due to MVD, if added to conventional medications at an appropriate time as the MVD progresses. Care must be taken to assure that the drug’s downsides do not interfere with the dog’s bodily systems. As for prescribing spironolactone to cavaliers in Stage B2, there is no scientific justification for any veterinarian to do so, whatsoever.

December 20, 2016:

Why do any veterinarians prescribe useless drugs
to MVD-affected cavaliers before heart failure?

ACE-inhibitors, loop diuretics, and spironolactone
have not been shown to work before heart failure

And, they may have damaging side effects

ACVIM Consensus Statement Stages of MVDThere is no question that, once cavalier King Charles spaniels (CKCS) affected by mitral valve disease (MVD) reach the point of congestive heart failure (Stage C of MVD), research studies have shown that some medications can delay the progression of their MVD to the ultimate end point, death. Those drugs include pimobendan (Vetmedin, Cardisure, Safeheart 5), ACE-inhibitors (e.g., enalapril, benazepril, imidapril), loop diuretics (e.g., furosemide, hydrochlorothiazide), and spironolactone.

However, there is only one research study showing that any of these medications can delay the progression of MVD of cavaliers before they reach congestive heart failure (CHF). Those CKCSs have enlarged hearts but are not in CHF, and are in Stage B2 of MVD. That medication is pimobendan, and the study is the EPIC Study, published in September 2016. Some cavaliers in Stage B2 of MVD may benefit from starting low doses of pimobendan, as long as they meet the strict minimum parameters of the EPIC Study findings.

So, as our main title asks, why do any veterinarians, even including some board certified cardiologists, prescribe the other drugs -- ACE-inhibitors, loop diuretics, and spironolactone -- to Stage B2 cavaliers since those drugs have not been shown to work in Stage B2?

We ask this question because, amazingly and unfortunately, many veterinarians do prematurely prescribe these drugs to cavaliers, and we are very concerned that these veterinarians are putting our CKCSs at risk of harm. None of these drugs, when given to a dog before they are medically needed, are harmless like sugar pills.


EnalaprilThe question of whether ACE-inhibitors can delay heart failure in CKCSs was answered with a definitive "NO" in 2002, when the SVEP Trial (Scandinavian Veterinary Enalapril Prevention Trial) was published. The SVEP study included 229 MVD-affected cavalier King Charles spaniels, of which 107 CKCSs also had heart enlargement (Stage B2). The researchers concluded that the ACE-inhibitor enalapril did not delay the onset of CHF, compared to the placebo group.

In addition to that SVEP Trial, in 2007 the manufacturer of enalapril sponsored a similar study (the VETPROOF Trial), which included 124 dogs of several breeds, only 10 of which were cavaliers. In that study, the authors found that the ACE-inhibitor enalapril "modestly delays the onset of CHF in dogs with moderate to severe mitral regurgitation."

They also grudgingly acknowledged the importance of the SVEP Trial results. They wrote:

"The VETPROOF, reported here, suggests that enalapril treatment provides a modest benefit in delaying onset of CHF, whereas the first and larger of these studies, the SVEP trial, does not."

The VETPROOF authors further acknowledged the importance of SVEP's 229 cavaliers versus their multi-breed enrollment with only ten cavaliers. They wrote:

"It is noteworthy that the natural history of mitral valve regurgitation and the RAAS in Cavalier King Charles Spaniels are different from those of other breeds".

Notwithstanding that conclusive peer-reviewed research evidence, even some cardiologists prescribe ACE-inhibitors before heart failure. In fact, a majority of the ten members of the 2009 ACVIM Consensus Statement panel recommended starting an ACE-inhibitor at Stage B2, although their reasoning was not included in the Consensus Statement, and the Consensus Statement recommendations apply to all breeds and not just CKCSs. Since the vote was not unanimous, the ACVIM Consensus Statement did not endorse ACE-inhibitor therapy of MVD dogs at Stage B2 MVD. Further, ACE-inhibitors have not been approved for veterinary medicine for MVD dogs in Stage B2 by regulating authorities.

Additionally, it is well established that ACE-inhibitors can have undesireable side effects, particularly to dogs' kidneys. ACE-inhibitors may contribute to renal dysfunction by activating the renin-angiotensin aldosterone system (RAAS). Other side effects include the accumulation of toxins which can damage the liver, anorexia or loss of appetite, vomiting, azotemia -- elevation of blood urea nitrogen (BUN) -- and the development of a dry cough due to the accumulation of bradykinin. Since a dry, hacking cough is a frequent symptom of progressing MVD, this side effect of the drug could be confused with the worsening of the disease.

So, why does any veterinarian prescribe ACE-inhibitors to MVD-affected cavaliers before heart failure?

Loop diuretics

LasixDiuretics, by definition, are intended to increase the excretion of water from the bodily system. When an MVD-affected cavalier reaches Stage C, congestive heart failure, that means that fluids are building up in the lungs or abdomen due to the heart not functioning properly. In fact, the word "congestive" refers to the build-up of fluids. So, it is very easy to understand why veterinarians would prescribe a loop diuretic, such as furosemide (Lasix), once the cavalier enters CHF.

The ACVIM Consensus Statement on MVD in dogs does not even suggest starting diuretics on MVD-affected dogs until the congestive heart failure stage.

But why would any veterinarian prescribe a diuretic to an MVD-affected cavalier which does not have any fluid build-up?


SpironolactoneThe most surprising MVD drug which we have found to be prescribed before heart failure is this one. Spironolactone is mild diuretic but also has other attributes which in some cases makes it a useful supplemental drug to cavaliers in CHF, when combined with the others -- pimobendan, ACE-inhibitor, and diuretic -- to delay the dog's death.

But there is no research evidence showing that spironolactone has any value at all when given to cavaliers not yet in CHF. Also, it has its own downsides. It is a potassium-sparing diuretic, meaning that it may lead to excessively high, life-threatening levels of potassium in the dog's blood, particularly when combined with ACE inhibitors.

Therefore, cautious veterinary cardiologists recommend that potassium levels be carefully monitored when using spironolactone in combination with ACE-inhibitors, by drawing blood at regular intervals until it is evident that the potassium level is or is not going to be a problem.

So, why would any veterinarian prescribe spironolactone to an MVD-affected cavalier before heart failure?

We suggest that you ask your vet, it if happens to your cavalier King Charles spaniel.

October 3, 2016:

Pimobendan’s EPIC Study: The BAD and the UGLY!

... And the cherry-picked GOOD news

Why have the researchers thumbed their noses at the CKCS?

Over-diagnosis can be good for the drug business

The long-awaited and highly vaunted final report on the EPIC (Evaluation of Pimobendan In Cardiomegaly) trial study was published on September 28, 2016. The trial has been of utmost importance to owners of cavalier King Charles spaniels (CKCS) because it has been thought that it could mean extending the lives and well-being of CKCSs suffering from mitral valve disease (MVD), which affects and kills more cavaliers than any other cause.

The questions the EPIC trial raised were whether daily oral administration of the drug pimobendan to MVD-affected dogs before they reached heart failure (CHF), (a) was safe and well tolerated, and (b) would prolong the length of time MVD-affected dogs lived before reaching CHF.

Pimobendan is a propriety drug owned and manufactured by the German pharmaceutical company, Boehringer Ingelheim Animal Health GmbH. The drug is not available as a generic. It is marketed primarily under the name Vetmedin, but also as Cardisure, Safeheart 5, and Fortekor Plus.

We have covered this trial from its inception in a series of articles on this blog site. (See our April 23, 2011, March 25, 2015, February 2, 2016, August 3, 2016, and September 30, 2016 articles.) As most of these previous articles indicate, we have been suspicious of the motives underlying this trial from the beginning. Our main concern has been that the trial has been fully financed by the manufacturer of pimobendan. The manufacturer’s underwriting included paying the 36 veterinary cardiologists involved in the study, including compensating them for their research, travel, speaking fees, consultancy fees, and preparation of educational materials, in addition to providing all of the pimobendan for the 360 dogs in the trial.

The hazards of pimobendan treatment before heart failure

Vetmedin Container WarningsPrior to release of the EPIC Study report, the universally recommended use of pimobendan had been limited to MVD-affected dogs only after they reached CHF. The reasons for delaying the start of pimobendan treatment until the dogs reached CHF has been due to prior peer-reviewed veterinary studies finding harmful side-effects if the dogs were treated before the need for the positive inotropic support of their hearts’ contractility, which pimobendan provides.

Specifically, these articles warned about the hazadous downsides of pre-CHF administration of pimobendan:

In “Comparative adverse cardiac effects of pimobendan and benazepril monotherapy in dogs with mild degenerative mitral valve disease: a prospective, controlled, blinded, and randomized study”, published in 2007 in the Journal of Veterinary Internal Medicine, the researchers found that "PIMO has adverse cardiac functional and morphologic effects in dogs with asymptomatic MVD."

In “Increased Mitral Valve Regurgitation and Myocardial Hypertrophy in Two Dogs With Long-Term Pimobendan Therapy”, published in 2005 in Cardiovascular Toxicology, the researchers concluded "This is the first report to describe an increase in mitral regurgitation under clinical conditions in dogs treated with pimobendan. We also suggest that pimobendan may induce ventricular hypertrophy."

In Cardiac Care for Pets (CVCA) “Pimobendan– A Silver Bullet?”, published in May 2009, the cardiology department stated: "In a small study performed by CVCA, it was determined that after two to three weeks of Pimobendan therapy about 75% of dogs had an increased frequency of ventricular arrhythmias documented on 24 hour ambulatory ECG monitoring."

In the U.S. Food and Drug Administration’s (FDA) 2007 report approving the use of pimobendan for dogs, it stated this conclusion in a four week toxicity study of pimobendan administered to 30 previously healthy lab Beagles:

“Conclusions: Pimobendan administered IV daily to healthy Beagles caused dose dependent increases in heart rate, mitral valve myxomatous thickening, left ventricular outflow tract endocardial thickening, and ventricular muscle ischemic lesions (multifocal subendocardial necrosis and scarring). The cardiac pathology seen in these dogs is typical of positive inotropic drug toxicity in normal dog hearts, and is related to the physiologic effect of the drug on contractility and exaggerated hemodynamic response.”

On Vetmedin’s website, it had this warning: “The safety of VETMEDIN has not been established in dogs with asymptomatic heart disease.”

Additionally, veterinary cardiologists spoke out against the pre-CHF use of pimobendan:

Dr. Amara Estrada warned: “There is evidence that treatment with a positive inotropic agent such as pimobendan prior to the development of systolic myocardial failure can have deleterious effects. ... Pimobendan ... should be reserved for use when systolic myocardial failure is detected or suspected.”

Dr. George A. Kramer warned: “Most dogs with chronic heart disease do not have decreased contractility and do not need positive inotropic support.”

Dr. Mark Rishniw warned: “One study in dogs with early mitral valve disease suggested an increase in valve damage in the dogs give pimobendan.”

Dr. Mark Kittleson, referring specifically to the EPIC trial while it was ongoing, warned:

“Because this study found pimobendan to be detrimental to dogs with MMVD it is the opinion of the author that further study was warranted prior to exposing 150 dogs to it in a large clinical trial (the EPIC study). Primum non nocere (first do no harm). It is also the opinion of the author that pimobendan should not be administered to dogs with MMVD prior to the onset of heart failure until the results of the EPIC trial are published. ... Will it prolong the time until a dog with MMVD goes into heart failure? That remains to be seen. Given the one study that has been done to date I don’t believe you can give this anything more than a 50:50 chance.”

Notice that the main focus of these warnings is about the damage that pimobendan could do to the hearts of pre-CHF dogs which are not in a depressed contractile state and therefore do not need the additional positive inotropic support which is the primary benefit of pimobendan. The measure of the need for positive inotropic support typically is determined by calculating left ventricle performance by such means as the ejection fraction or the fractional shortening percentage (FS%). While the baseline FS% of the dogs in the EPIC trial were calculated before administration of pimobendan began, no minimum or maximum FS% was a criterion in selecting or excluding the dogs for the trial, and there is no indication from the final report that any subsequent FS% measurements were taken. The initial median FS% were 43 (39-48) for the pimobendan dogs and 44 (41-49) for the placebo dogs.

Despite all of these warnings from peer-reviewed articles and board certified cardiologists (cited above), the EPIC trial was designed from the beginning to ignore the FS% as a parameter for the dogs to qualify for the study. Perhaps that was the factor which upset Dr. Kittleson so much. The designers of the study were willing to take the risk – a risk to be borne by the pimobendan dogs – that these dogs would survive the trial nonetheless.  They were intentionally flying blind.

The qualifications for dogs to be in the EPIC trial

The actual qualifications which the dogs had to meet were these: (a) A dog had to be 6 years of age or older; (b)have a mitral valve murmur of at least Grade 3 of 6; (c) have echocardiographic evidence of advanced MVD consisting of characteristic valvular lesions of the mitral valve, regurgitation through the mitral valve (MR) on the color Doppler echocardiogram, and have echocardiographic evidence of left atrial and left ventricular dilatation. All dogs entering the study met or exceeded three different heart size criteria. They are, first, the left atrial-to-aortic ratio (LA/Ao) equal to or greater than (≥) 1.6. Second, the normalized left ventricular internal diameter in diastole (LVIDDN) ≥ 1.7. Third, radiographic evidence of enlargement with a vertebral heart score (VHS) >10.5.

The unfortunate March 2015 press releases (advertisements)

Press ReleaseThe actual clinic phase of the trial for the 360 dogs started in early 2012 and was intended to last for three years, ending in early 2015. In March 2015 (notably early 2015), the three lead researchers quite surprisingly issued three press releases (two were identical) in which they announced that, because of an interim analysis that was performed in February, the trial was being ended “early”. The press releases boldly stated:

“A global clinical trial ... has found evidence of benefit of the drug pimobendan for dogs with mitral valve disease.”

“The interim analysis indicated that there was clear evidence of benefit of the administration of pimobendan in prolonging the time to the primary endpoint of the study, which was a composite of the development of left-sided congestive heart failure, or death presumed to be cardiac in origin. The interim analysis did not raise any concern over the safety of pimobendan administration.” (Link)

“A mid-study analysis in mid-February 2015 indicated that pimobendan is clearly beneficial and did not raise any concern over the administration of pimobendan.” (Link)

While the March 2015 press releases concluded with this statement – “Full and final results of the study are expected at a later date.” – the releases notably did not include the list of initial qualifications which the dogs in the trial needed to meet. So, while the readers of these press releases – essentially advertisements for the drug – knew of the success of prescribing pimobendan prior to heart failure, they were not told what the parameters needed to be to start the drug.

For eighteen months, from mid-March 2015 until September 28, 2016 when the EPIC Study report was published, all anyone not involved in the study knew was that pimobendan worked on pre-CHF dogs with MVD and some heart enlargement. And hundreds of veterinarians, including cardiologists, presumably fell for it, by prescribing pimobendan to asymptomatic MVD-affected dogs, without having any idea of what the dogs’ actual minimum echocardiographic and radiographic parameters needed to be.

What the final report DOES say

So now that the final report is out, what do the EPIC Study results show? Well, for sure, the end result has not Cherry Picking Warning Signdisappointed pimobendan’s manufacturer, in the least.

First of all, the researchers warn that:

“... it should be borne in mind when interpreting these results that all dogs included in the analyses also met the echocardiographic inclusion criteria and these results therefore might not be generalizable to all dogs with a VHS > 10.5 in the absence of concurrent echocardiographic measurements and a confirmed diagnosis of MMVD.”

Therefore, to apply the results of this study to future treatment of MVD-affected dogs, an x-ray of the heart showing a VHS value over 10.5 is not sufficient by itself, and that the two echo measurements must also be confirmed.

Of 354 dogs in the study, 161 (45.5%) were cavalier King Charles spaniels (CKCS) -- the largest breed group. Therefore, the results of this study obviously are of supreme importance to owners of cavaliers. Of those 354 dogs, 178 of the dogs were treated with pimobendan (77 CKCSs), and 180 received the placebo (81 CKCSs). Of those 178 dogs treated with pimobendan, 59 (33.1%) reached congestive heart failure (CHF), 15 (8.4%) died of cardiac-related deaths during the treatment. The others had not reached CHF by the time the study ended. Unfortunately, the report does not tell us how many cavaliers were in any of these categories.

Median time to the “primary endpoint” (CHF or death) was 1228 days in the pimobendan group and 766 days in the placebo group. Dogs in the pimobendan group lived longer, with a median survival time of 1059 days in the pimobendan group and 902 days in the placebo group. But, the study does not tell us how many of those deaths were attributable to MVD. Surely they have that information. Why they have failed to include it in their report is mystifying.

As for the dogs which died prior to reaching CHF, the authors explained that:

“Although a greater number of dogs in the pimobendan group experienced spontaneous cardiac death (12 versus 5), the proportion of dogs in each group experiencing this event was not significantly different.”

The report concludes:

“Chronic oral administration of pimobendan to dogs with echocardiographic and radiographic evidence of cardiomegaly secondary to MMVD, in the absence of concurrent cardiovascular medication, results in the prolongation of the preclinical period, and is safe and well tolerated. The median time to the onset of CHF or cardiac-related death was prolonged by approximately 15 months, and the risk of a dog experiencing this event was reduced by approximately one-third; the majority of the benefit observed was attributable to delaying the onset of CHF. This substantial degree of prolongation of the preclinical period is f clinical relevance and is of importance to veterinarians and owners of dogs affected by this common disease.”

So, the bottom line is:

(1) The dog must be in Stage B2 of mitral valve disease; AND
(2) Have a murmur of at least Grade 3; AND
(3) The dog must NOT be on any other cardiac medication; AND
(4) An echocardiogram must be conducted and show valvular lesions of the mitral valve, regurgitation through the mitral valve (MR) on the color Doppler echocardiogram, and have echocardiographic evidence of left atrial and left ventricular dilatation (defined as a left atrial-to-aortic root ratio [LA/Ao] equal to or greater than 1.6 and body weight normalized left ventricular internal diameter in diastole [LVIDDN] equal to or greater than 1.7); AND
(5) X-rays most be obtained, showing evidence of enlargement with a vertebral heart score (VHS) value greater than 10.5.

This essentially means that once the MVD-affected dog develops a Grade 3 murmur and an x-ray showing enlargement, the owner should have a board certified veterinary cardiologist perform a thorough echo exam.

The BAD and the UGLY!

But what is most disturbing is what is not in the EPIC Study report. We know the cherry-picked GOOD news -- that pre-CHF EPIC Faildogs which are treated with pimobendan and are were lucky enough not to die, could stave off the CHF much longer than dogs on sugar pills. But what about the BAD and the UGLY? The report is loaded with unanswered questions. Notable examples of the BAD and the UGLY:

• The recommended x-ray and echo measurement parameters were set at the outset of the study, rather than scientifically determined as a result of the study. Since the conclusion of the EPIC Study includes very precise minimum heart measurement criteria (VHS >10.5; LA/Ao ≥ 1.6; LVIDDN ≥ 1.7), one would have hoped that the researchers made those determinations by a careful analysis of the results of the study. But, no, the exact opposite was the case. The lead researchers made up those parameters before the study even began. And they did not re-visit those parameters after the study ended, to determine if their initial determinations are safe and otherwise appropriate. The fact is that at least one of the those three parameters -- the VHS measurement -- is so off base for cavaliers that it can be life-threatening.

The average heart-healthy cavalier has a VHS value above 10.5. It is troubling that the study report fails to note that normal, heart-healthy cavaliers typically have VHS measurements as high as 11.7, which is VHS Value Measurement Methodnotably higher than the 10.5+ criterion for beginning pimobendan treatment. Considering that nearly half of the dogs in the study were CKCSs, this oversight is rather inexplicable and potentially life-threatening.

Bizarrely, the researchers’ footnoted citation justifying this VHS score is an article which expressly states:

“The use of breed-specific VHS values is needed for the VHS method to have a high specificity for normal heart size.”

It previously has been customary when cardiologists determine heart enlargement using VHS values, to compare the current x-ray with previous ones, such as a baseline x-ray. Indeed, the ACVIM’s 2009 Consensus Statement specifically recommends, for Stage B dogs, to obtain baseline x-rays. It states:

“Thoracic radiography is recommended in all patients to assess the hemodynamic significance of the murmur and also to obtain baseline thoracic radiographs at a time when the patient is asymptomatic for CVHD.”

Therefore, it is perplexing as to why this EPIC Study, being hyped as “top tier” by its chief lead researcher, ignores breed-specific VHS values (which the same researcher previously had recommended as "needed for the VHS method to have a high specificity"), and establishes an unfounded and abnormal parameter for the cavalier King Charles spaniel. More importantly for cavaliers, it ignores the individual patient’s specific VHS value compared to the dog's baseline x-ray.

There is nothing "top tier" about a study which ignores the basic research principle that differences likely influenced by genetic factors should be taken into account when designing clinical trials, and also most particularly in this instance, when making recommendations about parameters to be followed by clinicians hereinafter.

But if the manufacturer’s goal is to sell more pills, then reducing the threshold VHS value to significantly below the average score of a healthy cavalier, will do just that -- sell more pills. Let’s face it, the CKCS breed will be its biggest customer.

The study glosses over pimobendan causing sudden deaths. It also is disappointing that the study Sudden Deathdoes not go into any details about 8.4% of dogs being treated with pimobendan and which suffered cardiac-related deaths while only in Stage B2. While the authors do acknowledge that “concerns had previously been raised about possible detrimental effects of the administration pimobendan to dogs with preclinical MMVD”, they provide nothing to explain why pimobendan played a role in those sudden and unexpected Stage B2 deaths. To the contrary, they seem to be patting themselves on the back for even including any data on these premature cardiac deaths, stating:

“If our primary endpoint had focused exclusively on the onset of CHF, with dogs that died being censored, it might have appeared that we were choosing to ignore potentially detrimental effects of the treatment.”

Well, it certainly does appear that they have chosen to ignore those detrimental effects. Instead, they minimize these premature deaths of pimobendan-treated dogs by stating:

“We found, not unexpectedly, that only a small number of dogs met the primary endpoint in this way. Although a greater number of dogs in the pimobendan group experienced spontaneous cardiac death (12 versus 5), the proportion of dogs in each group experiencing this event was not significantly different.”

 How many of the suddenly dead pimobendan group dogs were cavaliers? We are not told. What if all of the dead pimobendan dogs were cavaliers? (That is not so far-fetched, considering the unreasonably low VHS threshold of >10.5.) That would amount to 15.5% of all of the CKCSs in the pimobendan group. If 15.5% of the cavaliers in the pimobendan group died suddenly, would that make a “significant” difference?

In a prior peer-reviewed study of 317 human patients, the researchers found that: “In both pimobendan groups combined the hazard of death was 1.8 times higher than in the placebo group”, and those researchers made a big deal of that finding. Ironically, in this EPIC Study, the death hazard of pimobendan was 2.4 times higher than the placebo group, and the EPIC Study researchers just blow that significant fact off like it does not matter a whit.

How can they conclude that pre-CHF dosing of pimobendan “is safe and well tolerated”, when nearly 10% of the dogs died cardiac-related deaths suddenly while being given pimobendan, and the researchers made no effort to find out those dogs’ precise causes of death? Well, that is what the manufacturer wanted them to conclude. “Safe and well tolerated” was one of the two main goals for the EPIC Study. So, by minimizing the significance of all of the pimobendan-caused sudden deaths, that goal of “safe and well tolerated” has been attained.

The study ignored the affect of pimobendan on contractility and systolic function of the dogs’ hearts. Despite the researchers acknowledging that “concerns had previously been raised about possible detrimental effects of the administration pimobendan to dogs with preclinical MMVD”, they did not bother to report measurements of the contractility and/or fractional shortening of the dogs’ hearts during the treatment period. Since prior peer-reviewed studies cited above have shown that “long-term administration of PIMO in dogs with asymptomatic MVD is associated with an increase in systolic function and, concomitantly, a progressive worsening of MVD with development of specific mitral valve lesions”, this periodic measurement could have predicted (and presumably avoided) the sudden deaths among the pimobendan dogs. That is another messy little detail which would not have made the manufacturer very happy.

When a study ignores these previously detailed, scientifically determined hazards of the premature administration of pimobendan (over-stimulating the well-compensated heart’s contractility), and instead the study is based upon superficial appearances (an enlarged heart), that study can easily lead to false positives. False PositivesIn such a case, it really does not matter that the current study includes a larger number of dogs than the previous clinical ones. What matters is the damage done -- and to be done in the future -- because of the risks taken. The failure to examine that damage -- in this case, the causes of death of nearly 10% of the dogs in the pimobendan group -- aids and abets the potential for those false positives. Minimizing the negative results points to a manufacturer-driven study.

The report excludes the study’s own evidence of pimobendan shortening life spans after CHF. While it is not at all clear in the published article, at the ACVIM conference in June 2016, where the results of this study were orally presented to attending cardiologists, it was reported that once the dogs reached CHF, the subsequent life spans of the pimobendan dogs were shorter than the life spans of the placebo dogs. It therefore suggests that once CHF develops, life expectancy actually shortens for dogs treated with pimobendan, relative to untreated dogs. The researchers have not included this information in their article, but that missing data raises the question of whether the shortened life span of CHF dogs treated with pimobendan during Stage B2 is due either to drug toxicity or to an acquired pharmacological tolerance to the pimobendan.

The report does state that, “The median time to death by all causes was 1059 days in the pimobendan group [83 dogs] and 902 days in the placebo group [103 dogs]”. (Emphasis added.) But it fails to break out the numbers of dogs which died of MVD or MVD-related disorders. So, the data which the authors provide on this topic in their report is pretty much worthless, and they are silent on the topic which would have been most relevant: How much longer, or shorter, did pimobendan dogs live than did placebo dogs before dying MVD-related deaths?

One of the lead investigators. shortly after publication of the EPIC Study, stated that, “We intend to publish at least one further paper relating to the study, which will provide longitudinal follow up on dogs in the study." That is well and good, of course, but unless that further paper is published promptly, there will be another undue delay -- like the 18 month one between the March 2015 press releases and the report itself -- in finding out what value pimobendan, if any, may have in extending the lives of MVD-affected dogs. Meanwhile its Coulda Woulda Shouldamanufacturer will be able to continue to bask in the unsubstantiated hype and promises that pre-CHF administration of pimobendan will not only delay the onset of heart failure, but also extend the lifespans of the dogs. For example, that same lead investigator reportedly told the UK Telegraph in October 2016 that, “This is a major breakthrough in treatment and could extend the lives of dogs around the world.” “Could" is the operative word there,  because no evidence has been presented in the published report that pimobendan added to the longevity of any dogs dying of mitral valve disease.

• The researchers provide no breed-specific information.  There were 360 dogs in this study. Nearly half of them were cavalier King Charles spaniels. And yet, the report includes no data specific to cavaliers -- or to any other breed, for that matter. The authors had a year and a half after the conclusion of the trial, to sift through the data and analyze every aspect of them, before publication. But no breed-specific breakdown is to be found. No breed is going to be more affected by this study than the CKCS.

Researchers Thumb Their Noses At CavaliersThe researchers also ignored prior studies showing the importance of using breed-specific heart measurements for that breed -- thereby placing the CKCS at greater risk than other breeds when taking the drug prematurely. This is just about the least informative study of the safety and effectiveness of any drug with a prior record of toxicity, in this century. Why would experienced veterinary cardiology researchers ignore their own prior warnings of the vital importance of breed-specific heart measurements and also fail to calculate the breed-specific data they collected in this study? Why have the researchers thumbed their noses at the cavalier King Charles spaniel?

The report precludes treating pre-CHF dogs with any other cardiac medications. Since the EPIC Study excluded any dogs being treated with cardiac drugs other than pimobendan, this means that previous common protocols, such as prescribing an ACE-inhibitor (e.g., enalapril or benazepril) to MVD-affected dogs in Stage B2, are out the window from now on. In fact, the authors brag about not needing any other medications in Stage B2, stating:

“An additional strength of the study is the absence of the confounding effect of any concurrent cardiovascular medications”.

This is an added benefit to pimobendan’s producer, conveniently giving it a peer-reviewed monopoly on pre-CHF treatment of MVD-affected dogs.

The authors try to defend the manufacturer's total financial control over them. Interestingly, the authors bend over backwards to justify the full funding of this study by the manufacturer of pimobendan. They essentially explain that, ‘that’s the way it is in the veterinary field.’ Specifically, they state:

“that the majority of published clinical trials are sponsored by industry. In the veterinary field, there are no large independent funding organizations comparable to the National Institutes of Health (NIH) that are likely to be able to (or wish to) fund a study of the magnitude of the one we describe; therefore, such studies are only likely to be achieved with industry sponsorship. Potential explanations of the increased likelihood of industry-sponsored research having positive findings include the following: Industrial sponsors might be more likely to support studies that are likely to succeed, industrial sponsors might design studies with an inappropriate comparator group, or there might be publication bias with unsuccessful studies being less likely to be published.” (Emphasis added.)

There is a term used in the scientific research field for this type of defensive excuse making: “publication bias”, and the authors even use it in the quote above. When they write, “... unsuccessful studies being less likely to be published”, they could add, “unsuccessful results within studies” to the list of those being less likely to be published. And it is also apparent in the next topic discussed here: the glaring conflict between the March 2015 press releases and the actual findings in the September 28, 2016 journal article.

The report flatly contradicts the braggadocious press releases issued 18 months earlier. But the absolutely most irresponsible fact to be drawn from this report is the March 2015 press releases issued by the three lead researchers, which unqualifiedly stated:

“The interim analysis indicated that there was clear evidence of benefit of the administration of pimobendan in prolonging the time to the primary endpoint of the study, which was a composite of the development of left-sided congestive heart failure, or death presumed to be cardiac in origin. The interim analysis did not raise any concern over the safety of pimobendan administration.” (Emphasis added.)
“A mid-study analysis in mid-February 2015 indicated that pimobendan is clearly beneficial and did not raise any concern over the administration of pimobendan.” (Emphasis added.)

Nowhere in any of those self-laudatory press releases did any of the researchers warn of the vital importance of first performing two precise echocardiographic measurements and a radiographic measurement before dosing pimobendan to MVD-affected dogs prior to CHF.

Since the researchers knew in advance of those press releases what the essential parameters were for the dogs participating in the trial, they easily could have included those parameters in their press releases. But they did not. And so, for 18 months, from March 2015 to September 2016, every cardiologist and internal medicine specialist and general practice veterinarian was intentionally misled about the essential parameters which had to be met before prescribing pimobendan. This obviously indicates the danger of veterinary researchers ignoring their own professional judgment and instead signing their names to such irresponsible advertisements which must have been pushed upon them by the manufacturer with the checkbook.

It is a WIN-WIN for pimobendan’s manufacturer!

This study, unfortunately, has cut corners and added risks to cavaliers. Anyone with a cavalier should proceed with caution because the study has not been designed to take into account the special needs of cavaliers. It appears that the EPIC Study has not been about avoiding the risking of the lives of MVD-affected dogs, especially cavaliers. False positives and publication bias all point to a pre-determined goal: over-diagnosis so that one manufacturer may sell more of its exclusive product than ever before. It is a terribly unfortunate thing, but it is not a surprising thing.  A lesson to be learned is that veterinary researchers need to learn to say “NO!” to sole-source drug manufacturers.

September 30, 2016:

So your cavalier has a heart murmur. What do you do next?
UPDATED since the EPIC Study!

The ACVIM says: Get an x-ray, not an ultrasound!

Vet auscultating a cavalierSince over half of all cavalier King Charles spaniels may be expected to develop mitral valve murmurs by age 5 years, it should come as no surprise when your veterinarian tells you that your cavalier has one. But there is no reason to panic. The American College of Veterinary Internal Medicine (ACVIM*) has a sensible list of steps to take once a murmur is first detected in your CKCS.

For the record, the ACVIM recommends that cavaliers be screened annually by “auscultation” (examination by stethoscope) by board certified cardiologists. Specifically, ACVIM** states:

“Owners of breeding dogs or those at especially high risk, such as Cavalier King Charles Spaniels, may choose to participate in yearly screening events at dog shows or other events sponsored by their breed association or kennel club and conducted by board-certified cardiologists participating in an ACVIM-approved disease registry.”

For that reason, CavalierHealth.org has a list of upcoming heart screening clinics in the USA and Canada, which is updated weekly.

Once a murmur is detected by the vet, the first thing to realize is that you do not need to rush your dog to have an ultrasound (echocardiograph) scan of its heart. Instead of an ultrasound, the ACVIM recommends that you get your dog’s heart x-rayed to be a “baseline” for measuring the heart size against future x-rays after any heart enlargement takes place. The ACVIM states:

“Thoracic radiography [chest x-ray] is recommended in all patients to assess the hemodynamic significance of the murmur and also to obtain baseline thoracic radiographs at a time when the patient is asymptomatic for CVHD [chronic valvular heart disease].”

X-ray of cavalier's heartThe ACVIM does not recommend that cavaliers with new murmurs be ultrasounded unless the auscultation and the x-ray do not adequately satisfy the cardiologist about the true cause of the murmur and the heart does not appear to be significantly enlarged. Specifically, this is what the ACVIM states about ultrasounding cavaliers once a mitral valve murmur is detected:

“In small breed dogs with typical murmurs, echocardiography is recommended to answer specific questions regarding either cardiac chamber enlargement or the cause of the murmur if those questions are not answered adequately by auscultation and thoracic radiography.”

Note that the only “baseline” that the ACVIM recommends for cavaliers with new murmurs is an x-ray and not an ultrasound, as long as the cardiologist is satisfied that the stethoscopic exam and the x-ray confirm the cause of the murmur.

The EPIC Study's recommendations

In September 2016, a large team of board certified veterinary cardiologists issued a report, called the EPIC Study, revising how to diagnose and treat MVD-affected dogs once their hearts begin to enlarge significantly. Their conclusions do not change the above-described steps the cavalier's owner should take when a murmur is first detected, which is to get those baseline x-rays.

But the EPIC Study recommends that once an MVD-affected dog's heart murmur reaches Grade 3, if any x-rays -- the baseline or later ones -- show that the dog's heart has begun to enlarge (Stage B2 MVD), then the owner should have a cardiologist perform an ultrasound scan of the dog's heart -- an echocardiogram.

The EPIC Study's bottom line for starting pimobendan in Stage B2 is:

(1) The dog must be in Stage B2 of mitral valve disease; AND
(2) Have a murmur of at least Grade 3; AND
(3) The dog must NOT be on any other cardiac medication; AND
(4) An echocardiogram must be conducted and show valvular lesions of the mitral valve, regurgitation through the mitral valve (MR) on the color Doppler echocardiogram, and have echocardiographic evidence of left atrial and left ventricular dilatation (defined as a left atrial-to-aortic root ratio [LA/Ao] equal to or greater than 1.6 and body weight normalized left ventricular internal diameter in diastole [LVIDDN] equal to or greater than 1.7); AND
(5) X-rays showing evidence of enlargement with a vertebral heart score (VHS) greater than 10.5.

If and when the cardiologist determines from the x-ray and the measurements from the echocardiogram, that the dog's heart has enlarged enough, the EPIC Study's recommendation is that the cardiologist may prescribe treatment with pimobendan. Prior to publication of this EPIC Study, the consensus was to not treat MVD-affected cavaliers with any medications until the MVD progressed to heart failure.

* The ACVIM certifies veterinary cardiologists. A list of them in the USA and Canada is available here.    
See the ACVIM's "Guidelines for the Diagnosis and Treatment of Canine Chronic Valvular Heart Disease", page 1144.

August 18, 2016:

Is the University of Washington’s
“Rapamycin Intervention Trial in Pet Dogs” Unethical?

 Thus far, all we have is publication of it’s misleading “findings”
and an obvious fund-raising campaign

Peer ReviewOwners of cavalier King Charles spaniels are all excited about the prospects of a miracle drug called “rapamycin” curing their dogs’ mitral valve disease (MVD). They are being duped.

The University of Washington is conducting a series of studies of rapamycin*, boldly called the “Dog Aging Project”, with the announced goal of determining if “rapamycin is effective at improving cardiac function in dogs at doses without significant side effects.”

The researchers, mostly in the university’s pathology department, have divided their study into two phases. “Trial One”, concluded this month, was to “determine appropriate dosing of rapamycin and document cardiac improvements.” Only 24 dogs participated in this 9-month study, all golden retrievers, Labrador retrievers, and German shepherd dogs over 40 lbs. Half of those – twelve in all – received rapamycin, and the other half received a placebo. Interestingly, they started with 40 dogs, but specifically excluded any found by echocardiogram to have even an asymptomatic heart valve disorder. The second phase, “Trial Two” is seeking participants via their study’s dedicated website, which also includes a fund-raising campaign.

Our complaint is with the way they have publicized Trial One. Keep in mind these facts about it:

(1) Trial One ended this month (August 2016).
(2) The researchers immediately issued a press release announcing:
“As of August, 2016, we are finishing the analysis of the data for the dogs that completed the phase 1 study and hope to submit the results for publication within the next few months. The key findings are that there were no significant side effects associated with the rapamycin treatment, and there were statistically significant improvements in heart function in the dogs that received rapamycin relative to those that received the placebo, similar to what has been observed in older laboratory mice.
“... We view these initial results as highly encouraging, however, and feel that this phase 1 study provides a strong justification for the next phase of the intervention trial which will follow dogs for three to five years.**

So, not only has there been no peer-reviewing of this study, but the researchers admit that they have not even finished the analysis of the data. Nevertheless, they boldly make the assertion that the dogs receiving rapamycin had significant improvements in heart function!

Needless to say, the press has jumped on the bandwagon. For instance, the UK’s Telegraph’s headline on August 15 was “Trial to extend life of dogs shows ‘significant improvements’ in heart health, say scientists”. The Telegraph’s article goes on to state: “it could help dogs live for an extra four years.”

So, whatever happened to following the ethical rules of scientific research? For instance, what has become of the need for full analysis of the data, followed by a carefully drafted article, which then is peer reviewed before a whisper is heard about the results of the study?

If you have any doubts about whether the August 2016 press release was unethical, consider that in the world of scientific research, it is highly unusual for raw research data, much less any results, to be leaked publicly before peer-reviewing and the official publication of the peer-reviewed article. Further, it used to be unheard of for there to be an official public release of any such premature information, issued by the researchers. Any such prior disclosure normally is considered unethical and unprofessional in the scientific research arena.

See, “What is Ethics in Research & Why is it Important?”, by David B. Resnik, J.D., Ph.D. National Institute of Health website, 2011:

“There are many other activities that the government does not define as ‘misconduct’ but which are still regarded by most researchers as unethical. These are called ‘other deviations’ from acceptable research practices and include: ... Bypassing the peer review process and announcing your results through a press conference without giving peers adequate information to review your work.

Consider the fine print behind the University of Washington researchers’ boasts. The study was limited to twelve large-breed dogs – none of which had a hint of MVD – taking rapamycin for nine months. Whether any of these dogs really did display any improvement in heart function remains to be seen. One thing we know is that their hearts already were functioning properly, because dogs with any sign of a heart problem were excluded.

We have seen another instance of this kind of research abuse recently. The glorified (and apparently exaggerated) results of the EPIC Trial, about which we have written several articles, were announced in this same seemingly unethical manner in three press releases (one each from the three lead researchers), within days of the EPIC trial’s end in March 2015.  The actual peer-reviewed article has yet to be published.

Let us hope that this tactic, of falsely whipping up the hopes of owners of MVD-affected cavaliers, comes to an end quickly, and is not just a beginning.

* Rapamycin is a bacteria-produced immunosuppressive agent used mainly to prevent the rejection of transplanted organs. It also is known as “sirolimus” and the brand name “Rapamune”.

** The press release does contain this disclaimer, which nonetheless does not excuse the researchers from publishing anything at all at this stage:  “It is important to keep in mind that this is a small study that requires replication before we can be confident in these results. It is also important to recognize that we don’t have any evidence that the improvements in heart function indicate overall improvements in health or slower aging in these dogs or even what the long-term effects of rapamycin will be.” 

August 3, 2016:

Whither the EPIC Trial's final report?

Something about it smells terribly funny

Bad SmellLast February, we blogged that “EPIC trial results are scheduled to be announced at the ACVIM Forum in Denver on June 9”, and we added, “15 months from the end of the trial to publication of its results”. The trial ended in March 2015 and was promptly followed by tantalizing press releases claiming:

"The interim analysis indicated that there was clear evidence of benefit of the administration of pimobendan in prolonging the time to the primary endpoint of the study, which was a composite of the development of left-sided congestive heart failure, or death presumed to be cardiac in origin. The interim analysis did not raise any concern over the safety of pimobendan administration."

Apart from those extraordinarily inappropriate* March 2015 press releases, while it was true that a brief summary of the EPIC Trial findings was orally presented to a handful of veterinary cardiologists in June, very little of that information has leaked out, and the nitty-gritty data, findings, and conclusions remain under wraps. So that makes it 17 months now, since the end of the EPIC Trial, and still nothing published about it.

In the meantime, more and more veterinarians, seeing only those press releases, are prescribing pimobendan (Vetmedin, Cardisure, Safeheart 5, Fortekor Plus) willy-nilly to cavaliers with only the whispered hint of a mitral valve murmur, because they think that the EPIC Trial is all about starting doses of pimobendan as early as possible and with no exceptions. And, obviously, this is exactly what Vetmedin’s manufacturer must want to happen.

We know from prior peer reviewed veterinary journal articles and cardiologists’ observations that the premature use of pimobendan – prescribing it to dogs either not in heart failure or not needing augmentation of cardiac output – can accelerate the progression of MVD and irreversibly damage the dogs’ hearts. And yet, know-it-all vets – including some cardiologists – are jumping the gun and prescribing this dangerous drug to our cavaliers which are not even close to heart failure.

Cautionary Statements About Pimobendan

It is inexplicable as to why the EPIC Trial’s final report has not yet been peer reviewed and published in a veterinary journal. The latest rumor is that the report will be published “this fall”, probably in the Journal of Veterinary Internal Medicine. Whenever and wherever that may be, the premature prescribing of pimbendan has been rampant since those March 2015 press releases, and if the final report includes any exceptions to giving pimobendan to any cavalier with only a mild murmur and slight enlargement of the heart, somebody is going to have a lot of explaining to do. Something about this foot-dragging smells terribly funny, and appears to be all to the financial advantage to Vetmedin's manufacturer.

* See, "What is Ethics in Research & Why is it Important?", by David B. Resnik, J.D., Ph.D. National Institute of Health website, 2011: “There are many other activities that the government does not define as ‘misconduct’ but which are still regarded by most researchers as unethical. These are called ‘other deviations’ from acceptable research practices and include: ... Bypassing the peer review process and announcing your results through a press conference without giving peers adequate information to review your work.”

April 15, 2016:

OFA finally recognizes what mitral valve disease is all about

Two steps forward and one step sideways for the still-provincial
Orthopedic Foundation for Animals

OFAThe Orthopedic Foundation for Animals (OFA) has been mired in the mid-20th century since its inception in the 1960s. But, finally, at least in this month of April 2016, OFA has recognized that mitral valve disease (MVD) is not “congenital”*. For decades, OFA has maintained a database of heart defects titled “Congenital Cardiac Database”. Even though MVD is an “acquired”** disorder and therefore not congenital, OFA fortunately has included MVD test results in its Congenital Cardiac Database. We suppose that an organization with “orthopedic” in its name may be excused for not quite grasping the elementary aspects of the non-orthopedic but most widespread herditary disease and killer among cavalier King Charles spaniels.

* Congenital means that the disease or physical abnormality existed in utero or at birth.
** Acquired means that the disease began developing after birth.

Effective this month, OFA has attempted to right this wrong, although it still shows that it does not fully understand exactly what MVD is all about. As of April 1, OFA has joined with the American College of Veterinary Internal Medicine (ACVIM) to create a new “Advanced Cardiac Database” to distinguish between congenital and what OFA has labeled “adult-onset” cardiac diseases. It will serve two primary purposes:

“1. Develop an appropriate screening protocol for adult onset cardiac diseases; and

2. Begin collecting better data on cardiac disease prevalence and progression in the purebred dog.”
OFA Advanced Cardiac Database

According to OFA, the examinations for the Advanced Cardiac Database must be performed by board certified veterinary cardiologists. This is a huge step forward for OFA. Previously, practitioner veterinarians have been allowed to perform these tests for OFA’s database purposes.

The cardiologist will send the exam results to OFA and the ACVIM

The most significant change will be the reporting procedure to OFA. Previously, the only copy of the veterinarian’s exam report was given to the dog’s owner, to either submit to OFA for its database or to not do so. Hereafter, the new OFA advanced cardiac examination forms will be in triplicate. As in the past, one copy of the completed exam form will be given to the dog's owner. (See a copy of the new form, below.) However, regardless of whether or not the owner sends his copy of the form to OFA for official certification, the examining cardiologist will retain one copy of the form and submit it to OFA and the ACVIM, to be used only to record results on its database, in order to collect better heart disease prevalence and progression data by breed. If the cardiologist also performs an echocardiogram, the new form’s echo section is far more detailed, to collect statistics regarding flow rates, velocities, etc.

The dog owner’s responsibility for obtaining an official OFA clearance certification number remains the same as in the past. Owners must submit their copy of the completed, signed form to OFA along with the filing fee. OFA clearances under the Advanced Cardiac Database will be valid for only 12 months. If the owner wants the adult onset cardiac clearance to remain current, repeat exams will be necessary.

OFA still does not grasp how and when MVD develops in cavaliers

While this step obviously is progress, since previously OFA did not officially recognize the existence of non-congenital heart disorders, OFA still does not appear to fully grasp how MVD develops, particularly in cavalier King Charles spaniels. OFA seems to think that there are only two categories of cardiac diseases in dogs – the congenital type and the “adult-onset” type. In fact, MVD is not necessarily an adult-onset disorder, since statistics have shown that as many as 10% of cavaliers have developed MVD murmurs before their first birthday. Incidentally, OFA’s minimum age for dogs undergoing these cardiac examinations is 12 months, which is not quite the age of adulthood for CKCSs.

For more information, see OFA’s press release here.  The new Advanced Cardiac Database form is below. A pdf version is downloadable here.

OFA's Advanced Cardiac Database form

April 14, 2016:

A Giant Leap Backwards:

Some USA cavalier breeders boycott posting
health test clearances on the OFA website

They must want to keep other breeders and pet buyers in the dark

OFAThe Orthopedic Foundation for Animals (OFA) was founded in 1966 in the USA to “promote the health and welfare of companion animals through a reduction in the incidence of genetic disease.” Its main objectives include:

• To collate and disseminate information concerning orthopedic and genetic diseases of animals.

• To advise, encourage and establish control programs to lower the incidence of orthopedic and genetic diseases.

OFA’s primary means of carrying out its objectives is its on-line database of health testing clearances of breeding stock. As OFA explains it:

“The OFA databases are core to the organization’s objective of establishing control programs to lower the incidence of inherited disease. Responsible breeders have an inherent responsibility to breed healthy dogs. The OFA databases serve all breeds of dogs and cats, and provide breeders a means to respond to the challenge of improving the genetic health of their breed through better breeding practices. The testing methodology and the criteria for evaluating the test results for each database were independently established by veterinary scientists from their respective specialty areas, and the standards used are generally accepted throughout the world.”

Responsible cavalier breeders post all health clearances on OFA's website

Responsible breeders have their breeding stock tested by veterinary specialists according to OFA’s protocols, for such genetic disorders as hips, elbows, heart, eyes, and patellas. If a dog passes a test, OFA issues a certification number to the dog for that test and posts the test result in its databases on its website. That is, if the dog’s owner allows OFA to post the health clearance result. Responsible breeders, of course, authorize the posting of those clearances for their dogs. Irresponsible breeders do not.

Recently, more and more breeders of cavalier King Charles spaniels are announcing their intention to not allow OFA to post the health clearances of their breeding stock. (See one of their posters below.) They claim that a few disgruntled pet buyers are using missing health-testing information about dogs on OFA’s website to accuse the breeders of either not testing their breeding stock or not following breeding protocols based upon the results of those health tests.

Cavalier breeders' excuses for boycotting OFA are spurious

Boycott OFA's DatabasesThese cavalier breeders’ excuses for boycotting OFA are spurious. These breeders fall into three categories:

1. Previously, some of these breeders have allowed OFA to post on its public databases some of their dogs’ health testing clearances, but not all of them.

2. Others of these breeders have never allowed OFA to post any of their dogs’ health testing clearances.

3. And, in some instances, unfortunately, some cavalier breeders do not bother to health test their breeding stock, at all.

But regardless of which category they fall within, their argument for now not allowing OFA to publicly post any health clearances, is that disgruntled pet owners are using their dogs’ publicly posted clearances on the OFA website to accuse them of not testing their dogs before breeding them. The illogic of that excuse is stunning. Clearly, if all of these breeders’ dogs’ health-testing clearances are posted on OFA’s website, the complainers would have nothing to accuse the breeders of not doing.

The fact is, as we have witnessed so many times over the past decades, some cavalier breeders care only about their own breeding program and not one whit about the health and welfare of future generations of cavalier King Charles spaniels here in the USA.

They claim that whether and when their dogs have passed health tests is nobody’s business but their own. They claim that they will provide their puppy buyers with copies of the health test clearances, but no one else should be allowed to see those papers. These breeders are selfish and short-sighted, because they fail to recognize the importance of making available their dogs’ health test results for future generations of breeding stock to be bred by other breeders, even decades from now.

So, the bottom line clearly is that any cavalier breeder in the USA who refuses to allow OFA to publicly post all of their dogs’ health test clearances, by definition, is an irresponsible breeder.

February 2, 2016:

EPIC trial results are scheduled to be announced
at the ACVIM Forum in Denver on June 9

15 months from the end of the trial to publication of its results

Why wait so long?

The results of the EPIC* Trial, a five-year study of up to 360 dogs suffering from pre-heart-failure MVD, will EPIC Trialbe announced at ACVIM’s annual forum in Denver, Colorado on June 9, 2016. All three lead researchers, Drs. Adrian Boswood, Sonya Gordon, and Jens Haggstrom, are scheduled to participate in the “EPIC Trial Results” session that morning.

The EPIC Trial, fully funded by Boehringer Ingelheim, the manufacturer of pimobendan (Vetmedin), began in 2010 as a placebo-controlled clinical trial evaluating the effectiveness of pimobendan in the prevention of the onset of signs of congestive heart failure in dogs with cardiac enlargement secondary to pre-clinical MVD. Thirty-six veterinary cardiologists from all over the globe participated, each examining ten MVD-affected dogs over the following five years, ending March 1, 2015.

The boastful March 2015 announcements were unethical and premature

Peer ReviewSince publication of three clearly unethical**, premature public announcements*** in March 2015 of non-peer-reviewed “interim analysis”, claiming “clear evidence of benefit of the administration of pimobendan in prolonging the time to the primary endpoint of the study”, a Dr. Sonya Gordon's Pre-Peer-Review Comment About EPIC Resultslid has been firmly placed upon the actual results of the study.**** See, for example, Dr. Gordon's clearly inappropriate statement which she made in her March 2015 press release, at left.

It will have been an extraordinary length of time -- over fifteen months to be exact -- between the March 1, 2015 end date of the study and the June 9, 2016 release of the actual (and presumably) peer-reviewed results. The scheduled date of the release reportedly has been postponed twice, without explanation.

The March 2015 press releases had manufacturer Boehringer Ingelheim’s desired effect, because numerous veterinarians -- specialists and general practice vets alike -- have been ignoring the FDA guidelines which forbid the administration of pimobendan to MVD-affected dogs prior to heart failure. When questioned about the lack of any evidentiary support for violating the FDA ruling, many such veterinarians have referenced the March 2015 announcements as their sole justification. Thus, if the full report includes any conditions or qualifications to the press releases’ bold asssertion of “clear evidence of benefit”, then the lead researchers will have a lot of explaining to do.

Ironically, in a March 2016 veterinary journal article, a team of Japanese researchers succintly summarized the current peer-reviewed studies finding that pimobenan can cause adverse effects, including the acceleration of mitral valve degeneration, in dogs. They stated:

"Pimobendan (PIMO) can cause adverse effects, such as mitral valve degeneration, in dogs. ... Despite the benefits of treatment, adverse effects have been reported with the use of PIMO in dogs. In a case report of two dogs with mitral insufficiency, a long-term administration of PIMO worsened mitral regurgitation and ventricular hypertrophy. Similarly, in dogs with mild mitral insufficiency, the long-term administration of PIMO was shown to worsen mitral regurgitation and valve lesions. Adverse effects on mitral valves were considered to occur because of increasing cardiac contraction, but it was unclear whether PIMO directly affected the mitral valves."

Why wait so long to publish?Question Marks

A burning question remains: Why have the lead researchers waited over 15 months to disclose the peer-reviewed results of the EPIC Trial?

Obviously, in the interim, manufacturer Boehringer Ingelheim has been getting exactly what it has been paying for.

* "Evaluation of Pimobendan In dogs with Cardiomegaly caused by preclinical mitral valve disease".

** See, "What is Ethics in Research & Why is it Important?", by David B. Resnik, J.D., Ph.D. National Institute of Health website, 2011: “There are many other activities that the government does not define as ‘misconduct’ but which are still regarded by most researchers as unethical. These are called ‘other deviations’ from acceptable research practices and include: ... Bypassing the peer review process and announcing your results through a press conference without giving peers adequate information to review your work.”

*** See the releases here: 1, 2, and 3.

**** Dr. Boswood's March 7, 2015 press release was supplemented a month later with this addition in bold font:  "Please note – quantitative analysis of these results will not be discussed until the full results are available."

October 25, 2015:

Too Many Cavaliers Are Too Fat

Feed the fat cavalier less and exercise it more!

Overweight cavalier King Charles spanielUnfortunately, but perhaps not surprisingly, cavalier King Charles spaniels are pre-disposed to obesity. In other words, for whatever reason, it is easier for cavaliers to gain excess weight than nearly any other breed. Their pleading eyes and sweet demeanor are nearly impossible for many owners to resist. The CKCS’s only serious competition in this area are Labrador retrievers, boxers, Cairn and Scottish terriers, and Cocker spaniels.

Obesity in dogs is considered to be a medical disorder and is the canines’ most common nutritional disease. Its estimated prevalence, species-wide, ranges from 30% to 50%, with the percentage of fat cavaliers probably even higher. Obesity is defined as “an accumulation of excessive amounts of adipose tissue in the body. ” While some other health disorders may cause cavaliers to gain too much weight, scientifically speaking, it usually is the result of either eating too much and/or not exercising enough. Veterinary specialists call this “overnutrition”.

Overweight cavalier King Charles spanielsObesity is unhealthful because it can lead to other disorders and accelerate the effects of still more of them. For instance and most importantly, it can shorten their life spans. It can have severe effects upon the dogs’ respiratory system function, especially as an added risk factor for breathing difficulties due to brachycephalic airway obstruction syndrome (BAOS), another disorder to which cavaliers are pre-disposed due to their shortened muzzle lengths. It can affect cardiac function, cardiac rhythm, and left ventricular volume, all of particular concern to the CKCS because of the breed's prevalence of mitral valve disease (MVD). It can be a major risk factor for hip dysplasia and intervertebral disc disease, two other disorders more common in cavaliers than the average purebred.

What to do? Feed the fat cavalier less and exercise it more! It usually is as simple as that. It may not be easy, because maybe you already have conditioned your dogs and yourself to feeding them upon their demand. But the remedy is simple. Don’t feed as much per meal. Eliminate junky treats; if you must treat, do so infrequently and only as a reward for good behaviors, and use healthful, nutritious dog food as that reward. And, most importantly, walk your fat dogs – every day. If you already walk them, then take them on longer walks.

What should be your goal – an ideal weight? The weight is not as important as the shape of the body. Veterinarians have devised a couple of charts called “Body Condition Scoring” or “Body Condition System”, showing either five or nine different shapes of the canine body, from extremely fat to far too thin. The goal is to reach the middle number of, essentially, an hour-glass figure. See the two charts below:

5 Point Dog Body Condition Scoring Chart

9 Point Dog Body Condition Scoring Chart
October 14, 2015:

Cardiologists focus on bionic fixes
to the leaking mitral valve

Four man-made devices are in the works

Noah recovering from heart surgerySince the first realization that some purebred dogs, particularly cavalier King Charles spaniels, regularly develop mitral valve disease, veterinary cardiologists have dealt with MVD-caused congestive heart failure by trying to “manage” its consequences with drugs. They started with digoxin, a relative of the 18th century herbal digitalis from the foxglove plant. Then they added diuretics (and ACE-inhibitors, to offset the negative side effects of the diuretics). And now we have pimobendan, which its manufacturer anxiously is trying to get approved for use as a preventative of heart failure in dogs.

In the past decade, veterinary surgeons, particularly in Japan and the USA, have tried their hand at replacing defective mitral valves with transplants from pigs, or even mechanical valves. But serious drawbacks to such surgeries include the need to by-pass the heart’s pumping system during the procedures and the requirement that the patient be young and otherwise healthy enough to endure the operation and recovery without dying from stress or transplant rejection. And, it has gone without saying that the costs of such procedures, from thirty thousand dollars and up, is prohibitive to all but the wealthiest of cavalier owners.

So now, some inventive cardiologists are focusing upon simplified surgeries which would not require by-passing the heart during the brief procedure and are designed to prevent the deteriorating mitral valve from allowing blood to backflow through it.

All four of these quick-fixes involve inserting man-made devices onto or into the heart while it continues to Mitral Valve Implant Devicebeat normally. The first of these, with the full name of “epicardial mitral annuloplasty device” but nicknamed “Mitrex”, is essentially a U-shaped clamp (right) which is wrapped around the mitral valve leaflets and tightens them so that they are prevented from allowing blood to backflow through the valve. The Mitrex clamp reportedly has been inserted on dogs’ beating hearts in less than 30 seconds. The device currently is being tested by veterinary cardiac surgeons at clinics in California and Florida on MVD-affected dogs in congestive heart failure.

Tucker valve in place through tricuspid valveVeterinary cardiologist Dr. George Kramer, is researching the viability of a balloon device, called the Tucker valve (left), which is inserted through either the mitral or the tricuspid valve in order to block regurgitation of blood through the valve back into the atrium.

Veterinary cardiologist Simon Swift has begun research on a valvular prosthesis that is to be implanted but does not require the use of cardiopulmonary by-pass during the installation procedure. While he has not yet publicly published details of the device, he proposes to reduce the cost of the prosthesis by manufacturing his own valves.

Injecting Alginate Hydrogel into HeartIn June 2013, a team of California medical cardiologists reported that they had found that injecting alginate hydrogel directly into the left ventricle (LV) of the hearts of 7 dogs in advanced heart failure, increased the thickness of the LV wall, and LV structure and function improved. Alginate is a naturally derived polysaccharide that is used in drug delivery and as cell encapsulation material. (See a diagram of the injection at right.)

For more information about these devices, see our section on them on our MVD webpage.

July 1, 2015:

Heart failure in the MVD-affected
cavalier King Charles spaniel

What it is, and what it is not

Sick Cavalier King Charles SpanielThe terms “heart failure” and “congestive heart failure” are used almost interchangeably by many veterinary cardiologists when discussing mitral valve disease (MVD) in the cavalier King Charles spaniel. Nevertheless, there can be a difference between the two.

What is “heart failure”?

In the ACVIM’s 2009 “Guidelines for the Diagnosis and Treatment of Canine Chronic Valvular Heart Disease” (ACVIM Consensus Statement), it claims to be providing a definition of “heart failure”, but it really does not. The ACVIM introduces its “new system” of “4 basic stages of heart disease and failure”, and yet the ACVIM uses the term “heart failure” in them without defining it. Nevertheless, the ACVIM’s Consensus Statement gives us hints as to what that definition might be.

First, by way of introduction to the topic, it states:

“Heart failure is a general term that describes a clinical syndrome that can be caused by a variety of specific heart diseases, including CVHD [chronic valvular heart disease]. Heart failure from any cause is characterized by cardiac, hemodynamic, renal, neurohormonal, and cytokine abnormalities.”

So from that, we learn that heart failure is a “clinical syndrome”, characterized by “abnormalities”.

ACVIMThe Consensus Statement goes on to cite the 2001 American College of Cardiology/American Heart Association [ACC/AHA] classification system for the treatment of heart disease and failure in human patients*, stating the ACVIM has adapted that human classification system to the management of canine MVD. Fortunately, the ACC/AHA does provide a useable and understandable definition of heart failure. It states:

“Heart failure [HF] is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. ... Because not all patients have volume overload at the time of initial or subsequent evaluation, the term ‘heart failure’ is preferred over the older term ‘congestive heart failure’.
“... HF is defined as a clinical syndrome that is characterized by specific symptoms (dyspnea and fatigue) in the medical history and signs (edema, rales) on the physical examination. There is no single diagnostic test for HF because it is largely a clinical diagnosis that is based on a careful history and physical examination.”

The “bottom line” as to what is and is not heart failure -- particularly congestive heart failure -- seems to be that it is a combination of the heart not pumping sufficient quantities of blood to the body plus outward signs or symptoms of the consequences of the body not receiving those sufficient quantities. The examining veterinarian must both determine if the heart is pumping adequately and look for those outward signs. So essentially, within reasonable limits, a veterinary cardiologist can “call it as he sees it” in terms of diagnosing heart failure in an MVD-affected cavalier.

ACVIM Consensus Stages of MVDTo get back to the ACVIM Consensus Statement, even though it fails to adequately define “heart failure”, it is crystal clear that only dogs in either Stage C or Stage D are in heart failure, and that dogs in Stages A or B1 or B2 are not. Therefore, a dog with a loud murmur and an enlarged heart is not in heart failure unless it also displays some specific clinical symptoms and signs, such as coughing, dyspnea/orthopnea (difficulty breathing / shortness of breath while lying down), anorexia / cachexia (lack of appetite/involuntary weight loss), ederna / ascites (fluid collecting in cavities and tissues), restlessness especially at night; tire easily, reluctance to exercise, less playful, lethargic, depressed, collapse / syncopal (fainting or nearly fainting). It is for this reason that counting respiratory rates is so important in being able to identify the onset of heart failure.

Is “congestive heart failure” different from “heart failure”?

Yes, it can be, in the context of MVD. The term “congestive” often mistakenly is assumed to refer to fluid from the heart, which collects in the lungs. However, medically speaking, “congestive” simply means that the heart is unable to pump adequate blood to the body, and as a result, the blood that is not being pumped out of the heart is being retained within the heart. Some of that fluid may also back up into the lungs, and so fluid detected in the lungs can be a sign of congestive heart failure.

What are “systolic dysfunction” and the “ejection fraction”?

Ejection Fraction“Systolic dysfunction” occurs when the heart muscle does not contract with enough force to pump enough oxygen-rich blood throughout the body. It also is referred to as “diminished contractility”. During an echocardiogram, the cardiologist is able to calculate the “ejection fraction”, which measures how well the heart pumps with each beat. That ejection fraction determines whether there is systolic dysfunction.

For many years, heart failure has been considered by many veterinarians to be synonymous with a systolic dysfunction, despite research evidence to the contrary.** Cardiologists have discovered that some MVD-affected dogs – particularly among toy breeds and especially many CKCSs – display classic signs and symptoms of heart failure without having a low ejection fraction or systolic dysfunction or diminished contractility. Dogs in heart failure but which nevertheless have an ejection fraction greater than about 50% are considered to be adequately “compensating” for their MVD condition or have a “preserved ejection fraction”.

This distinction is particularly important when deciding when to begin medicating the MVD-affected dog in heart failure. Some standard MVD drugs for dogs in heart failure are designed to compensate for systolic dysfunction and to increase the ejection fraction. In particular, pimobendan (Vetmedin, Cardisure) is one of those drugs. But if the cavalier in heart failure is adequately compensating for its condition with a normal ejection fraction and therefore no systolic dysfunction, those drugs could over-stimulate the heart muscle and cause damage, rather than manage the dog’s heart failure.


* ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult: Executive Summary. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J. American College of Cardiology. July 2001;38(7):2101-2113.
** Myocardial function in small dogs with chronic mitral regurgitation and severe congestive heart failure. Kittleson MD, Eyster GE, Knowlen GG, Bari Olivier N, Anderson LK. JAVMA. February 1984;184(4):455-459. (“This study suggests that the contractile performance of the left ventricle in most dogs with chronic mitral valve fibrosis and clinical evidence of severe congestive heart failure is either normal or mildly depressed. This suggests that congestive heart failure in these patients is due to severe regurgitation and subsequent volume overload of the left ventricle and atrium. Heart failure secondary to mitral regurgitation can be due not only to myocardial failure, but also to severe regurgitation by itself or in combination with myocardial failure.”).

April 30, 2015:

The CKCSC,USA makes part of its ethics code optional!

It’s real motto: “Forever Guardians of the Cavalier BREEDERS!”

CKCSC,USA mottoThe Cavalier King Charles Spaniel Club, USA (CKCSC,USA), like all other nationwide cavalier clubs, has a Code of Ethics. Traditionally, ethics codes, like the Ten Commandments, command breeders either to always do something or to never do something. For instances, the CKCSC,USA’s code has stated:

“If I decide to breed a litter, I will ...”
“As the owner of a stud dog, I realize that I must exercise exemplary conduct in the use of my dog in order to abide by the standards set forth in this Code of Ethics. Therefore I will ...”
“As the owner of a brood bitch, I realize that I must exercise exemplary conduct in breeding from her in order to abide by the standards set forth in this Code of Ethics. Therefore I will not: ...”

But no longer. As of March 14, 2015, the CKCSC,USA has made portions of its ethics code optional! Specifically, it has added this non-mandatory (and therefore meaningless) statement to the ethics code section on breeding brood bitches*:

“The CKCSC,USA recommends a minimum breeding age of 2½ years, and following the health testing guidelines as published on the CKCSC,USA website.”

It is bad enough that the club’s so-called “health testing guidelinesdo not even include the MVD breeding protocol, but to make health testing optional in its ethics code shows that, in reality, the CKCSC,USA is Forever Guardian of the Cavalier BREEDERS!

* Not even this recommendation applies to stud dogs!

April 19, 2015:

“Purebred breeding” is a euphemism
for accelerated genetic entrophy

Toss out that closed studbook now!

The End Is NearResearchers estimate that more than 50% of cavalier King Charles spaniels (CKCSs) may have the genetic neurological disorder called syringomyelia (SM), also known as “neck scratcher’s disease”. And, they estimate that up to 95% of CKCSs may have Chiari-like malformation (CM), which purportedly is at least part of the cause of SM. And, we know from statistics that more than half of all cavaliers may be expected to develop mitral valve disease by their fifth birthday. So what are we doing wrong? And what do these severe genetic problems – among several others* -- foretell about the future of our breed?

* To name the rest: various hereditary eye disorders, progressive hereditary deafness, low blood platelets (idiopathic asymptomatic thrombocytopenia), cerebellar infarcts (strokes), chronic pancreatitis, brachycephalic airway obstruction syndrome (BAOS), curly coat syndrome, intervertebral disk  disease (IVDD), diabetes mellitus, eosinophilic stomatitis, idiopathic epilepsy, episodic falling syndrome, fly catchers syndrome, primary secretory otitis media (PSOM) – glue ear, chronic kidney disesase, masticatory muscle myositis (MMM), muscular dystrophy, obesity, patellar luxation, hip dysplasia (HD), and pneumocystis pneumonia.

Breed StudbookFor starters, it means that the breed clubs’ proverbial “closed studbook*” is destined to fail, and bring the entire breed down with it.

* In the parlance of dog breeding, the “studbook” is the list of pedigrees of the dogs of a particular breed. In turn, “pedigree” means the record of the ancestors of a breed, showing that it is “purebred”. “Purebred” means that all of the dogs in the breed descended from other dogs of the same breed. Therefore, no dogs of any other breed (or multi-breed) are allowed entry into a breed club’s closed studbook. If a mating occurs between a purebred dog and a dog of some other breed, their offspring are ostracized by that breed club, banned from participating in purebred activities, especially conformation shows, much less being allowed to mate with any other dogs of that breed.

The second law of thermodynamics applies to closed studbooks

A basic tenet of physics is Rudolf Clausius’ and Lord Kelvin’s statement of the Second Law of Thermodynamics:Second Law of Thermodynamics

“The amount of energy available for useful work in a given isolated system is decreasing. The entropy is always increasing.  Therefore, closed systems cannot perpetually sustain themselves.”

In other words, a closed system inevitably always is expending its store of energy and is constantly winding down. An isolated system has no additional source of energy with which to replenish itself. And no system is more “isolated” than a dog breed club’s closed studbook. Its “energy” component is its pool of genes. Every breeding decision results in eliminating more and more genes from the very limited pool which a closed studbook contains at its start. Therefore, in no way can the closed studbook be capable of perpetually sustaining itself.  From the beginning of the concept of “purebred” breeding, the closed studbook has been destined to degrade into accelerated, irreversible exhaustion.

The breed standard does not mention “pedigree” or the “studbook”

The stated goal of purebred breeding has been to produce dogs which meet a defined “breed standard”, which mainly pertains to appearance, structure, and temperament. Breed standards typically do not even mention a requirement that the dogs be descended only from dogs listed in the breed’s studbook.

CKCS Breed Standard

The closed studbook has never really been a necessary corollary to achieve that goal. For example, it is possible to mate together a variety of “mongrels” – note how class snobbery so easily seeps in to the purebred vocabulary – and produce, within as few as three or four generations, a dog which actually meets the breed standard of the cavalier King Charles spaniel. Indeed, if the CKCS breed standard included a “health clause” – that is, requiring that the dog not have certain genetic disorders, such as Chiari-like malformation or mitral valve disease – it would be easier to produce a dog matching the CKCS breed standard from mongrels than it would be by mating purebred cavaliers.

Because the national kennel clubs decreed that their breeds’ studbooks be closed, the second law of thermodynamics kicks in and guarantees a foreseeable end point to those breeds’ existence. As evidence, the American Kennel Club, founded in 1884, has been predicted to run itself into the ground within the next ten years. This is based upon the rate of declining annual puppy registrations, from a high of over 1,500,000 in 1992 to around 400,000 in 2014*, a decline of over 75% in only the last twenty-two of its 131 years. And just why is that? Pure irrational snobbery, perhaps.

* The AKC was so embarrassed by the declining registrations that it stopped publicizing their numbers in 2008.

So, why not toss out the closed studbook, or at least open it up to outsiders, and let the offspring of any parents vie for matching the breed standard?

Case Study: The low uric acid (LUA) Dalmatian

A tragic example: Up to 2011, all AKC-registered Dalmatians reportedly carried a mutated version of the SLC2A9 gene, which causes exceedingly high levels of uric acid – about ten times that of a normal dog. In research studies, high majorities of males were found to have uric sediment in their bladders, and an estimated 13% to 34% produce potentially painful urate stones which can cause blockages and which may require repeated surgeries to remove.

In an effort to come to the rescue of that breed, in 1973 a very knowledgeable and courageous breeder, Dr. Robert Schaible, cross-bred a Dalmatian bitch with a German shorthaired pointer (not affected with the mutated SLC2A9 gene), producing a litter half of which also did not have the dreadful mutation. These dogs since have been labeled “low uric acid” or LUA Dalmatians. Within three generations after back-crossing those healthy offspring, only the most biased Dalmatian fanciers could detect which dogs were from that cross breeding when compared to champion purebred Dals.

Fiona Grand Champion LUA DalmatianNevertheless, the ever so particular members of the AKC's parent club, the Dalmatian Club of America (DCA), voted twice – in 1984 and 2008 (by then, the tenth generation of LUA Dals had been produced) – to reject these healthy dogs’ bids to obtain AKC registrations. In the meantime, all AKC Dalmatian breeders necessarily produced only litters of dogs with the version of the gene which was certain to cause exceedingly high levels of uric acid. They all did this intentionally!

 Finally, by the twelfth generation of LUA Dals, which were 99.97% purebreds (see Fiona, at right), even the AKC board of directors had reached the limit of its patience. In November 2010, the AKC board warned the Dalmatian parent club that if its membership did not vote to approve admission of the LUA Dals into the AKC within the following six months, then AKC would take the matter into its own hands and rule on admitting the LUA dogs into the breed’s studbook. The parent club read the signals and finally voted to admit the LUA Dals in 2011, after 38 years of irresponsible foot-dragging, during which the club’s breeders gleefully continued to produce Dals suffering this potentially agonizingly painful genetic urinary disease.

BBC's Pedigree Dogs ExposedSo, almost invariably the purebred dog clubs’ studbook fetish trumps the genetic health of generation after generation of the dogs their breeders produce. Thus, these degenerate offspring continue to be bred, and their reputations for sever genetic health defects grow and grow. The recent BBC documentary television program “Pedigree Dogs Exposed” is evidence of that. As a consequence, the dog owning public is turned off, repulsed even, by the selfish, snobbish, anti-health policies of the national kennel clubs.

The cavalier clubs still irresponsibly ignore the MVD and the CM/SM breeding protocols

Added to that is the fact that purebred breed clubs often refuse to recognize either the severity of the genetic disorders their breeding practices have brought upon their dogs, or the often simple solutions to dealing with those disorders. For example, both of the CKCS national breed clubs in the United States have refused to endorse the Mitral Valve Disease Breeding Protocol, designed by cardiologists and geneticists to eliminate early-onset MVD in the breed. And, both clubs refuse even to acknowledge the existence of the SM Breeding Protocol, designed by neurologists and geneticists to reduce the incidence of CM/SM in the breed.

AKC's TombstoneSo, we have a combination of (a) the inevitability of the second law of thermodynamics to waste away an isolated system, like the ubiquitous and totally unnecessary closed studbook, and (b) the breed clubs’ persistent denial of the reality of at least a partial solution to some of the severe genetic health disorders which their closed studbooks have brought about. All this is wrapped in the breed clubs’ tuxedo-dressed attitude of elitism, snobbery, and condescension towards anyone who dares to suggest that the clubs could be doing something terribly wrong and also could be refusing to do something absolutely necessary. The victims, of course, are these purebred dogs, as their genetic health deteriorates with each future generation.

Perhaps as predicted, by the year 2025 the purebred dog will be put out of its misery, as the closed studbooks of these miserable dog clubs follow the second law of thermodynamics and degrade into total exhaustion.

March 25, 2015:

The EPIC trial ends on schedule,
but could a whitewash be in the works?

Study's objective is changed and findings are disclosed prior to peer review

Such advance disclosures normally are unethical and unprofessional

White WashIn 2010, Boehringer Ingelheim, the manufacturer of Vetmedin (a brand name for pimobendan) announced the start of the EPIC Trial, a 360-dog study by 36 veterinary cardiologists around the world, to determine if the drug could be effective in delaying the onset of clinical signs of congestive heart failure in dogs with mitral valve disease. In that announcement, Boehringer Ingelheim's senior brand manager is quoted stating:

“The EPIC trial will definitely answer the question: Does pimobendan delay the onset of clinical signs?”

In a press release issued by EPIC Trial co-lead researcher Dr. Jens Häggström* on March 16, 2015, it was announced that “The EPIC study has been terminated”. No surprise there, because from the beginning of the EPIC Trial back in 2010, it was announced that it would end in early 2015. But, really! A press release to announce the end of a drug study which was scheduled to end anyway? Could that announcement have been just an excuse for issuing a press release at all?

What is surprising is this comment included in that press release:

“The interim analysis indicated that there was clear evidence of benefit of the administration of pimobendan in prolonging the time to the primary endpoint of the study, which was a composite of the development of left-sided congestive heart failure, or death presumed to be cardiac in origin. The interim analysis did not raise any concern over the safety of pimobendan administration.” (Emphasis added.)

Unfortunately, there is a lot wrong with that dreadfully vague statement.

Can you spell p-e-e-r  r-e-v-i-e-w?

First of all, in the world of scientific research, it is unusual for research data, much less any results, to be leaked publicly before peer-reviewing and the official publication of the peer-reviewed article. Further, it is unheard Peer Reviewof for there to be an official public release of any such premature information, over the name of one of the researchers. Any such prior disclosure normally is considered unethical and unprofessional in the scientific research arena.**

So, what is so special about the EPIC Trial that this seemingly unethical, unprofessional, and unheard of press release has been issued? It is far from clear, within the four corners of that press release.

The answer may be tucked into the highlighted portion of that quote above – “or death presumed to be cardiac in origin.” You see, from the outset, it never was intended that the EPIC Trial's pre-heart-failure administration of pimobendan end at death.

Here is how the EPIC trial researchers originally stated the objective of their study:

“Investigators will determine if chronic oral administration of pimobendan in dogs with evidence of increased heart size secondary to preclinical MMVD can delay the onset of signs of CHF. Complete EPIC results will be published and distributed, regardless of the outcome.
“Does chronic oral administration of pimobendan in dogs with evidence of increased heart size secondary to preclinical MMVD delay the onset of signs of congestive heart failure?”

In other words, pimobendan would be given to dogs with Stage B2 mitral valve disease (dogs with a loud murmur and some enlargement of the heart but not in heart failure), and once congestive heart failure signs appear, the study ends for that dog. There is nothing there about intending to give the dogs pimobendan until they die, or that doing so would “benefit” the dog.

 Now, granted, in the FAQs on the EPIC Trial website, it does state that “The primary endpoint is a composite of the development of left-sided congestive heart failure (CHF) or cardiac death.” (All that means is that a particular dog's testing ends either when the dog reaches CHF or if the dog dies instead of reaching CHF.) But surely that did not mean that cardiac death prior to CHF meant that the pimobendan treatment had been a success. It meant the opposite -- that the pimobendan had failed to allow the dog to reach CHF at all. In other words, there would be no “evidence of benefit” if the pimobendan killed a dog which otherwise would have reached CHF.

Since one of the main concerns about administering pimobendan prior to heart failure always has been that it can cause death, and since death before the usual progression to heart failure always has been considered to be a bad thing and not a desirable one, it would be very curious if death prior to heart failure has been added to the EPIC Trial’s objective as a normal, desirable end point. ***

A bad smell pervades this EPIC Trial

Bad SmellThis press release is very troubling because it reeks of an effort to placate the manufacturer of Vetmedin. We feared this from the beginning, when we urged cavalier owners to not particpate in the EPIC Trial in our Blog entry, “Beware the pimobendan/Vetmedin ‘EPIC clinical trial’: There is no upside.” 

Hopefully, between now and when the actual (presumably peer-reviewed) article on the EPIC Trial is published, responsible professionals will re-take control of this process back from the manufacturer and not suggest that death before reaching congestive heart failure is an acceptable end result of giving their dogs pimobendan.


*Lead researcher Adrian Bosworth issued a nearly identical press release on March 17, 2015. Co-lead researcher Sonya Gordon issued an even more egregious press release on March 24, 2015.
** See, "What is Ethics in Research & Why is it Important?", by David B. Resnik, J.D., Ph.D. National Institute of Health website, 2011: “There are many other activities that the government does not define as ‘misconduct’ but which are still regarded by most researchers as unethical. These are called ‘other deviations’ from acceptable research practices and include: ... Bypassing the peer review process and announcing your results through a press conference without giving peers adequate information to review your work.”
*** In the "Pimobendan in Congestive Heart Failure (PICO) trial", a 1996 study of 317 human patients, the researchers found that: "In both pimobendan groups combined the hazard of death was 1.8 times higher than in the placebo group."

March 19, 2015:

Is it 'Back to the Future' for the American Kennel Club?

A degenerate breeding program masquerading as the dogs’ champion

AKC Chairman Ron MenakerThe new Chairman of the Board of the American Kennel Club is the same old chairman who led the AKC into its decline earlier in this millennium. Ron Menaker (right) was re-elected chairman by AKC’s board of directors this month, after a three year hiatus while interim chairman Alan Kalter fiddled around trying to figure out how a million or so “Likes” on Facebook could reverse AKC’s rapid decline.

Yes, the same Ron Menaker whom we chided in a July 2011 blog entry for not only condemning the factually accurate (as far as cavalier King Charles spaniels are concerned) 2008 BBC television program “Pedigree Dogs Exposed” (PDE), but also actually petitioned the UK Parliament to have the BBC do a documentary attacking PDE’s producer, called “Jemima Harrison Exposed”!

To re-hash a bit, Mr. Menaker described PDE as a “piece of sensationalist fiction and tabloid journalism masquerading as a documentary” and an “exercise in media sensationalism”. Ironically, he pretty much could have used similar words to describe the AKC these days:

“A degenerate breeding program masquerading as the dogs’ champion.”

It should come as no surprise that closed studbooks have led to rapid declines in genetic diversity and the Arrow Downproduction of sicker and more exaggerated versions of each purebred breed of dogs. AKC's mantra should be something more like “Cross-breed or die”, but Mr. Menaker appears incapable of seeing that viewpoint.

So, the question becomes: Will Chairman Menaker’s tired old head-in-the-sand ideas speed up AKC’s annual double-digit drop in litter and puppy registrations? We all must wait and see, although perhaps not have to wait as long as the statistically predicted death date of 2025.

February 10, 2015:

All that cavalier owners need to know about
the “Reverse Sneeze” or “Cavalier Snort”

Elongated Soft PalateOccasionally, excited cavalier King Charles spaniels will suddenly stand still and start making a very loud snorting sound, over and over, as if they are gagging and having difficulty breathing. In cavalier circles, this is known as the “Cavalier Snort” or the “Reverse Sneeze”. A YouTube video of a cavalier making this sound is here.

In cavaliers, this gagging sound usually is due to the dog having an elongated soft palate. The palate is the roof of the mouth. It is divided into two parts, the front bony hard palate, and the rear fleshy soft palate. The soft palate separates the nasal passage from the oral cavity. (See the soft palate at the top of the sketch to the right.)

An elongated soft palate is too long for the length of the mouth, so that its tip protrudes into the front of the airway and may get sucked into the laryngeal opening where it may obstruct the normal passage of air into the trachea. This is because the CKCS has a shorter muzzle than the average dog, and therefore all of the dog’s breathing apparatus is compressed into a shorter space than the average dog.

When the elongated soft palate protrudes and partially or totally blocks the airway, the dog no longer can breathe through its nose. Since dogs normally breathe through their noses, they continue to try to do so, thereby causing the gagging or snorting sound.

Block the dog’s nostrils and make it breathe through its mouth

If the palate is only moderately elongated and does not totally block the airway, most cavaliers are able to pull out of these blockages by themselves. Snorting may be relieved by forcing the cavalier to breathe through its mouth instead of its nose. This may be done by holding the dog's head down and mouth open with one hand while blocking air from entering the nose with the other hand.

In severe instances, the dog may collapse if the airflow is obstructed completely for too long. In such cases, surgical removal of excess tissue from the palate may be necessary. One of those procedures is called “folded flap palatoplasty” (FFP), which both shortens and thins the soft palate. Post surgery prognosis is good for young dogs. They generally may be expected to breathe much easier, with significantly reduced respiratory distress, and display more energy and stamina. Older dogs may have a less favorable prognosis.

In all cases, it is strongly recommended that only board certified veterinary surgeons who also are very experienced at airway surgery, be permitted to perform any type of airway surgery on cavaliers.

(This article has been excerpted from  “Brachycephalic Airway Obstruction Syndrome (BAOS) in the Cavalier King Charles Spaniel” on this website.)

October 20, 2014:

Just Asking: What’s up with Vetmedin’s ‘EPIC Trial’?

It’s due to end next year, but some recent indications are ominous

Keep Calm -- Just AskingWhen the EPIC Trial was announced in 2010 by the manufacturer of Vetmedin (a brand name of pimobendan), we did not think it was a wise approach for studying whether the drug could safely delay the onset of heart failure in dogs with mitral valve disease (MVD). We went so far as to warn all cavalier owners to “Beware the pimobendan/Vetmedin ‘EPIC clinical trial’: There is no upside” in an April 2011 blog entry on this page.

The trial, of up to 360 dogs with MVD murmurs and enlarged hearts (but not yet in heart failure), is scheduled to end in 2015. Each dog was to receive either two pimobendan tablets or placebos daily until the dog reached heart failure. Since the trial started over 4 years ago, presumably many of those dogs by now have reached the heart failure stage of MVD, and their reports should be piling up in the in-boxes of the study’s leaders, including Dr. Sonya Gordon of Texas A&M University in the USA and Professor Adrian Boswood in the UK.

We may assume that the 36 cardiologists participating in the EPIC Trial are sworn to secrecy until the final report, which entails drafting, review, approval by at least a majority of them, and peer review before publication in a veterinary journal. However, there are curious indications that some of the results are known and do not look so good for the wannabe peddlers of early-use Vetmedin.

Owners of some of the dogs in the trial are reporting that their dogs died suddenly, shortly after its start. Some cardiologists who are among the 36 participants now are talking with renewed emphasis about the importance of waiting for signs of heart failure before starting Vetmedin. At least one other cardiologist recently has openly attacked the trial as being risky. The EPIC Trial’s own website – epictrial.com -- with its videos and graphics Just Askingand list of names of those 36 cardiologists and its map showing their locations around the globe and all of its optimistic hype about Vetmedin before heart failure, has disappeared from the Internet*. Inquiries to Vetmedin’s manufacturer, Boehringer Ingelheim GmbH, go unanswered.

Are these indications that the EPIC Trial has been an epic failure? Just asking ...

* Finally, as of early December 2014, the Epic Trial website is back on line.

October 13, 2014:

So your cavalier has a heart murmur. What do you do next?

The ACVIM says: Get an x-ray, not an ultrasound!

Vet auscultating a cavalierSince over half of all cavalier King Charles spaniels may be expected to develop mitral valve murmurs by age 5 years, it should come as no surprise when your veterinarian tells you that your cavalier has one. But there is no reason to panic. The American College of Veterinary Internal Medicine (ACVIM*) has a sensible list of steps to take once a murmur is first detected in your CKCS.

For the record, the ACVIM recommends that cavaliers be screened annually by “auscultation” (examination by stethoscope) by board certified cardiologists. Specifically, ACVIM** states:

“Owners of breeding dogs or those at especially high risk, such as Cavalier King Charles Spaniels, may choose to participate in yearly screening events at dog shows or other events sponsored by their breed association or kennel club and conducted by board-certified cardiologists participating in an ACVIM-approved disease registry.”

For that reason, CavalierHealth.org has a list of upcoming heart screening clinics in the USA and Canada, which is updated weekly.

Once a murmur is detected by the vet, the first thing to realize is that you do not need to rush your dog to have an ultrasound (echocardiograph) of its heart. In fact, rarely does a cavalier with a mitral valve murmur ever need an ultrasound before the disease reaches heart failure. Instead of an ultrasound, the ACVIM recommends that you get your dog’s heart x-rayed to be a “baseline” for measuring the heart size against future x-rays after any heart enlargement takes place. The ACVIM states:

“Thoracic radiography [chest x-ray] is recommended in all patients to assess the hemodynamic significance of the murmur and also to obtain baseline thoracic radiographs at a time when the patient is asymptomatic for CVHD [chronic valvular heart disease].”

X-ray of cavalier's heartThe ACVIM does not recommend that cavaliers with new murmurs be ultrasounded unless the auscultation and the x-ray do not adequately satisfy the cardiologist about the true cause of the murmur. Specifically, this is what the ACVIM states about ultrasounding cavaliers once a mitral valve murmur is detected:

“In small breed dogs with typical murmurs, echocardiography is recommended to answer specific questions regarding either cardiac chamber enlargement or the cause of the murmur if those questions are not answered adequately by auscultation and thoracic radiography.”

Note that the only “baseline” that the ACVIM recommends for cavaliers with new murmurs is an x-ray and not an ultrasound, as long as the cardiologist is satisfied that the stethoscopic exam and the x-ray confirm the cause of the murmur.

* The ACVIM certifies veterinary cardiologists. A list of them in the USA and Canada is available here.    
See the ACVIM's "Guidelines for the Diagnosis and Treatment of Canine Chronic Valvular Heart Disease", page 1144.

October 11, 2014:

Do MVD-affected cavalier King Charles spaniels
really need taurine supplements?

Taurine There is a popular notion that dogs with mitral valve disease will benefit from adding taurine (right) to their daily diets. Taruine (2-aminoethanesulfonic acid) is essential for cardiovascular function as well as for playing a variety of other fundamental roles in keeping animals functioning. Fortunately, most all dogs produce sufficient taurine themselves, as long as they ingest an adequate amount of animal-based protein. There is no published evidence that dogs with mitral valve disease are deficient in taruine or would benefit from supplementing it.

There were a couple of reports published in 1997 that found that American Cocker spaniels affected with dilated cardiomyopathy (DCM) became taurine-deficient and in need of taurine supplementation. Apart from the fact that American Cockers and cavaliers have the same last name, there is no established connection between the CKCS and a need for added taurine. Cavaliers are not inherently taurine-deficient, and as a breed, they are not known to develop DCM. Mitral valve disease (MVD) and DCM both affect the dog’s heart, but otherwise, they are not related.

Nevertheless, many canine heart supplements include taurine, and even some cardiologists recommend adding taurine to the diets of dogs with mitral valve disease. We are not sure why, because research studies have shown that MVD-affected dogs tend to have higher plasma taurine concentrations than unaffected dogs. In a 1995 study by George A. Kramer, Mark D. Kittleson, Philip R. Fox, Julia Lewis, and Paul D. Pion, for example, they found:

"[P]lasma taurine concentrations were highest in dogs with AVD [acquired valvular disease, e.g, MVD] ... We conclude that plasma taurine concentrations may be increased in dogs with AVD."

Now Brand Taurine PowderEven DCM-affected dogs other than American Cockers usually have no taurine deficiency. In board certified veterinary cardiologist Dr. Rebecca E. Gompf's 2005 article on nutritional therapies, she wrote:

“Because dogs readily make taurine from free sulfur amino acids, only lose a small amount in their bile acids, and can maintain normal blood levels of taurine despite their diets, they do not tend to develop taurine-deficient DCM.”

In a 2002 presentation, board certified veterinary cardiologist Dr. Bruce Keene (who conducted one of those 1997 studies of the American Cocker) stated:

"Taurine supplementation is indicated whenever plasma or whole blood taurine concentrations are found to be low. ... [S]upplementation is generally only recommended after discovery of deficiency."

So, the bottom line is that, if you are thinking about giving your cavalier a taurine supplement, check its blood first to see if the dog needs it. The odds are great that no MVD-affected cavaliers will be low in taurine, and remember the old saying: “Too much of a good thing is not a good thing!”

July 12, 2014:

When NOT to start giving your cavalier
pimobendan (Vetmedin)

Vetmedin boxesUnfortunately, a few veterinary cardiologists, and a huge number of general practice vets, have been prescribing pimobendan (brand names Vetmedin and Cardisure) to cavaliers which have mitral valve disease (MVD) murmurs but definitely are not yet in heart failure. This is very disturbing because the premature dosing of pimobendan can kill the dog which does not need it.

Even some dogs already in heart failure cannot tolerate pimobendan, because one of its consequences is that it strengthens the heart muscle and enables it to pump harder. This is called improving the heart’s contractility. If a dog in heart failure still has a strong heart muscle, it does not need to be strengthened, and the pimobendan thereby forces the heart to work much harder than it should.

This is what happened to one of our cavaliers. We noticed that his heart was beating so hard after being given pimobendan that we could see the beats causing his chest hair to vibrate. So we cut back the dosage by half, and then by half again, so that he was getting a quarter of the typical dosage. Finally we discontinued it completely. He had an enlarged heart and he was in heart failure, but the heart muscle remained strong and was doing its job.

Premature administration of pimobendan can overwork the heart to the point of shredding some of its chordae tendineae and thereby causing instant death.

Ask your vet, "WHY?"

So, if you have a cavalier with a mitral valve disease murmur but has no symptoms of heart failure, and your veterinarian recommends starting pimobendan, the first thing you should do is ask him "Why?".

And, show him the manufacturer's warning on the box, about not prescribing it prior to heart failure. It states:

Contraindications: Vetmedin should not be given ... in cases of hypertrophic cardiomyopathy, aortic stenosis, or any other clinical condition where an augmentation of cardiac output is inappropriate for functional or anatomical reasons.
Warnings: Only for use in dogs with clinical evidence of heart failure.”

See for yourself:

Vetmedin label warnings

And, point out that Vetmedin's website has this warning:

“The safety of VETMEDIN has not been established in dogs with: Asymptomatic heart disease.
“Use only in dogs with clinical evidence of heart failure.”

And, show him the ACVIM consensus statement,  which states (on page 1145, top of second column):

“A few panelists considered the use of the following medications for patients in Stage B2 under specific circumstances: pimobendan, ... . The panel felt in general that these treatment strategies needed additional investigation into their efficacy and safety in this patient population before a consensus recommendation could be made.”

And, ask him about the current “EPIC study” of 360 pre-heart-failure dogs, being sponsored by Vetmedin's manufacturer and not due to end until 2015, to determine whether or not Vetmedin should be given to pre-heart-failure-dogs. On the EPIC Study website, it specifically states:

“Currently there is no treatment licensed to delay the onset of CHF [congestive heart failure].”

Elsewhere on the EPIC Study website it states:

“There is currently no treatment licensed for the management of preclinical, myxomatous mitral valve disease (MMVD).”

And still on another page of the EPIC Study website it states:

“Treatment of CHF due to MMVD begins when the dog shows clear clinical signs of heart failure, and is Luci & Rickytailored for the individual dog.”

As you see, pimobendan's own manufacturer repeatedly warns against giving the drug to dogs before they are in heart failure.

In other words, ask your veterinarian to satisfy you that his way is better than ALL of the evidence against premature dosing of pimobendan! As Ricky Ricardo would say to Lucy, "You got some splainin' to do!"

June 18, 2014:

Do-it-yourself diagnosing of congestive heart failure
in your cavalier King Charles spaniel

“Only respiratory rate predicted the presence of CHF with high accuracy.”

CavalierHealth.org Copyright © 2004 Blenheim CompanyExcept for prescribing pimobendan, veterinary cardiologists’ consensus about medicating cavalier King Charles spaniels with mitral valve disease (MVD) is to wait until the dog enters “congestive heart failure” (CHF), or just “heart failure” (to avoid having to define “congestive”). They tell us cavalier owners that our dogs with MVD should be brought in and re-examined regularly – be it every six months or as frequently as every three months – so that if and when the dog is on the cusp of CHF, the vet will be ready and able to prescribe a combination of medications – usually a diuretic, an ACE-inhibitor (in addition to the pimobendan) – immediately. 

If it is so important to know exactly when our cavaliers enter CHF, so the drugs may be given promptly thereafter, then exactly how is CHF diagnosed? Can only a veterinarian make that diagnosis? Do only the vets have the necessary equipment? If so, what will happen to our dog if CHF shows up sometime between those periodic visits to the vet?

We know that vets, especially cardiologists, have some very expensive diagnostic equipment for our dogs’ heart problems. They include x-ray machines, Doppler echocardiographs (ultrasounds), and electrocardiograph devices (ECG or EKG), all of which may be used to detect CHF. In addition, the vets have expensive blood tests (cardiac biomarkers) to detect CHF. But what good are all of these tools and equipment if our dog enters CHF between visits to the vet?

15-second stop watchSimply count the dog's breaths for 15 seconds

The answer is counting the dog’s “respiratory rate”, which is something that cavalier owners can do anytime they are with their dogs. As fancy and complex as all of the cardiologists’ electronic devices may be, and as sophisticated as their cardiac biomarkers may be, the best single means of determining when a cavalier enters congestive heart failure is when the dog’s respiration rate consistently exceeds 30 breaths per minute.

Top cardiologists in the UK and USA have concluded that respiration rate counts are more accurate in predicting the onset of CHF than any other means. In a 2011 study at Ohio State University’s veterinary school, Dr. Karsten Schober and a team of researchers compared the respiratory rates of 45 dogs with MVD (including 13 CKCSs) with their cardiac biomarkers and their Doppler echocardiographic indices, and they found that “Only respiratory rate predicted the presence of CHF ... with high accuracy.” They concluded that “home monitoring of respiratory rate is simple and very useful in the assessment of CHF in dogs with ... MVD.”

In a 2012 study conducted by an international team of cardiologists, they found that “apparently healthy adult dogs generally have mean sleeping respiratory rates [less than] 30 breaths/min and rarely exceed this rate at any time.”

As a result of these studies, several cardiologists are recommending that owners become familiar with their MVD-affected cavaliers’ normal resting breathing rate and effort and keep logs of their sleeping respiratory rates, to establish a baseline rate for each dog, and report when the dogs’ rates increase to consistent rates approaching or above 30 to 40 breaths per minute. For example, the University of Pennsylvania’s veterinary school advises in a handout available on-line

“When your dog is at rest, watch their sides rise and fall as they breathe normally. One rise and fall cycle is equal to one breath. Count the number of breaths they take in 15 seconds, then multiply this number by 4 to get total breaths per minute. For example, if you count 8 breaths in 15 seconds, that is equal to 32 (8 x 4) breaths per minute. Texas A&M Respiratory Rate BrochureA normal dog at rest should have a respiratory rate less than 40. If you notice this number increasing consistently, or notice an increase in the effort it takes to breathe, contact your veterinarian.”

The vet school at Texas A&M University also has published a handout (right) explaining how to keep track of dogs’ respiratory rates. An excellent YouTube video shows when How to measure a respiratory heart rate in your dogand how every cavalier owner can count the breaths of their MVD-affected dogs while they are sleeping or at rest.

 Bottom Line: Ask your cavalier’s cardiologist (you do have one, don’t you?) whether and how you should monitor your dog’s respiratory rate for congestive heart failure.

March 10, 2014:

Dog food companies may be turning a grain-free corner

Some truths about carbohydrate-laden kibbles ooze out of
the petfood industry magazine's March 2014 issue

Petfood Industry, March 2014Petfood Industry magazine’s March 2014 issue has a picture of a wolf on its cover. It’s cover story is “Should domestic dogs really eat like wolves?” It’s subhead asks “Bio-appropriate petfoods are often meat-first and grain-free, but are they based on nutrition science?”

Considering that Petfood Industry is the marketing association of the USA's commercial petfood industry, and that the petfood manufacturers’ bread-and-butter has been machine-extruded, carbohydrate-laden dry kibble for the past fifty years, one would expect the answer to both of those questions is “No!” – “No, dogs should not eat like wolves” and “No, biologically-appropriate petfoods are not based upon nutrition science”.

Well, think again. Petfood companies’ “conventional wisdom” is turned on its head in this remarkable issue of the industry’s magazine. The wolves article lays waste to the “validity” of feeding dogs carbohydrate-laced kibble, making such heretical politically-incorrect statements as:

“According to ‘The Biologically Appropriate Food Concept’, conventional dry dog and cat foods appear to be created on the premise that the digestive system of the dog and cat is similar to humans -- with an emphasis on grains and carbohydrates. While some would argue that dogs and cats have adapted since kibble foods were introduced, bio-appropriate petfood makers would counter that their digestive systems remain unchanged.
“‘Such evolutionary adaptations require much more time than a mere hundred years or so, and the evolutionary change -- from gross anatomy down to the molecular level -- that would be required for the development of such different digestive capabilities would take much longer than the time that dogs have been living with humans,’ the Champion Pet Foods whitepaper points out.
“In the short digestive systems of dogs and cats, plant proteins are far less digestible than meat proteins. High levels of trypsin inhibitors in grain legumes can cause substantial reductions in protein and amino acid digestibilities (up to 50%) in rats and pigs. Certain protein sources are better than others by providing a richer blend of amino acids. These proteins have a high biological value (BV). BV refers to how well the body can actually use the protein.”

Veterinary nutritionists' "Pet Humanization" slur is turned against them

In addition, the March issue’s second article, “Grain-free petfood: A top trend in the US pet market” (subhead: “Desire for natural products, pet humanization drive this growing segment”) reports that discerning pet owners finally are having an impact on the petfood industry by choosing more grain-free foods for their dogs and cats. Admittedly, the author of this article uses the more demeaning slur of “pet humanization” to describe the pet owners’ choices of meat protein over corn and other grains. She writes:

“Pet humanization is still a hot topic in the petfood industry today and is characterized by exactly what it sounds like -- pet owners increasingly taking the well-being of their furry companions every bit as seriously as that of any other member of their family. ‘Consumers are clearly comfortable splurging on pets because they see them as valued family members, not just everyday animals,’ said [Maria Lange, senior product manager for GfK Retail and Technology].”

The fact is that if anyone is guilty of “pet humanization”, it is the kibble manufacturers and their bought-and-paid-for "board certified veterinary nutritionists", who have falsely contended that the digestive systems of dogs have evolved to be similar to humans and less wolf-like.

Grain-free pet food sales increased 32% in 2013

Kibble BowlThe bottom line of the second article is that grain-free pet food sales increased 32% in the United States in 2013. Pet owners spent US$1.4 billion on grain-free dog food products at US pet stores in 2013, according to GfK. Perhaps, within a year or two, the Science Diet kibbles and their ilk will become just a nasty experience of the past.

A follow-up question is: What will all of those pro-corn and anti-meat "board certified veterinary nutritionists" do for a living?

December 12, 2013:

The accordion-muzzled cavalier King Charles spaniel

Why do cavaliers have so many unique disorders of the head?

AccordionThe cavalier King Charles spaniel breed suffers from some fairly unique hereditary disorders in their beautiful heads, including Chiari-like malformation (CM), primary secretory otitis media (PSOM), progressive hearing loss, dry eye syndrome, cerebellar infarcts (strokes), episodic falling syndrome (EFS), fly catchers syndrome, and temporomandibular joint dysplasia. CKCSs may not be the only breed with these disorders, but they clearly have more than their fair share, particularly of CM, PSOM, dry eye, strokes, and EFS.

What is there about the cavalier that explains this uniqueness?

There has been much discussion of late about “brachycephalic” breeds of dogs. The term "brachycephalic" means short-nosed and refers to dogs with short muzzles, noses, and mouths. "Brachy" means short and "cephalic" means head. The throat and breathing passages in brachycephalic dogs often are undersized or flattened. The head's soft tissues are not proportionate to the shortened nature of the skull, and the excess tissues tend to increase resistance to the flow of air through the upper airway (nostrils, sinuses, pharynx and larynx). The consequent disorders are labeled "brachycephalic airway obstruction syndrome" (BAOS).

Teeth OvercrowdedMany cavalier fanciers will argue, vehemently, that cavaliers are not brachycephalic. They point out that most CKCS muzzles are significantly longer than such breeds as the English bulldog, pug, King Charles spaniel (English toy spaniel), French bulldog, and Pekingese. And, indeed, they have an obvious point; the muzzle of the average cavalier appears to be proportionally longer than those other breeds.

Nevertheless, cavaliers seem to have at least their share of brachycephalic disorders – inhalation issues caused by their compressed breathing apparatus – especially an elongated soft palate – not to mention sets of very jumbled teeth and gums (see photo at right). Also, veterinary researchers have unanimously classified the cavalier King Charles spaniel as brachycephalic in their research articles on the subject.

The CKCS's head has been treated like an accordion!

Skulls of King Charles Spaniel & Cavalier King Charles SpanielApart from their relatively longer muzzle, cavaliers’ brachycephalism stands apart for one other reason: The cavalier is the only brachycephalic breed that was created by purposefully elongating an already snub-nosed snout. While the English bulldog, pug, King Charles spaniel (KCS), French bulldog, and Pekingese were fashioned by generation after generation of selective breeding to shorten the muzzle, the CKCS was bred to lengthen the already quite snub-nosed King Charles spaniel. Thus, the cavalier’s head has been treated as if it was an accordion – first shortening it to attain the King Charles spaniel breed standard (see KCS skull at near right), and then, beginning in the 1920s, selecting KCS breeding stock, and perhaps out-crossing, to produce longer snouts (see CKCS skull at far right).

(Specimens from the collections of the Albert Heim Foundation, Museum of Natural History, Bern.)

Consider this series of profiles (below), beginning at the left with an 1850 King Charles spaniel, then a 1910 champion King Charles spaniel, then a 1930 second generation champion cavalier King Charles spaniel, then a 1960 champion CKCS, and finally a 2010 champion cavalier. The accordion affect between the 1850, 1910, and 1930 versions is most noticeable.

Accordion-Muzzled Spaniels 1850-22010

If you consider that breeding to shorten the head will compress the dog’s breathing apparatus, what happens when those jumbled contents then are stretched out again? Certainly, there can be no assurance that the end result would be perfectly relocated airway passages and teeth in the exact position they would have been had no bunching had taken place to begin with. Unlike an accordion, the dog's skull is not equipped with a built-in spring. Once jumbled by compression, it is very possible that the decompressed airways remain confusingly jumbled but just in some other manner. We know that to be the case just by looking in the cavalier’s mouth. Despite a longer muzzle than the KCS, many of the cavalier’s overcrowded teeth are in anything but a functional position.

We also know that the CKCS’s hereditary head disorders, particularly PSOM, dry eye, and CM, are the result of the jumbled consequences of brachycephalism, while cerebellar infarcts are believed to be due to CM altering blood flow to the brain. But, in no other brachycephalic breed are these hereditary diseases anywhere close to being so prevalent. As an example, in a March 2006 article, the radiologists authors noted that, while the canine "tympanic cavity is usually quite large and rounded", in the cavalier, "it is smaller and flatter." The accordion effect of breeding cavaliers could explain the uniqueness of these disorders.

PDFSeptember 23, 2013:

All that cavalier owners need to know
about primary secretory otitis media (PSOM)

Cavalier Being BAER TestedPrimary secretory otitis media (PSOM) has become more frequently diagnosed in cavalier King Charles spaniels. It consists of a highly viscous mucus plug which fills the dog's middle ear and may cause the tympanic membrane to bulge. PSOM has been reported almost exclusively in cavaliers.

Because the pain and other sensations in the head and neck areas, resulting from PSOM, are similar to some symptoms caused by syringomyelia (SM), some examining veterinarians may have mis-diagnosed SM in cavaliers which actually have PSOM and not SM.

The cause of PSOM is unknown. It is suspected to be due to a dysfunction of the middle ear or the Eustachian (auditory) tube: either (a) the increased production of mucus in the middle ear, or (b) decreased drainage of the middle ear through the auditory tube, or (c) both.

The principal symptoms are moderate to severe pain in the head or neck, holding the neck in a guarded position, and tilting the head. Other signs may include scratching at the ears, itchy ears, head tilt, excessive yawning, crying out in pain, ataxia, drooping ear or lip, inability to blink an eye, rapid eyeball movement, facial paralysis or nerve palsy, Vestibular disease, some loss of hearing, seizures, and fatigue. These symptoms, in many cases, are very similar to those of syringomyelia and, to some extent, to those of progressive hereditary deafness. Therefore, the examining veterinarian should take care to consider these other possible causes of the dog's symptomatic behaviors.

PSOM may be detected by veterinary neurology or dermatology specialists from either magnetic resonance imaging (MRI) or a computed tomography (CT) scan. Both require that the dog be under general anesthesia. It also may be observed using an operating microscope with good lighting and at a suitable magnification.

Treatment traditionally has consisted of performing a myringotomy, making a small cut in the eardrum (tympanic membrane), followed by flushing the middle ear to force out the mucus plug. Topical and/or systemic corticosteroids and antibiotics then are administered. The procedure may have to be repeated, in some cases several times, depending upon how the dog responds. An alternative procedure is a ventral bulla osteotomy,which involves making an incision on the under side of the neck behind the jaw bone. The auditory bulla, a hollow bony sheath that encloses parts of the middle ear, then is exposed and is opened.

Some specialist veterinarians have been prescribing N-Acetyl-L-Cysteine (NAC), a mucolytic -- mucus thinning agent or expectorant -- for cavaliers with PSOM, following surgeries.

(This article has been excerpted from "Primary Secretory Otitis Media (PSOM) in the Cavalier King Charles Spaniel" on this website.)

PDFAugust 26, 2013:

All that cavalier owners need to know
about their dogs' blood platelets

Veterinarian examing cavalier King Charles spanielUp to half of all cavalier King Charles spaniels may have both an abnormally low number of blood platelets and oversized platelets. Despite the low platelet counts, the typical cavalier's blood platelets function normally, and the dog does not appear to experience any health problems due to either the size or fewer numbers of its platelets. There are, however, limited exceptions to this typical situation.

An excessively low platelet count normally is a sign which tends to alarm general practice veterinarians, and so it is vitally important that cavalier owners alert their vets about this benign condition in the breed when blood tests are ordered.

No treatment is recommended unless the dog shows other symptoms of a blood-related disorder. Cavaliers should not be treated for immune-mediated thrombocytopenia (IMT) as a precaution. Dog really suffering from IMT must be treated quickly, usually with intravenous doses of immunosuppressive drugs -- steroids, azathioprine, cyclosporine A and others -- to save the dog's life. Such treatments are severe and could do major damage to the healthy cavalier with nothing more than a low platelet count.

Most commercial laboratories use an automated counting system for blood cells, which determine cell types on the basis of their size and volume. Because cavaliers' platelets are so large, automated blood cell counters may not recognize platelets as being platelets and undercount them, thereby inaccurately lowering the platelet count. Researchers have found that CKCS platelet counts using three different automated systems underestimated the actual counts determined manually. Antech Diagnostics, the largest veterinary diagnostic laboratory, has specifically stated on its website that:

"Platelets in this breed should be counted manually, because automated blood cell counters cannot distinguish the large platelets from erythrocytes and therefore underestimate the true platelet count."

An accurate platelet count can be obtained by visually counting the cells. Also, because the large platelets are so fragile, any blood samples should be extracted very carefully. Therefore, all blood samples from cavaliers should be taken in a very careful manner and preferably only from the dog's jugular vein, using a large bore needle, and then should be examined only under a microscope by an experienced clinical pathologist before making a diagnosis of low platelet count.

(This article has been excerpted from "Blood Platelets in Cavaliers" on this website.)

August 10, 2013:

What if the American Kennel Club ceased to exist?

The cavalier’s future after the AKC’s death spiral

akc_tombstoneThe American Kennel Club (AKC) reportedly is withering away. Every year since 1992, its litter and puppy registration numbers have been dropping by as much as double digit percentages. Over the course of the last 21 years*, registrations have declined by over two-thirds, even as the number of dogs in American homes has increased. Observers have predicted that if AKC’s registrations continue to drop at the same rate, it will be out of business by 2025.

* From 1.528,392 in 1992 to 479,404 in 2013.

To continue to survive financially, the AKC has been upping its event fees, such as for conformation shows, obedience, rally, and agility trials, and tracking tests. It even has increased its litter and puppy registration fees, despite the declining registrations. But such counter-intuitive alternative fund-raising initiatives have not stanched its cash crisis. AKC also has cut back on its funding of its programs of kennel inspections, DNA profiling, canine good citizens, search-and-rescue, Canine Health Foundation, legislative issues, etc.

So, what would no AKC mean to the cavalier King Charles spaniel? There are two national CKCS clubs in the United States. One, the American Cavalier King Charles Spaniel Club (ACKCSC), is an official “parent club” for the breed, in the AKC. The other, the Cavalier King Charles Spaniel Club, USA (CKCSC,USA), is independent of the AKC and has been in existence since the 1950s, long before AKC recognition of the cavalier in 1995.

ACKCSC Up-Side-DownIf AKC goes kaput, so too would its CKCS parent club. Except for the occasional “specialty” conformation shows, parent clubs rely totally upon the AKC for direction, litter and puppy registration, rules, judging, and show organization. To survive post-AKC, the parent club would have to learn how to do what the CKCSC,USA has been doing all along for the past 57 years. It would have to re-organize completely, from the ground up, including registering dogs, creating rules, approving judges, organizing its own shows around the country, and finding enough volunteers to do what has been done for them by AKC kennel (all-breed) clubs up to now.

Ironically, after AKC’s demise, the CKCSC,USA may end up being the only show in town for those cavalier breeders who, since 1995, have turned their backs and thumbed their noses at the original cavalier club in the USA.

July 9, 2013:

All that cavalier owners need to know about
natriuretic peptides tests (ANP and BNP)

Veterinarian examining cavalier King Charles spanielThere has been much research into attempting to diagnose mitral valve disease (MVD), and more particularly, to diagnose the onset of congestive heart failure (CHF) in dogs by measuring "cardiac biomarkers", such as blood plasma concentrations of the natriuretic peptides: atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP).

Natriuretic peptides are hormones manufactured and secreted by areas of the heart. A test of natriuretic peptides measures the quantity of the natriuretic peptides in the dog's blood. Elevated levels of these natriuretic peptides in the blood may be directly related to heart defects, and natriuretic peptides in the blood become elevated only after the heart has to pump harder to compensate for the disorder. In particular, BNP is secreted by the left ventricle in response to heart wall stretching or stress.

Our bottom line on this topic has best been stated by Dr. Jennifer L. Garcia in "The NT-proBNP assay: A portent of heart health." in dvm360:

"For conditions such as mitral valve disease, this test may be of limited value because a diagnosis can be readily made by thorough auscultation and documentation of a heart murmur. In these cases, the assay also has limited utility in determining disease severity; thoracic radiography is preferred."

Translated, she is saying that stethoscopic examinations, combined with periodic x-rays of the heart, are more effective in diagnosing MVD and CHF than any blood tests.

History of natriuretic peptide testing

A 2003 study (conducted by Drs. Kristin A. MacDonald, Mark D. Kittleson, Coralie Munro, and Philip Kass of the University of California at Davis) has shown a positive correlation between BNP and heart disease and CHF in dogs. In that study, BNP increased with the progressively increased severity of mitral valve disease and CHF. For every 10-pg/mL increase in BNP, the 2003 study's dogs' mortality rate increased approximately 44% over the four months of the study. In a 2005 study, Drs. William E. Herndon, Justine A. Lee, Kenneth J. Drobatz, and Matthew J. Ryan concluded that "With further investigation, this new BNP assay may someday provide a widely available noninvasive diagnostic test with rapid turnaround time to help diagnose and/or treat heart disease and congestive heart failure in the dog."

However, in earlier studies (1994 and 1997) conducted by Drs. Jens Häggström, Kjerstin Hansson, Clarence Kvart, and others, the researchers have suggested that BNP levels in cavaliers with mitral regurgitation did not rise as dramatically as in humans, and that N-terminal (NT)-proANP (NT-proANP) may better reflect the severity of mitral regurgitation in cavalier King Charles spaniels than NT-proBNP tests.

Four trademarked names for NT-proBNP tests are Canine CardioCare (Veterinary Diagnostics Institute), Canine VetSign CardioSCREEN (Guildhay Ltd.), Cardiopet proBNP (IDEXX Laboratories), and Antech Cardio-BNP (Antech Diagnostics). There have been studies showing the effectiveness of these types of tests for dogs suffering from asymptomatic occult dilated cardiomyopathy (DCM), which is not the same disorder as MVD and is not known to be a genetic problem for cavalier King Charles spaniels.

Natriuretic Peptides Whichever test (NT-proBNP or NT-proANP) is found to be more accurate for detecting MVD, it is believed by some researchers that the test may be useful in assisting examining veterinarians in deciding whether or not detected heart murmurs are innocent or are pathologic in nature. However, in a 2007 study of 54 CKCSs by Drs. Tarnow, Pedersen, Kvart, and others from Denmark and Sweden, they found that "Natriuretic peptides are elevated in cavalier King Charles spaniels with congestive heart failure but not in dogs with clinically inapparent mitral valve disease."

In a May 2008 report by Drs. Mark A. Oyama, Philip R. Fox, John E. Rush, Elizabeth A. Rozanski, and Michael B. Lesser of 119 dogs, they found that "Serum NT-proBNP concentration was significantly higher in dogs with cardiac disease than in control dogs, and a serum NT-proBNP concentration > 445 pmol/L could be used to discriminate dogs with cardiac disease from control dogs with a sensitivity of 83.2% and specificity of 90.0%. In dogs with cardiac disease, serum NT-proBNP concentration was correlated with heart rate, respiratory rate, echocardiographic heart size, and renal function." They concluded that, "For dogs with cardiac disease, serum NT-proBNP concentration could be used to discriminate dogs with and without radiographic evidence of cardiomegaly and dogs with and without congestive heart failure." And that, "Results suggested that serum NT-proBNP concentration may be a useful adjunct clinical test for diagnosing cardiac disease in dogs and assessing the severity of disease in dogs with cardiac disease."

In a May 2009 report from Sweden, the researchers concluded: "Plasma concentrations of the natriuretic peptides measured at re-examination could predict progression in regurgitant jet size."

In a 2012 study of 1,134 dogs, including 37 cavaliers, Stephen J. Ettinger, Giosi Farace, Scott D. Forney, Michelle Frye, and Andrew Beardow concluded that "This biomarker [NT-proBNP] may be a useful tool for staging of cardiac disease and identifying cardiac-related coughing or dyspnea in this species."

In a 2013 study of 36 dogs, none being CKCSs, a team of Japanese researchers concluded: "These results indicated that plasma ANP rose with an increase in the volume overload of the left side of the heart. Plasma ANP discriminated cardiomegaly from non-cardiomegaly caused by asymptomatic MMVD. We conclude, therefore, that plasma ANP concentrations may be a clinically useful tool for early diagnosis of asymptomatic MMVD in dogs."

In an April 2013 report, a team of German veterinary cardiologists studied 352 dogs and found that: "NPs [natriuretic peptides] in canine MMVD are useful to discriminate between asymptomatic dogs and dogs with CHF. Due to a large overlap of NP-concentrations between the groups, NPs do not seem to be useful to differentiate between dogs in stages B1 and B2. Interpretation of NT-proBNP and proANP values should include consideration of sex-specific differences."

 In a January 2017 report, researchers focused upon the inherent variability of NTproBNP in all dogs -- both healthy and MVD-affected -- and how those random variations, called biologic variability, affects the accuracy of population-based reference ranges of NTproBNP readings. They measured NTproBNP in healthy dogs and dogs in stages B1, B2, and C of mitral valve disease, to estimate biologic variability and calculate an Index of Individuality (IoI) for each dog. Of the 28 MVD-affected dogs in the study, 14 -- 50% -- were cavalier King Charles spaniels, along with 10 healthy control dogs. They found that MVD-affected dogs had a lower inherent variability of NTproBNP compared to healthy dogs, and that, as a group, MVD-dogs required a change of 58.2% for NTproBNP to be outside the range of inherent biologic variability and indicate a change in disease. They determined that population-based reference ranges for NTproBNP may have limitations. They stated that:

"It is important for veterinarians to have an understanding of how much a biomarker value could change over time due to randomness vs. disease progression in an individual dog. ... Monitoring serial individual changes in NTproBNP values may be clinically relevant in addition to using population-based reference ranges to determine changes in disease status."

This study suggests that a one-time test may not provide an accurate result, and that many repeats of that test are required over an extended period of time.

Why these blood tests are not necessary to diagnose MVD and CHF

Nevertheless, it appears that veterinary cardiologists and other cardio-specialists should be quite capable of detecting mitral valve prolapse (MVP) murmurs and distinguishing between them and flow murmurs or other innocent varieties of heart murmurs. Since BNP in the blood becomes elevated only after the heart has to pump harder to compensate for the disorder, the question then is: When does the heart start working so hard that BNP levels start to go up? In the cavalier King Charles spaniel's version of heart defects -- mitral valve disease due to deteriorating valve flaps -- there are no immediate external symptoms. It is not yet clear from research studies thus far, as to whether the heart becomes labored enough to produce increased levels of BNP before auscultation is able to detect the murmurs from minimal backflow of blood leaking through the mitral valve flaps. Advocates of BNP testing do represent that that studies of BNP and cardiomyopathy show that BNP is elevated before the onset of signs and murmur. But it does not yet appear that BNP testing is an any earlier warning system for MVD than auscultation.

One possible uniquely valuable use for natriuretic peptides tests is if the dog is approaching congestive heart failure (CHF) without any symptoms. In that case, natriuretic peptides tests, combined with "Left Chambers on Aorta ratio" greater than 4,5, the veterinarian may begin administering ACE inhibitors, pimobendan, and other drugs immediately even though the dog is asymptomatic.  See Dr. Gerard Le Bobinnec's proposal in this report to the 2010 WSAVA Congress. See, also, the 2012 report of the PREDICT Cohort Study, which found that measurements of left heart size (using the "left atrial to aortic root dimension ratio [LA:Ao]") and plasma NT-proBNP concentration independently estimate risk of first-onset of CHF in dogs with MVD. It correctly predicted first-onset of CHF in 72.5% of cases out of 82 dogs, which included cavaliers.

Dr. Oyama has stated that natriuretic peptide tests may also be useful to properly diagnose a dog known to suffer from congestive heart failure and also is in respiratory distress. He said that, “When dogs come into veterinary hospitals in respiratory distress, it’s sometimes difficult to know if they are having a respiratory or heart problem. Such a test could speed effective treatment and also help decide if a dog should be referred to a veterinary cardiologist before undergoing more expensive testing.”

(This article has been excerpted from "Mitral Valve Disease and the Cavalier King Charles Spaniel" on this website.)

July 7, 2013:

The cavalier King Charles spaniel is pre-disposed to ...

The list gets longer

Sick Cavalier King Charles SpanielIn the past two months, we have added two more webpages to CavalierHealth.org – kidney disease and pneumocystis pneumonia. Contrary to some breeders’ claims, we hate to do that; we hate to have to increase our list of genetic disorders to which the cavalier King Charles spaniel is pre-disposed. But when dogs are suffering and dying of genetic diseases and their owners don’t know why, we feel the need to continue their education about the extraordinary list of serious genetic problems in our breed.

Chronic kidney disease and pneumocystis pneumonia are killers. The recent deaths of some CKCSs have prompted us to upload these two new webpages. We urge you all to read about them and become aware of their symptoms. You may save your dogs’ lives by recognizing signs which often elude your veterinarians. One of the unfortunate facts about owning cavaliers is that many vets are totally clueless about some of these serious diseases, mainly because they are either unique to our breed or darn close to it.

The cavaliers’ “pre-disposed” list? Here it is:

Mitral valve disease (MVD)
Chiari-like malformation (CM)
Syringomyelia (SM)
Low blood platelets (idiopathic asymptomatic thrombocytopenia)
Cerebellar infarcts – strokes
Chronic pancreatitis
Brachycephalic airway obstruction syndrome (BAOS)
Curly coat syndrome
Deafness – progressive hereditary hearing loss
Intervertebral disk disease (IVDD)
Diabetes mellitus
Dry eye syndrome
Eosinophilic stomatitis
Idiopathic epilepsy
Episodic falling syndrome
Fly catchers syndrome
Primary secretory otitis media (PSOM) – glue ear
Chronic kidney disesase
Masticatory muscle myositis (MMM)
Muscular dystrophy
Patellar luxation
Hip dysplasia (HD)
Pneumocystis pneumonia
Temporomandibular joint dysplasia

March 26, 2013:

CKCSC,USA embarks on an offensive “charm offensive”

"Forever Guardians of the Cavalier" is its new spin on a BIG LIE!

Old CKCSC,USA LogoThe Cavalier King Charles Spaniel Club, USA has noticed its ever-declining membership over the past several years and has determined that the problem is not its fault, but instead has been due to the "economy" and  poor public relations. At its 2012 Annual General Meeting, president Bruce Henry noted that membership has dropped from 2,000+ five years ago to the current 1,500 range. He attributed this decline “to the general economy since there is no change in the way our club operates.”

If president Henry wanted to be more pointed about the growing insignificance of the CKCSC,USA, he could have added that over the past ten years, membership has dropped by well over half!

Apparently, the CKCSC,USA president is oblivious to the more likely real reason for the membership drop, which is that “there is no change in the way our club operates.” The way the CKCSC,USA has been operating since the departure of president Anne Eckersley (below right) in 2002 perhaps is the real reason for the lack of interest in joining -- and renewing memberships in -- the “Old Club”. It made a major change for the worse back then, and, as Mr. Henry noted, it has not changed since.

The big change

Cavalier's Year of the HeartThe 2002 change? When the post-Eckersley presidents and their boards took charge of the CKCSC,USA, they rejected the health-consciousness of the Eckersley-led board of directors (BOD). Recall that in 1998, president Eckersley presided at the International Symposium on Mitral Valve Disease (MVD), where a panel of veterinary cardiologists and geneticist unveiled the MVD Breeding Anne Eckersley RobinsProtocol. Remember that? At the time, in 1998 (CKCSC,USA’s “Year of the Heart!” -- see its logo at left), it was a major announcement, offering cavalier breeders the solution to breeding litter after litter of cavaliers with early-onset MVD. The Eckersley BOD also unanimously endorsed the MVD Breeding Protocol and actually urged its members to follow it! They also created the CKCSC,USA Health Registry, to keep track of cavaliers which did not develop MVD until after their fifth birthday. Remember the CKCSC,USA Health Registry?

Soviet CensorshipBut with the retirement of the Eckersley administration, her successors unanimously have dumped the MVD Breeding Protocol. In their narrowed minds, it effectively has been air-brushed away, as if that 1998 MVD Symposium never happened, just like old-fashioned Soviet Union censorship.

Soviet Air Brushing Example

Since then, the CKCSC,USA's memberships -- largely non-breeder pet owners -- have plummeted by 50+%, and it has become an indistinguishable step-sister of the AKC’s parent club, the American Cavalier King Charles Spaniel Club. The ACKCSC has been notorious for ignoring the breed’s genetic health problems, and since 2002, the CKCSC,USA has been tagging along right behind. Both clubs deny the existence of the MVD Breeding Protocol and the Syringomyelia Breeding Protocol.

The big lie

The Big LieSo, back to the present: The current CKCSC,USA BOD has unveiled its much-heralded solution to its lousy membership numbers. It is a combination of a new slogan, “Forever Guardians of the Cavalier” (below at right), and a chant of tedious “Watchwords” (which includes a Big Lie):

New CKCSC,USA Logo“We are Forever Committed to the goodwill of the Cavalier;
We are Forever Historians of the Cavalier – we are the history of the breed, and will always be;
We are Forever Protectors of the Cavalier;
We are Forever Dedicated to the health of the Cavalier;
We are Forever Joyful owners of the Cavalier;
We are Forever in Love with the Cavalier;
   and lastly, and most important,
We are Forever Guardians of the Cavalier.”

And so it goes. The Old Club’s solution to the lack of interest in it is to Spin a Big Lie about cavaliers’ health. Maybe this should be its new logo:

Forever Guardians

December 18, 2012:

AVMA’s House of Nannies aims at homeopathic vets

AVMA is bent upon endorsing veterinary malpractice

Nanny BloombergObviously, the AVMA (American Veterinary Medical Association) leadership feels threatened by the complexity and success of homeopathy. So what does it do? It lashes out in ignorance ... again. (It lashed out in August against raw food diets because they were hurting the vets' sales of kibble. See here.) In both instances, AVMA defends its hostility upon the pretext of baseless concerns about health and hygiene. The AVMA is beginning to look like a mass version of the Nanny of New York, Mayor Bloomberg (left).

At its January 5, 2013 meeting, the AVMA’s House of Delegates (read: House of Nannies) probably will pass overwhelmingly this resolution:

"Homeopathy Has Been Identified as an Ineffective Practice and Its Use Is Discouraged

"RESOLVED, that the American Veterinary Medical Association (AVMA) affirms that —

"1. Safety and efficacy of veterinary therapies should be determined by scientific investigation.

"2. When sound and widely accepted scientific evidence demonstrates a given practice as ineffective or that it poses risks greater than its possible benefits, such ineffective or unsafe philosophies and therapies should be discarded.

"3. In keeping with AVMA policy on Complementary and Alternative Veterinary Medicine, AVMA discourages the use of therapies identified as unsafe or ineffective, and encourages the use of the therapies based upon sound, accepted principles of science and veterinary medicine.

"4. Homeopathy has been conclusively demonstrated to be ineffective."

AVMA's premise is a thoughtless lie

Of course, the entire premise of this resolution is a thoughtless lie, as the much more competent American Holistic Veterinary Medical Association has pointed out in its response. Click here to read it.

The AVMA nannies' arrogant adulation of "scientific investigation" is known as "scientism". In his recent article in The New Atlantis, titled "The Folly of Scientism", biologist Austin L. Hughes nails these AVMA hypocrites when he points out:

"Advocates of scientism today claim the sole mantle of rationality, frequently equating science with reason itself. Yet it seems the very antithesis of reason to insist that science can do what it cannot, or even that it has done what it demonstrably has not. ... Scientism claims that science has already resolved questions that are inherently beyond its ability to answer ... Continued insistence on the universal competence of science will serve only to undermine the credibility of science as a whole. The ultimate outcome will be an increase of radical skepticism that questions the ability of science to address even The AVMA's a hurtin' dogthe questions legitimately within its sphere of competence."

AVMA reacts like a hurtin' dog

It is quite ironic that a group of veterinarians whose bag-o-tricks pretty much is limited to antibiotics, steroids, vaccines, indiscriminate neutering, and Science Diet, would condemn homeopathy as "conclusively demonstrated to be ineffective." So, the AVMA leadership is proving once again that its instinctive reaction to successful veterinary care that they do not understand, is to lash out like a hurtin' dog (see at right). When will the AVMA learn that it is not wise to endorse veterinary malpractice? When it forbids vets from using diagnostic and treatment modalities which have been proven to be effective for thousands of years, it is asking to be sued, big time.

Post Script: On January 5, 2013, the AVMA's House of Delegates chose to kick this resolution back for further review. It may raise its ugly head again, at its Spring 2013 meeting. We shall see ...

September 27, 2012:

Dog food companies lie, and allergic dogs may die

Examine the label; then cross your fingers.Let's say that your dog has a raging skin condition that is driving him crazy with itching and has resulted in gooey infections all over his body.  Your veterinary dermatologist suspects a severe allergic reaction to beef and pork, and so he prescribes venison for your dog to eat. You feed your pet a dog food which states clearly on the can that it contains venison and no beef or pork. But, your dog's allergy gets worse instead of better. What's up?

What's up is that dog food companies lie about the ingredients of their products.

In an August 2012 study by ELISA Technologies Inc., manufacturers of ten out of twenty-one tested commercial dog foods falsified the contents of their products by either including ingredients specifically excluded on the label or not including ingredients specifically advertised on the label. For instance:

• A food labeled as containing venison, contained no venison or deer at all, and instead contained beef and pork;

• A food labeled "lamb" contained no lamb and contained pork instead;

• A food labeled "chicken meal" contained pork instead;

• Foods labeled "no gluten" or "grain-free" in fact contained gluten and grain levels four times higher than allowable amounts.

False Pet Food Labeling Table 1

Commercial dog food companies are notorious for switching advertised ingredients, depending upon the varying costs of those ingredients. This August 2012 report clearly substantiates that fact.

When a dog is suspected of having a serious food allergy, veterinary dermatologists typically recommend that the dog be fed an "elimination" diet, by feeding ingredients, usually protein sources, the dog has never had before. For example, if the dog has been fed a typical dry food, usually containing corn, wheat, or other grains, the vet's recommendation is to exclude the corn and grains and feed a particular meat as the protein source. If the allergic dog has been fed beef, the vet might prescribe venison instead.

This study proves that owners of food-allergic dogs cannot rely upon the ingredient lists of dog foods to assure themselves that their dogs are no longer being fed the foods which are causing their allergic reactions. These dog food manufacturers are putting allergic dogs at great risk by falsifying the ingredients described on the packaging, all to save a buck.

September 26, 2012:

Update on Hill's Science Diet junk food

Hill's finally dumps its "superior nutrition" corn and chicken by-products

Kibble versus Real MeatEarlier this year we blogged "The insidious mind control over clueless veterinarians by Hill's Pet 'Nutrition'", in which we pointed out that many veterinary students have been brainwashed by Hill's about its Science Diet dog food, and that these veterinarians continue their nutritional cluelessness throughout their professional careers.

In that blog entry, we emphasized the horrendous main ingredients in Hill's Science Diet dry food: (a) because its corn and chicken by-products really are totally indefensible as being "superior" to real meat as daily sources of protein for dogs; and (b) because so many veterinarians, including "board certified veterinary nutritionists", have prostituted themselves by actually declaring that corn and by-products are better than real meat.

Well, on September 11, Hill's announced* that it is re-formulating its crappiest dry food, Science Diet, by offering a "quality protein first ingredient" (instead of the current "ground whole grain corn"), and "no chicken by-product". This is the first change of ingredients in Science Diet's 44 year history!

* Go to Hill's news release.

Wow! Without corn and chicken by-products, what will Hill's lapdog veterinary nutritionists and all the other sycophantic veterinarians have to rave about? Will they recant their prior praise for Hills' junk food ingredients of corn and by-products? Will they stop claiming that non-meat chicken by-products are "superior" for dogs than, say, a fresh chicken breast? Will they stop boasting that if corn was good enough for the American Indians, it is good enough for dogs? Has Hill's thrown all of these bootlicking vets under the bus?

Hill's Science Diet's New PackagingMind you, Hill's did not make this change willingly. Hill's U.S. President Kostas Kontopanos brags in its news release that its "Science Diet is Veterinarians' #1 choice to feed their own pets." (Imagine the scary thought that, for the past 44 years, more veterinarians have chosen Science Diet to feed their own pets than any other pet food. And we have been trusting their judgment to keep our pets healthy!) He goes on:

"We took a food that already delivered precisely balanced nutrition, industry leading quality and great taste and will make it even better by adding the natural ingredients that pet parents want."

So, Hill's grudgingly concedes that, despite Science Diet's "superior nutrition, backed by clinical research", we stupid pet owners no longer are falling for the hype like all of those veterinarians have. Hill's president pleads further: "We also want to be pet parents' #1 choice, with the ingredients you prefer, the uncompromising nutrition that more than 50 precisely balanced nutrients deliver and the quality you can trust."

So, this sea-change after 44 years is not being done to improve the nutritional quality of Science Diet's ingredients. Oh no. Hill's insists that its corn and by-products always have been the best source of pet nutrition there can be. Hill's is doing this solely because picky pet owners are more concerned about "natural ingredients".

Now, don't get too excited about this "new-but-not-necessarily-improved" Science Diet. We don't know yet what the "quality protein first ingredient" will be. And, we also realize that "natural ingredients" means absolutely nothing in the pet food industry. All we know for sure is that Hill's claims that the current first two ingredients, corn and chicken by-products, will be gone from the top of the ingredients list. Is it just a coincidence that corn and chicken prices have skyrocketed recently?

Post Script: It is January 2013 already, Hill's. Where is this new Science Diet? Hill's promised in September 2012 that it would introduce its new version of Science Diet, with "natural ingredients", in December 2012. So, where is it? And, what is it?  Hill's still has not even told us what the new ingredients are.

August 3, 2012:

The US cavalier clubs contemptuously
keep whistling past our breed's graveyard

Advisory Council on the Welfare Issues of Dog BreedingIn November 2011, the UK's Advisory Council on the Welfare Issues of Dog Breeding identified its "first eight problems which cause serious health and welfare issues for some dogs" as follows:

• Brachycephalic airway obstruction syndrome
• Limb defects (including hip and elbow dysplasia)
• Ocular disease secondary to conformational problems
Heart disease with a known or suspected inherited basis
• Epilepsy
• Skin conditions with a known or suspected inherited basis
• Issues arising from lack of responsible ownership (including problems such as separation-related behavioural issues and obesity)

Do any of these sound familiar to owners of cavalier King Charles spaniels? Well, seven of them certainly are the most serious problems affecting the CKCS. And, two of them -- inherited heart disease and syringomyelia -- are, by far, more severe in the cavalier than in any other breed of dog. Among these eight serious problems, only inherited skin conditions are not commonplace among the cavalier. Otherwise, the UK Advisory Council might just as well have been writing about only one breed -- ours.

So, what are the US cavalier King Charles spaniel clubs doing about these serious problems? Thus far, absolutely nothing. And there really is no reason to expect that they ever will do anything.

Mitral valve disease (MVD) has been identified as a widespread genetic problem in the breed for several decades. Over half of all cavaliers are expected to have MVD by their fifth birthday, and nearly 100% by their tenth year. It is the leading killer of CKCSs. In most breeds, death is more often due to cancer or accidents, RIP Cavalier King Charles Spanielbut in the cavalier it is MVD. In 1998, a panel of veterinary geneticists and cardiologists recommended to the US cavalier clubs a breeding protocol designed to eliminate early-onset MVD in the breed within as few as three generations. Neither national cavalier club endorses the breeding protocol, and one of those clubs, the AKC's parent club for cavaliers, refuses to acknowledge the breeding protocol's existence.

Similarly, syringomyelia (SM) has been identified as an excruciatingly painful genetic problem in the CKCS for over a decade. It is rampant in the breed; over half of all cavaliers are believed to have SM, and 95% to have Chiari-like malformation, which is part of the cause of SM and its severe pain. Since 2005, veterinary neurologists have designed breeding protocols to rid the breed of SM. However, neither US cavalier club has even acknowledged the existence of any such breeding protocol, much less recommended that it be followed by breeders.

The US cavalier clubs continue to skirt along their merry ways, ignoring any realistic solutions to these severe, breed-wide genetic health problems, and thereby encouraging their breeders to compound the extent and severity of MVD and SM in each and every future generation of cavalier King Charles spaniels. 

June 14, 2012:

The insidious mind control over clueless veterinarians
by Hill's Pet "Nutrition"

Hill's Science DietEver wonder why so many veterinary clinics have stacks of bags of Science Diet dog food for sale in their waiting rooms? It probably is because so many vet schools do not teach companion animal nutrition to their students. Instead, these many schools delegate to Hill's Pet Nutrition, the maker of Science Diet, the diet and nutrition curriculum taught to their veterinary students.

Vet's Shelves of Science DietDr. Karen Becker, DVM, who authored Dr. Becker's Real Food for Healthy Dogs and Cats, observed recently:

"Most veterinary students don't learn about species-appropriate pet diets in vet school. The only food discussed is processed, commercial pet formulas."

For nearly all vet students, their schools' nutrition classes have consisted of visits by commercial pet food marketeers to talk about their products. Consider this observation by a veterinarian who graduated from the University of Pennsylvania's veterinary school:

"When I was in veterinary school, we received little education in nutrition (and from walking into the average veterinary clinic today, I assume nothing has changed). Precious little was taught on how to keep the pet carnivore healthy for longevity. The small animal nutrition text was published by a major pet food company and given (not sold) to students."

That major pet food company was Hill's. Consider this telling admission in DVM Newsmagazine:

"Hill's provides financial and educational support to nearly every veterinary college in North America, as well as to veterinary students attending those institutions. This commitment to the profession includes Hill's sponsored teaching programs, residencies and faculty programs in veterinary schools and teaching hospitals all over the world. ...
"Hill's has shown its commitment to the partnership with MSU by providing support to many student groups and student activities; covering costs for students to attend the SCAVMA Symposium; providing students with the textbook Small Animal Clinical Nutrition and other various handouts; ... ." DVM Newsmagazine. Aug. 2004;35(8):38.

That veterinary school textbook, "Small Animal Clinical Nutrition", is published by Mark Morris Institute, which is owned by Hill's. Dr. Mark Morris was the creator of Science Diet kibble.

Hill's " Feeding Programs" -- like pabulum to vet students

Hill's Pet Nutrition Spoon Feeds Vet StudentsIn most USA vet schools, Hill's offers "Feeding Programs", by which it sells its pet foods to students and faculty at majorly reduced cost and donates the sales funds to student groups and scholarships. At each school, one or two students are appointed as "Hill's Contacts" -- not unlike Lenin's useful idiots -- to keep lines of communication open between the unsuspecting students and the pet food conglomerate.

Some vet schools have taken the Hill's bait, hook-line-and-sinker. The University of Florida has a large, permanent display of Hill's Science Diet in the middle of its emergency clinic waiting room. Hill's also is a major benefactor at this vet school, even funding a professorship. See this JAVMA article, "Ethical considerations raised by the provision of freebies to veterinary students", for more details and the ethics involved.

Now, this academic/business relationship would not be so insidious if Hill's Science Diet was a good, nutritive dietary product. But it is not. Here is the list of ingredients in Science Diet adult dry food:

"Ground Whole Grain Corn, Chicken By-Product Meal, Animal Fat (preserved with mixed tocopherols Dry Dog Foodand citric acid), Dried Beet Pulp, Soybean Oil, Dried Egg Product, Flaxseed, Potassium Chloride, Iodized Salt, Choline Chloride, vitamins (L-Ascorbyl-2-Polyphosphate (source of vitamin C), Vitamin E Supplement, Niacin, Thiamine Mononitrate, Vitamin A Supplement, Calcium Pantothenate, Biotin, Vitamin B12 Supplement, Pyridoxine Hydrochloride, Riboflavin, Folic Acid, Vitamin D3 Supplement), Vitamin E Supplement, minerals (Ferrous Sulfate, Zinc Oxide, Copper Sulfate, Manganous Oxide, Calcium Iodate, Sodium Selenite), preserved with Mixed Tocopherols and Citric Acid, Beta-Carotene, Rosemary Extract."

Where's the meat???

NO MEAT!!!Ingredients must be listed on the label in decreasing order by weight. For Hill's Science Diet, the first item is corn, which means that there is more corn in the mix than anything else. Corn is a cheap filler ingredient with little nutritional value. It is not a natural source of food for dogs and is very difficult for them to digest. The second item is chicken by-product meal. Chicken by-products in dog food do not include meat and instead contain cheap, unsavory ingredients ground into the mix, like stomach contents, beaks, feathers, feet, and entrails. But have no fear, because all of it then is cooked to death two separate times, changing the structure of proteins for the worse, and destroying vitamin A, vitamin E, and the B-group vitamins.

No dog should be required to live on this junk. And yet, seemingly intelligent veterinarians tout Science Diet to their patients' owners as "Vets' #1 Choice for their Own Pets".*

* By the way, Hill's Science Diet kibble cat food does not include any meat, either.

Some veterinarians have been so taken by the Hill's mind-numbing indoctrination efforts, that they actually endorse corn and by-products as nutritional ingredients in pet food. Dr. Bridget Edgren, DVM, of All Pets Animal Hospital in Boulder, Colorado, a Colorado State University vet school graduate (where Hill's Feeding Program lures the students) recently authored an article titled "Finding the right food for your pet". Her ignorance about dog nutrition is obvious when she writes:

"Corn ... is a nutritionally superior grain compared to the others because it provides a balance of nutrients not found in other grains. ... Contrary to popular belief, by-products are not hooves, feathers, and beaks, which have no nutritive value. By-products are not harmful and actually have excellent nutritive value."

Yeah, sure.

After all, corn was good enough for the Indians

Indians & Corn StereotypeDr. Sherry Lynn Sanderson, DVM, PhD, of the University of Georgia's veterinary college and a University of Minnesota vet school graduate (both schools have Hill's Feeding Programs) wrote "Raw Diets: Do They Make You Want To BARF?", in which she fervently defends corn as a main ingredient in dog food. She writes:

"If one considers that corn was a main staple in the diet of Native Americans for many years, it is difficult to understand how critics can claim that corn is a filler used in pet foods."

Sad. Her point? She offers no clue. Chickens eat more corn than the American Indian ever did, but neither humans nor fowl are dogs. And this lady is a board certified veterinary nutritionist!

And, Dr. Sanderson is not unique. Another board certified veterinary nutritionist, Dr. Lisa M. Freeman, DVM, PhD, of Tufts University's Cummings School of Veterinary Medicine (another sucker-school for Hill's Feeding Program), also sings the praises of corn and by-products as the major sources of protein, instead of real meat. She writes in "Answering Owners' Questions About Pet Foods" (as if she actually is trying to be helpful to those owners), this incredible statement:

"Some owners are concerned about using diets that contain any vegetable-based proteins, such as soybean or corn. These are NOT added as fillers and contain important nutrients. There is no reason why 'grain free' foods are better for either dogs or cats. ... Pet food ingredients have strict definitions so meat by-products, for example, are not allowed to contain the non-nutritious animal parts that people sometimes worry about (by-products refer to the non skeletal muscle meat – in other words, the organs)"

THE LIAЯ SOCIETYNot true, and totally irresponsible. Remember, by definition, "meat by-products" do not include any meat.*

* The AAFCO definition of "poultry by-product meal: Consists of the ground, rendered, clean parts of the carcasses of slaughtered poultry, such as necks, feet, undeveloped eggs, and intestines, exclusive of feathers except in such amounts as might occur unavoidably in good processing practices."

Why this love affair of so many veterinarians with corn and by-products as the major ingredients in dog foods? The answer likely is Hill's indoctrination programs at the earliest stages of their veterinary education. Junk in; junk out.

Logically, what these "nutritionists" claim makes no sense. Humans, who are far less carnivorous that dogs, are not advised to eat highly cooked, dry, and processed foods instead of fresh, whole food-based diets. Why, then, are kibble and other highly-processed non-meat foods more appropriate for pets?  To the contrary of all this pro-kibble hype from these "nutritionists", research studies that have not been funded by commercial pet fund manufacturers have reached the opposite -- and more obvious -- conclusion that balanced home-prepared meals are much more healthful for our dogs than commercial diets prepared by pet food conglomerates. For example, in a 2003 Belgium study of 522 dogs*, the researchers found that dogs fed a species-appropriate homemade diet lived 32 months longer on average than dogs fed commercially available dog foods.

* Relations Between the Domestic Dogs’ Well-Being and Life Expectancy. Lippert, G., & Sapy, B. Prince Laurent Foundation Price, 2003.

Stop Bad VetsPost Script: Has the AVMA now legitimized veterinary nutrition malpractice? On August 3, 2012*, the American Veterinary Medical Assn. (AVMA) voted overwhelmingly to condemn the feeding of home-prepared raw food to dogs and cats. Not surprisingly, the AVMA's meeting was heavily funded by Hill's and by Purina, another producer of junk dog food. So, these vets apparently have learned nothing beyond what the commercial pet food manufacturers indoctrinated them about in vet school, and continue to wallow in their self-imposed ignorance. The question now is: Has the AVMA legitimized veterinary nutrition malpractice?

* According to the AVMA website, in the four months preceding this AVMA vote, over 60 commercial brands of dog and cat food were recalled, nearly all for "possible Salmonella contamination". Despite these massive recalls of kibble and canned pet foods, AVMA chose to condemn only pet owners for feeding healthful raw food diets to their dogs and cats. Pet owners have been feeding raw diets to their dogs and cats for decades, yet to date, not one documented case of raw pet food causing illness in humans has been reported.

June 3, 2012:

Congratulations to Her Majesty, lover of cavaliers!

Her Majesty, Queen Elizabeth's Diamond JubileeThe Diamond Jubilee of Her Majesty, Queen Elizabeth II! This is a once in several lifetimes' event for the peoples of the United Kingdom and the Commonwealth realms. For the first time in 115 years, their monarch has served 60 years, and only for the second time in the history of the monarchy.

Ruby & Her MajestyThe ties of the cavalier King Charles spaniel to Britain are many and obvious. The breed's name owes itself to one of its kings. But for the prompt and willing response of UK breeders of the English toy spaniel  to the challenge of an American, Roswell Eldridge, in 1926 (the same year the Queen was born), there would be no CKCS breed. Through World War II, those British breeders rescued and salvaged the fledgling breed.

And, thanks to Her Majesty for her total dedication to her life-long job of serving as her realm's sovereign. At age 86 years, she seems indefatigable in dutifully offering herself this weekend in ceremony after ceremony, rain or shine, hours on end, all with grace and dignity. She truly is an amazing person, "a living flag"!

And while she may be a backyard breeder of a lengthy royal line of inbred corgis, the photo above attests that she also loves cavalier King Charles spaniels! May God save the Queen and the cavalier King Charles spaniel!

May 9, 2012:

When ignorance (stupidity?) guides cavalier PSOM research, and the federal government funds it

Dr. Charles Bluestone doesn’t even know what “PSOM” stands for

Dr. ChimpWhat do you get when a medical researcher who thinks chimpanzees are in his own pedigree and that the cavalier King Charles spaniel “has been bred over 300 years to have a short snout”, decides to solve the mystery of what he calls “persistent secretory otitis media” in our breed? Answer: You get Charles D. Bluestone, M.D., professor of otolaryngology at the University of Pittsburgh School of Medicine (UPMC).

Yes, this man is convinced that his ancestors were chimpanzees, despite the lack of any evidence to prove it.* He apparently has blind faith in such unproven theories, which is not a good thing for a research scientist. And yes, he obviously knows nothing factual about the cavalier King Charles spaniel, beyond being able to identify one in a photograph.

* His alleged “evidence”? He irrelevantly and erroneously asserts: “Chimpanzees share an astounding 98.4% of their genetic code with us.” Actually, using Dr. Bluestone’s intellectually shallow means of DNA comparisons, the similarity is more like below 70%, under the most optimal alignment conditions. The 30+% difference represents almost 35 million single nucleotide changes and 5 million insertions or deletions. By his same simplistic standard, the lowly house mouse shares more of our genetic code -- 99% -- than does the chimpanzee. The notion of man's alleged descent from chimpanzees has long been rejected by knowledgeable evolutionists and creationists, alike. (See, e.g.: "The common chimp [Pan troglodytes] and human Y chromosomes are 'horrendously different from each other', says David Page of the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts." The fickle Y chromosome, Nature, Jan. 2010;463[14]:149.)  Why Dr. Bluestone bothers to bring the topic up in a report about PSOM is beyond comprehension. Click here for some more interesting reading about Dr. Bluestone's credibility.

He doesn’t even know the name of the disease he claims to be researching. He repeatedly has called PSOM “persistent secretory otitis media” instead of its real name, “primary secretory otitis media”. Scientists really ought to know the name of what they are researching.

But, with the full weight of federal funding behind him and his co-conspirator, UPMC’s J. Douglas Swarts, Ph.D., he is determined to prove that 300 years of breeding the cavalier for its “short snout” altered its palate muscles to keep its Eustachian tube from operating correctly, thereby causing “persistent secretory otitis media” in “up to 40%”, or “50%”, or “greater than 50%” (pick one) of the breed. Never mind that the modern-day cavalier was created less than 85 years ago and has been bred to have a longer snout – not a shorter one – and that the percentage of cavaliers with PSOM has not been determined.*

* If you want to learn more about PSOM, click here.

When does ignorance morph into stupidity?

Dr. Bluestone's lack of knowledge about the cavalier King Charles spaniel goes way beyond sloppy research. He is so wrong about this breed in so many ways that it is impossible to determine whether he is monumentally ignorant or just flat stupid. Where is his intellectual curiosity? Has he not researched the breed’s founding in the years following Roswell Eldridge’s challenge in 1926? Has he not learned that the cavalier’s longer muzzle sprung from the shorter muzzle of the King Charles spaniel? Does he not even care to learn the actual name of the disorder he has decided to research?

Skulls of King Charles Spaniel (right) and Cavalier King Charles Spaniel (left)

(Specimens from the collections of the Albert Heim Foundation, Museum of Natural History, Bern.)

Note in the comparison of the breeds’ skulls above: the King Charles spaniel skull is at the left, and the skull of the cavalier King Charles spaniel is at the right.

How does federal funding fit into this mess? Leave it to the National Institutes of Health (NIH)* to have wasted our tax dollars on this “research”: Human evolutionary history: Consequences for the pathogenesis of otitis media, published in Otolaryngology -- Head & Neck Surgery in December 2010.

* Federal NIH funding fits Dr. Bluestone's modus operandi: "Bluestone submitted numerous grant applications to the NIH throughout the 1970s and 1980s and ultimately was awarded approximately $17.4 million. At the same time, Bluestone began receiving funding from various pharmaceutical companies to test the effectiveness of their antibiotics in treating otitis media.   Collectively, this industry funding totaled approximately $3.4 million. ... Cantekin claims that as early as 1976, he raised with Bluestone his failure to list his industry funding on his NIH grant applications, but Bluestone allegedly brushed him off, saying that he was not going to tell the 'federal feather merchants' because it was 'none of their business' and would 'muddy up the waters'." Click here for source.

What next for Dr. Bluestone?

Dr. Bluestone stated in his 2010 article that “The underlying pathogenesis of the Cavalier’s ME disease is currently under investigation in our laboratory.” He re-affirmed this disquieting news in his 2011 video, when he redundantly said “It’s a current research project which we are undergoing now.” Most recently, in February 2012, he stated:

“Another ongoing research project involves a potential animal model, Cavalier King Charles Spaniel, which has a greater than 50% incidence of chronic otitis media effusion.* Research being conducted with his colleagues in this animal involves histopathology of the middle-ear cleft in cadavers, and Eustachian tube function tests in live animals, conducted at the Ohio State University School of Veterinary Medicine in Columbus Ohio. ”

* It seems he keeps increasing the percentage of incidence of PSOM in the breed, each time he makes a public comment, and this time, he has re-named the disorder “chronic otitis media effusion.” So, apparently his new acronym for PSOM would be “COME”!

We can only pray that some wild hair will distract him from his focus on the cavalier King Charles spaniel. Otherwise, we will have to endure more of his ignorance, hopefully not on our tax dime.

March 14, 2012:

AKC's CHIC program is a farce for cavaliers

Don't be fooled by cavalier breeders who brag about CHIC

CHICThe American Kennel Club* (AKC) sponsors the Canine Health Information Center, also known as CHIC, with the stated mission "To provide a source of health information for owners, breeders, and scientists, that will assist in breeding healthy dogs." Unfortunately, for the cavalier King Charles spaniel, CHIC not only does not work; it actually encourages bad breeding practices and allows bad CKCS breeders to hide behind the CHIC "Good Housekeeping" seal (see right).

*And its partners, the Canine Health Foundation (CHF) and the Orthopedic Foundation for Animals (OFA).

The two major genetic diseases affecting the cavalier King Charles spaniel are mitral valve disease (MVD) and syringomyelia (SM). Contrary to its "mission", CHIC provides absolutely no useful MVD or SM "health information ... that will assist in breeding healthy" cavaliers.

MVD is the leading killer of cavaliers. Statistics have repeatedly shown that over half of all cavaliers are expected to have MVD by their fifth birthday and nearly 100% by age ten years. SM is a spinal disorder which can cause excruciating pain. Statistics show that up to 25% of cavaliers may have SM by their first birthday and up to 70% by age 6 or older.

One would think that if AKC's CHIC program really wanted to "assist in breeding healthy" cavaliers, CHIC would recommend that breeders follow the breeding protocols* designed to reduce MVD and SM in future generations of cavalier puppies. Well, CHIC does nothing of the sort.

* Read the details of the MVD Breeding Protocol here, and the SM Breeding Protocol here.

Test for MVD? Yes ... but pass that test? Not necessarily!

As for MVD, all CHIC requires is that the breeding stock be examined by a veterinary cardiologist. It does not require that the results of the examination show no mitral valve disease. A cavalier of any age can be examined, flunk the exam, and still qualify for a CHIC certificate and be bred! See for yourself, from the CHIC policies webpage:

CHIC Number





Syringomyelia? Never heard of it!

As for SM, CHIC has no requirements at all! As far as CHIC is concerned, syringomyelia is not a problem in the breed, and any cavalier may be bred without testing for it, much less found not to have it.

So, if a cavalier breeder brags to you about her dog having a CHIC certificate, tell her you know exactly what a CHIC certificate means, and most importantly, what it does not mean.

March 1, 2012:

Pedigree Dogs Exposed: The Sequel, or The End?

Most all cavalier breeders still refuse to get the message

Pedigree Dogs ExposedPedigree Dogs Exposed was a televised investigatory documentary about the British purebred dog scene. It was first broadcast in the United Kingdom in 2008 and then on PBS in the United States in 2009. Since then it has been available on YouTube.

The program focused on a handful of dog breeds, but it had an enormous impact on the cavalier King Charles spaniel (CKCS) because it included video clips of cavaliers writhing in agonizing pain from syringomyelia (SM). (See photo below.) So, for many cavalier owners it was particularly eye-opening because, for the first time, many who viewed it were able to recognize similar symptoms of SM in their own pet cavaliers.

The program produced howls of protest from many corners of purebred dogdom, including over here in the US. The chairman of the American Kennel Club, Ron Menaker, referred to it as "sensationalist fiction and tabloid journalism masquerading as a documentary." But, he's an ignoramus. As far as the CKCS is concerned, every second of that program was factually accurate and needed to be publicized.

"From creation to ruination in less than 100 years"

PDE Cavalier Writhing In Pain From SMEarlier this week, its sequel, Pedigree Dogs Exposed -- Three Years On, was broadcast in the UK. It, too, now is available periodically on YouTube. The cavalier remained a prime topic in this sequel, and the conclusion to be drawn from it is that, with early-onset mitral valve disease (MVD) -- nearly 100% affected by age 10 years -- as well as syringomyelia -- over 70% affected -- it is time for pet buyers to seriously avoid getting cavaliers. As the program's commentator put it, "From creation to ruination in less than 100 years." The rationale is that if the breeders persist in refusing to follow the MVD breeding protocol and SM breeding protocol, so as to avoid producing future generations of only terminally ill cavaliers, then this breed should come to an end.

What has been the response of many cavalier breeders, to this sequel? Pretty much the same as to the 2008 broadcast: hostile condemnation. So, we are likely to see no progress on the breeding front. For the most part, the only people who "get" the truth are the pet buyers.

The likelihood of finding a cavalier puppy in the USA that either won't develop a heart murmur before its fifth birthday or won't have Chiari-like malformation and syringomyelia, is pretty much nill. Many US cavalier breeders have known about the MVD breeding protocol since 1998 and the SM breeding protocol since 2005, and yet most all of them have ignored both protocols.

For the rest of the US breeders, well they just don't even know about these real breeding protocols. In the US, there are two national breed clubs, one in the AKC and one out of it. Both of them refuse to recommend that their members follow either protocol. In fact, both of them recently have concocted their own phony MVD breeding protocols which no panel of cardiologists has ever approved, and neither club has even acknowledged the existence of the SM breeding protocol.

So, with breed clubs like those two, the CKCS appears to be on an unstoppable downward slide. The end result in the US probably will be generation after generation of sickly cavaliers, with high price tags and even higher veterinary and medicine bills. Surely that cannot go on very long. And then we will have none.

December 24, 2011:

Will the next SM breeding protocol be

Breeding under age 2.5 years would increase early-onset MVD

Wrong Way -- Right WayThe cavalier King Charles spaniel has TWO severe genetic health disorders, NOT JUST ONE! While syringomyelia (SM) is very widespread in the breed, so is mitral valve disease (MVD), and it is MVD – not SM – that is the cavaliers’ leading killer!

While the next SM Breeding Protocol, scheduled to be released in 2012 by the British Veterinary Association and the Kennel Club (BVA/KC), still is a work-in-progress, a preliminary draft of it (see below) would permit the breeding of cavaliers as young as 12 months old! If so, this certainly would violate the MVD Breeding Protocol, which sets the MINIMUM AGE for breeding cavaliers at 2.5 years of age.*

* A September 2010 statistical report has shown that anything less than following the MVD Breeding Protocol has not worked.

Proposed New SM Guidelines

Have the new BVA/KC's SM protocol drafters forgotten about MVD?  Are they giving CKCS breeders a deadly choice? Is the SM protocol really going to recommend that breeders ignore the MVD Breeding Protocol and thereby produce future generations of many more cavaliers which will die early, painful deaths from congestive heart failure?

Some background

It has been five years since the International Syringomyelia Conference issued its “Revised CKCS MRI Screening and Breeding Recommendations” in November 2006. The introduction to those breeding recommendations, also called the SM Breeding Protocol, stated:

“These breeding recommendations are made using current information and in response to CKCS breeder request for guidelines. It has yet to be proven if this guide is appropriate. The aim of these recommendations is to reduce the incidence of symptomatic syringomyelia (SM) in the breed, not to create litters of puppies guaranteed not to have SM as the chance of producing an affected dog cannot be predicted without knowing the inheritance.”

The general principle of the 2006 guidelines is that dogs graded “Code A” are more desirable to use than those graded “Code B”, and so on, but that dogs with a higher letter code may still be used in some limited circumstances.

Significantly, the protocol was predictively accurate. Statistics reported in October 2010 showed that:

• 75.9% of the offspring of matings of a Code A sire to a Code A dam were SM-clear.
• 41.9% of the offspring were SM-clear if only one parent was Code A.
• 0% of the offspring were SM-clear if neither parent was Code A.

Statistics reported a year later, October 2011, were similarly on target:

• 70% of the offspring of matings of a Code A sire to a Code A dam were SM-clear.
• 23% of the offspring were SM-clear if only one parent was Code A.
• 8% of the offspring were SM-clear if neither parent was Code A.

Still, much more has been learned about SM in the cavalier since the “current information” available to the International Syringomyelia Conference in 2006.

A June 2011 UK study of 555 cavaliers (Parker Report) showed that:

• 25% of 12 month old asymptomatic CKCSs had SM.
• 70% of asymptomatic CKCSs six years and older had SM.

These figures do not include SM-affected cavaliers which displayed symptoms, so, as the researchers concluded, “The true prevalence of syringomyelia in the general CKCS population is expected to be higher.” They also concluded that, based upon their statistics, the minimum age of the SM Breeding Protocol ought to be raised from 2.5 years to 3.0 years, although they recognized that “many breeders would consider 36 months unduly old.”*

*There is irony for you! The fact is that most cavalier breeders consider 2.0 years unduly old for initial matings.

In an October 2011 UK study (Knowler Report), the researchers go even farther. First, they concur with the Parker Report that “the optimum age for this early MRI screening is 36 months.” Then, they recommend that, if only one of the breeding pair is SM-clear, it be “five years or older”.

This is a matter of veterinary ethics!

So, with those two recent reports on the table urging raising the minimum breeding age to three or even five years, how can the BVA/KC possibly – even ethically – decrease that age from 2.5 years to one year?

The clear answer is that they should not! If the final, approved version of the new BVA/KC SM Breeding Protocol allows breeding any cavalier under the age of 2.5 years, then it will undercut the MVD Breeding Protocol, and it will be encouraging rampant early-onset MVD in the breed!

At the very least, the final version of the BVA/KC guidelines chart should change Age from "1-3" to "<3".

October 14, 2011:

What do the two USA CKCS clubs have against
breeding healthy cavalier King Charles spaniels?

Call 'Em!The syringomyelia (SM) breeding protocol works! (See the October 2011 statistical report.) And, anything less than the mitral valve (MVD) breeding protocol has not worked! (See the September 2010 statistical report.)

BUT ... STILL ... neither of the USA cavalier King Charles spaniel clubs will recommend that their members follow either of these breeding guidelines.

Email "Em!Why don't these two breed clubs, the American Cavalier King Charles Spaniel Club (ACKCSC), and the Cavalier King Charles Spaniel Club, USA (CKCSC,USA), oppose SM and early-onset MVD in future generations of CKCSs?

Why don't they endorse the MVD and SM breeding guidelines?

Ask their presidents. Call and email them.

The president of the ACKCSC is Patricia Kanan, telephone 805-688-7830, email torlundy@comcast.net

The president of the CKCSC,USA is Anne Eckersley, telephone 203- 616-5443, email ChadwickCavaliers@comcast.net

September 13, 2011:

A neurologist answers our August 13 questions:
"Okay syringomyelia researchers:
What now? Where do we go from here?"

Cash!Lo and behold! For a moment there, I thought we might have had a definitive answer to the query: "So, where do we go from here ...? Yo, researchers, do you have any suggestions?" in our August 13 editorial.

In the September 10, 2011 issue of the Veterinary Record, UK veterinary neurologist Rita Gonçalves wrote an editorial titled, "Understanding Chiari-like malformation: where are we now?"

"Ah ha", I thought! What wisdom does she have to impart? Well, not much, actually. After a brief but thorough and concise review of CM research in the cavalier King Charles spaniel, up through mid-2011, along with comparisons to the research of human Chiari malformation, Dr. Gonçalves reaches this painfully disappointing but quite obvious conclusion:

"Chiari-like malformation has for a decade now been widely identified in the CKCS population but despite its high prevalence, little is still known about its pathogenesis. Further studies are necessary to increase our understanding of this condition in order to allow the development of new treatment options and improve the welfare of the CKCS affected."

So, the answer essentially is that we need more money to continue the research, so that we can close in on the mysteries of the causes and solutions to CM and SM in our precious breed.

August 29, 2011:

Plucking the MVD genes:
The first shoe has dropped!

Canine ChromosomeThe headline of the September 2011 Journal of Heredity article says it all: "Identification of 2 Loci associated with development of myxomatous mitral valve disease in cavalier King Charles spaniels." Translation? It means that the first step towards finding a DNA test for early-onset MVD genes has been taken. The first shoe has dropped.

Soon there should be a second shoe heard hitting the floor, when the researchers announce they've identified the actual genes themselves. In their report, they state:

"We will initiate studies of the most promising candidate genes in the 2 candidate regions which hopefully will lead us to the mutations affecting the development of mitral valve disease."

And then the thud of a third shoe (yes, we are talking about a triped here) will be felt when the researchers offer the DNA test to determine which cavaliers do or do not carry the offending genes.

That will be when the shoes hit the fan! For it has been well over a dozen years since the MVD breeding protocol was offered to cavalier breeders in the USA as the means of eliminating early-onset MVD in the breed. Since that announcement in 1998, nearly all of those "reputable", "responsible" cavalier breeders have declined, claiming that they would prefer to wait until the MVD genes are identified. Instead of trying to reduce MVD in their breeding stock, they chose to hide behind that excuse, and they continued to produce generation after generation of cavaliers with worse and worse early-onset MVD.

But now, those breeders' big bluff is about to be called. Soon enough, they will have what they claimed they've been waiting for. They claimed that they would not risk following the MVD breeding protocol because they feared that it would eliminate too much of their breeding stock. If they thought the MVD breeding protocol would have that much of an effect, just imagine what the DNA test will do to their bloodlines! It may wipe out entire kennels of breeding cavaliers!

So, it looks like they're going to have to come up with a new excuse for ignoring the DNA test. Start thinking hard now, you "reputable", "responsible" breeders. You don't have much time left!

August 18, 2011:

Will the CSF-space gap predict
future syringomyelia in cavaliers?

MRI from April 2012 studyIn a recent research study of cavalier King Charles spaniels with Chiari-like malformation (CM) and some with both CM and syringomyelia (SM), the researchers reported:

"When [cerebrospinal fluid] CSF space between the cerebellum and brainstem was compared in CKCS with and without SM, there was a significant increase in CSF space in CKCS with CM alone compared to those with CM/SM when head position was flexed. In their cine MR imaging study of CSF flow dynamics in CKCS with CM or CM/SM, Cerda-Gonzalez and others (2009a) found that turbulent CSF flow and jets are associated with SM presence and severity and CSF flow velocity at C2/3 is inversely related to the presence of SM. The reduced CSF space in CM/SM dogs reported in this study could explain this jet like CSF flow in dogs with CM/SM compared to those with CM alone."

Translation? We THINK it means that there is more space for cerebrospinal fluid (CSF) between the cerebellum and the brainstem of cavaliers with just CM than there is of cavaliers with both CM and SM.

Now, one of the current issues about CKCSs is that those younger ones with only CM still may develop SM as they age. Another recent study found that most cavaliers do not develop SM until after their third birthday and as late as age 6 years. Most all cavalier breeders believe that it is unreasonable to have to wait until their breeding stock is over 3 years old before being bred for the first time.

It would be a very valuable piece of information for any breeding program to be able to predict if a young cavalier (say, at age 18 or 24 months) will or will not ever develop syringomyelia.

This study may lead to the answer to the question: Can an MRI at an early age, showing the amount of CSF space between the cerebellum and the brainstem, predict whether the cavalier will or will not end up with SM?

August 13, 2011:

Okay, syringomyelia researchers:
What now? Where do we go from here?

What? Where? When?HERE IS THE SITUATION: In June, a team of veterinary neurologists issued a devastating report. They examined the MRI scans of 555 cavalier King Charles spaniels, and found that at age 12 months, 25% had syringomyelia (SM), and by age six years, 70% had SM. And, all 555 of these were cavaliers which reportedly had no symptoms of SM.

THINK OF IT: Not only did 25% of these cavaliers already have SM by their first birthday, but in the five years between age 1 and age 6, 45% of the rest of the cavaliers acquired SM.

Previously, these neurologists thought that most dogs afflicted with SM would start to show symptoms before age 3 years. When the International Syringomyelia Conference issued its revised CKCS MRI screening and breeding recommendations in 2006, the panel of researchers stated:

“The age cut off at 2.5 years has been decided so as to tie in with MVD recommendations and because most dogs with symptomatic SM will show signs before 3 years of age.”

That cut off age meant that cavaliers at least 2.5 years old without SM would be classified as Code “A” and could be mated with any other cavaliers over 2.5 years, even if they had asymptomatic SM.

Now, we find, most cavaliers do not even contract SM until after they are 3 years old, much less also become symptomatic.

The authors of the June 2011 report, J. E. Parker, S. P. Knowler, C. Rusbridge, E. Noorman, and N. D. Jeffery, carefully worded the serious impact of these findings upon the current SM breeding protocol:

“The evidence for a lower prevalence in younger animals is more reliable ... and this effect lasts until dogs are at least three years of age. This finding has important implications for the design of a screening test procedure and may conflict with the current recommendations that the optimum age for screening should be 30 months. These data would imply that it is probable that dogs aged up to three years may yet have reduced odds for the diagnosis of syringomyelia. However, there is a need for the dogs to be screened when they are reasonably young so that breeders can decide at an early stage whether their animals are suitable for breeding; many breeders would consider 36 months unduly old.”

GET IT? This means that more cavaliers develop SM after age 2.5 years than before that age. So, the current SM breeding protocol is ineffective. But, they also observe that breeders would not consider waiting until their MRI-clear cavaliers are 3 years old (“unduly old”). Thus the dilemma in which we CKCS fanciers find ourselves.

WHAT TO DO? WHAT TO DO? Well, the researchers don’t give us much hope. They go on:

“The high lifetime prevalence of syringomyelia raises concerns for the welfare of the CKCS breed and also suggests that eliminating the genetic risk factors for the disease by selective breeding may be difficult, because the heritability has previously been shown to be complex ... and the prevalence of the determinant genes within the population is therefore likely to be high. The true prevalence of syringomyelia in the general CKCS population is expected to be higher than that found in this sample population because symptomatic dogs were specifically excluded.”

RAISES CONCERNS!!! To say the least! MAY BE DIFFICULT!!! What an understatement! We now know that SM is far more widespread in the breed than anyone, even the experts, ever thought. We now know that the 2.5 year cut off in the SM breeding protocol is way too early, but that many breeders would not stand for extending that age by even another six months.

(Actually, the dirty little secret is that nearly all US cavalier breeders always have been ignoring the current SM breeding protocol. Neither of the two CKCS national clubs in the US will even acknowledge that the breeding protocol exists, much less recommend that breeders follow it.)

So, where do we go from here, cavalier fanciers? Yo, researchers, do you have any suggestions?

July 24, 2011:

AKC's chairman Ron Menaker condemns
"Pedigree Dogs Exposed"

Then reinserts his head firmly back underground

AKC Chairman Ron MenakerIs this any way to lead the American Kennel Club through the genetic morass it is facing?  On July 19, the chairman of the board of the American Kennel Club, Ron Menaker, signed a petition to the UK's Parliament to prevent the British Broadcasting Company from broadcasting a sequel to "Pedigree Dogs Exposed" (PDE), the 2008 BBC documentary which has turned the British purebred dog world upside-down.

Chairman Menaker did not stop at just adding his name to the petition to Parliament. He also wrote:

"Responsible dog owners, the dog loving public and responsible dog breeders should not be subjected to another piece of sensationalist fiction and tabloid journalism masquerading as a documentary. Any investigation of dogs, breeding or health matters should be balanced and fair. If the BBC insists on repeating this exercise in media sensationalism, why not present the truth about the progress that has been made as a result of responsible dog breeding and scientific research projects funded by organizations that truly care about dogs. For the BBC's next installment, how about 'Jemima Harrison Exposed'?"

Thus, the AKC chairman wants UK's Parliament to both ban the BBC from broadcasting its upcoming PDE-2, and to force the BBC to present an exposé of PDE's producer, Jemima Harrison. Putting aside all of the anti-Freedoms of Speech and Press and censorship aspects of AKC Chairman Menaker's comments, it is jaw-dropping that the highest ranking officer of the American Kennel Club would wage so public and vicious an attack against PDE and its producer, just as that same producer is putting together the sequel which Mr. Menaker so desperately seems to want to prevent.

Hullo, Mr. Menaker?  Can you spell "Good Public Relations"?

Head In SandOne of the reasons PDE has had such a dramatic impact upon the British pedigree dog world since 2008 is that the UK Kennel Club and its breed clubs, including the UK's cavalier King Charles spaniel club, refused to substantively cooperate during its production. CKCS club members literally turned their backs on PDE's cameraman. But even those UK clubs had enough savvy to not publicly and personally lash out at Ms. Harrison, its producer.

On the one hand, AKC Chairman Menaker attacks PDE and it’s producer for not being "balanced and fair", and yet on the other hand, instead of offering information to help make PDE-2 more balanced and fair, he wants the British government to ban it! And investigate its producer, to boot! His head-in-the-sand approach is not going to work for the AKC, and if Chairman Menaker is not careful, soon Ms. Harrison may cross the pond to produce PDE-3, and re-pay him for his courtesies.

June 13, 2011:

How the syringomyelia breeding protocol
could lead to the Popular Sire Syndrome

Many "D" bitches mated with the same "A" stud =
another genetic crisis for the CKCS

Popular Sire In ActionFor corner-cutting breeders of cavalier King Charles spaniels, trying to follow the syringomyelia (SM) breeding protocol could lead to a uprising of the dreaded Popular Sire Syndrome*.

*A Popular Sire has been defined in canine research papers as having produced more than 100 offspring.

The current SM breeding protocol, introduced to the cavalier King Charles spaniel community in 2006 by the International Syringomyelia Conference, only requires that one of a breeding pair of cavaliers not have syringomyelia. The other cavalier of that pair may either have syringomyelia but without any symptoms – according to its magnetic resonance imaging (MRI) scan – or it may not even have been MRI scanned at all.

Specifically, the protocol provides that a dog classified as an "A" must be over 2.5 years of age and that SM is "absent or less than 2mm central canal dilatation in the C2-C4 region only". A "D" cavalier is one which is over 2.5 years and diagnosed by MRI to have "asymptomatic" SM, meaning that the dog has the disease but does not act like it does. That is one way a cavalier may be classified as a "D". The other way is to be over 2.5 years but to not be MRI scanned at all. So, as long as the dog is over 2.5 years and does not behave like it is suffering from SM, it is a "D" dog. This is known as a "default D" dog.

Most cavalier breeders have more female breeding stock than males. Having too many – in some cases even just one – intact males around can cause more problems than the males are worth. So, most cavalier breeders who do not rely much upon line breeding, will hire other breeders’ studs for mating, rather than keep the dogs in their own households with all those bitches around.

When a financially-challenged CKCS breeder with, say, a half dozen bitches as her breeding stock, considers the SM breeding protocol, she finds that MRI scanning can be quite costly. One thorough scan for just one bitch can cost thousands of dollars, when the ancillary procedures are taken into account, such as blood tests, anesthesia, radiologist and neurologist fees, transportation, etc. Multiply that cost by the number of bitches in the breeder’s kennel, and then maybe double that figure, since more than one MRI scan could be necessary during the breeding years for each bitch. Dealing with just this one protocol for this one genetic disorder could wipe out any hopes of the breeder breaking even on the litters all of her bitches could be hoped to produce.

An apparent solution to this breeder’s dilemma is the option under the SM protocol to not scan her breeding stock at all. If they don’t have symptoms of SM, then she can call all of them "D"s, hence the term, "default D". And if she can find a sire which has been MRI scanned and classified an "A", she could use that sire on all of her "default D"s and still satisfy the SM protocol.

But what about using that one "A" sire on so many "D" bitches? And what about all the other cavalier breeders who decide to take the same approach and also use that "A" male on all of their "D" bitches?

That would be a classic case of Popular Sire Syndrome (PSS). Yes, the current SM breeding protocol encourages corner-cutting breeders, with "default D" bitches, to use the same limited pool of sires, called "Popular Sires", in this case "popular" because they are among a very limited number of "A" dogs.

The PSS is believed to be one of the main causes for the spread of genetic disorders in any breed. As a result, geneticists have urged all breeders to avoid using the same dog for mating all or most of their own breeding stock, and also to avoid using the same sires that several other breeders have been using. Even the owners of the sires themselves have been urged to limit the usage of their dogs by breeders.

Cavalier breeders should not take the short-cut of calling their unscanned bitches "D" (for default), and then breeding them to the same "A" male, to satisfy the SM breeding protocol. But, if past history is a guide, many of corner-cutting cavalier breeders will do just that, and the CKCS community will face another genetic crisis soon enough, thanks to another round of the Popular Sire Syndrome.

May 11, 2011:

CKCSC,USA's board admits Its ignorance
... but not its stupidity!

You Can't FIX Stupid, But You CAN Vote Them Out!After repeated denials, the CKCSC,USA's current board of directors finally admitted that its 1998 predecessor board really did endorse the real MVD Breeding Protocol.  In the official minutes of the board's October 14, 2010 meeting, it says:

"In response to numerous inquiries and comments regarding the guidelines adopted by the CKCSC-USA, David Frederick clarified that guidelines are not medical protocols. The protocol suggested by a cardiology symposium held in conjunction with the 1997 [really was in 1998] National Specialty specified 2.5 years as the minimum age for first time breeding of dogs and bitches. This protocol was endorsed by an earlier Board." (Emphasis added, of course.)

So, there you have it. The current CKCSC,USA board admits that it was wrong when it claimed that its April 2010 breeding recommendations were "historic" and that "none had existed before"*. Unfortunately, what it did not do at its October 2010 meeting is re-instate the real, one-and-only MVD Breeding Protocol, which this current board un-ceremoniously dumped at its April 2010 meeting. Read "CKCSC,USA Dumps MVD Breeding Protocol" for those details.

The current CKCSC,USA board still endorses only a worthless breeding guideline which no panels of cardiologists or geneticists researchers have ever recommended, and which, they have told us, has not worked and would not work! Stupidity and callous disregard for the hearts of future generations of cavaliers still reign at the Cavalier King Charles Spaniel Club, USA!

*Interestingly, one of the current board members was also on the 1998 board which unanimously endorsed the real MVD protocol. Notwithstanding her inexplicable memory lapse, she now can say that she voted for it before she voted against it!

April 23, 2011:

Beware the pimobendan/Vetmedin "EPIC clinical trial":
There is no upside

If your cavalier is in it, PULL OUT!

BewareThere comes a time when owners of cavalier King Charles spaniels must say “NO!” to participating in a pharmaceutical company’s study of its proprietary brand wonder drug. The on-going “EPIC Clinical Trial” of pimobendan is a prime example. EPIC is being sponsored by its developer, Boehringer Ingelheim GmbH, a German pharmaceutical company, which markets the drug under the registered brand name “Vetmedin”.

Background of pimobendan

Cavalier King Charles spaniels suffering from mitral valve disease (MVD) and in the late stage of congestive heart failure (CHF), often are prescribed pimobendan. This drug has been shown to improve the quality of life for dogs suffering from CHF due to MVD. It can be very effective at increasing the strength of the heart muscle contractions, thereby improving the heart’s efficiency to function as a pump, and increasing the blood flow to major organs. It even has been shown, in some studies, to actually reduce the amount of backflow of blood through the mitral valve and reverse the enlargement of the heart chambers.

But, there also can be negative aspects to pimobendan. It can have life-threatening (or worse) side-effects when prescribed for asymptomatic dogs or to dogs which, even though they have enlarged hearts and are in CHF, also still have strong heart muscles and good contractility. For those dogs, pimobendan has over-increased their hearts’ pumping ability and contractility to the extent that their mitral valves’ major chordae tendineae have been overworked and, in some cases, have actually ruptured, causing immediate death. (Click here for summary of three disturbing research reports about the inappropriate administration of pimobendan to dogs not in CHF, and a dire warning from Vetmedin's manufacturer itself.)

Cautionary Statements About Pimobendan

US Food & Drug AdministrationThe U.S. Food and Drug Administration’s (FDA) 2007 report approving the use of pimobendan for dogs also contained the warning that the drug not be prescribed by dogs which are not in congestive heart failure. On each container of Vetmedin is the warning that “Vetmedin should not be given in cases ... where an augmentation of cardiac output is inappropriate for functional or anatomical reasons. Warnings: Only for use in dogs with clinical evidence of heart failure.”  (Click here to read more about pimobendan and its downsides.)

The bad news EPIC trial

Pimobendan’s manufacturer’s EPIC Clinical Trial has no upside for cavaliers. The trial’s criteria are that cavaliers with some heart enlargement due to MVD but which do not have any clinical signs and are not in CHF, are to be given twice-daily doses of either pimobendan or a worthless placebo and nothing else. This daily medication (or placebo) is intended to go on until the dog develops heart failure.

We already know, from the extensive studies relied upon by the FDA in its approval report, that pimobendan should not be prescribed to dogs if they are not in CHF. Even the EPIC Trial's own website contains this pointed reason to not prescribe pimobendan at such an early stage. It states:

"In the recently published ACVIM Consensus Statement, there is no treatment recommendation for dogs in this stage of heart disease."

We also know that treating a progressive disorder like MVD with only a worthless placebo -- and nothing but a worthless placebo -- until heart failure results, can be an extremely risky protocol for any cavalier. It would be irresponsible of the cavalier’s owner and its cardiologist.

So, much like Hobson’s choice, you can allow your cavalier to risk pre-mature death due to being given pimobendan when it could do more harm than good, or you can allow your cavalier to not be treated with anything at all until it develops heart failure.

Just say NO!

Just Say NO!Occasionally, or perhaps even more often than that, pharmaceutical companies’ motivations to sell their products tend to outweigh the ethical prudence they should display to not encourage inappropriate marketing. We are not suggesting that this manufacturer’s current EPIC Clinical Trial is such a marketing ploy. But knowing what we do know about the lethal dangers of prescribing pimobendan to cavaliers too early in the progression of their MVD, or to cavaliers even in congestive heart failure but still with strong contractility, this is a potentially terribly flawed study, and cavalier owners should not allow their dogs to participate in it.

Research Report Summaries:

In "Comparative adverse cardiac effects of pimobendan and benazepril monotherapy in dogs with mild degenerative mitral valve disease: a prospective, controlled, blinded, and randomized study", published in 2007 in the Journal of Veterinary Internal Medicine, the researchers found that "PIMO has adver se cardiac functional and morphologic effects in dogs with asymptomatic MVD."  

In "Increased Mitral Valve Regurgitation and Myocardial Hypertrophy in Two Dogs With Long-Term Pimobendan Therapy", published in 2005 in Cardiovascular Toxicology, the researchers concluded "This is the first report to describe an increase in mitral regurgitation under clinical conditions in dogs treated with pimobendan. We also suggest that pimobendan may induce ventricular hypertrophy."  

In Cardiac Care for Pets' (CVCA) "Pimobendan– A Silver Bullet?", published in May 2009, the cardiology department stated: "In a small study performed by CVCA, it was determined that after two to three weeks of Pimobendan therapy about 75% of dogs had an increased frequency of ventricular arrhythmias documented on 24 hour ambulatory ECG monitoring."

In the U.S. Food and Drug Administration’s (FDA) 2007 report approving the use of pimobendan for dogs, it stated this conclusion in a four week toxicity study of pimobendan administered to 30 previously healthy lab Beagles: "Conclusions: Pimobendan administered IV daily to healthy Beagles caused dose dependent increases in heart rate, mitral valve myxomatous thickening, left ventricular outflow tract endocardial thickening, and ventricular muscle ischemic lesions (multifocal subendocardial necrosis and scarring). The cardiac pathology seen in these dogs is typical of positive inotropic drug toxicity in normal dog hearts, and is related to the physiologic effect of the drug on contractility and exaggerated hemodynamic response."

On Vetmedin's website, it has this warning: "The safety of VETMEDIN has not been established in dogs with asymptomatic heart disease."

January 30, 2011:

Chiari-like malformation HAS been re-defined!

Emily Litella, "Never mind!"Our January 28, 2011 editorial, "Maybe Cavaliers Don’t Even Have Chiari-Like Malformation (CM)!", pointed out that, in view of recent research reports, either cavalier King Charles spaniels do not have CM ("decreased caudal fossa volume") or CM needs to be re-defined to fit within these current research findings.

Well, apparently CM has been re-defined! On the website of syringomyelia researcher Dr. Clare Rusbridge, CM now is defined as "a condition characterized by a mismatch in size between the brain (too big) and the skull (too small). There is not enough room for the brain and the back part (cerebellum and medulla) is pushed out the foramen magnum." The foramen magnum is a hole in the back of the skull -- in the occipital bone -- leading to the spinal cord. Dr. Rusbridge goes on to explain that the cavalier appears to have a brain more appropriate for a bigger dog.

This new definition of Chiari-like malformation pretty much neutralizes the point of our January 28 editorial, so in the inimitable words of Saturday Night Live’s Gilda Radner’s character, Emily Litella, "Never mind!"

January 28, 2011:

Maybe cavaliers don't even have
Chiari-like malformation (CM)!

Exploding BrainIt may be time to let Chiari-like malformation (CM) off the hook! For many moons, CM has been tagged as the "usual suspect" in the blame-game for a cause of syringomyelia (SM) in the cavalier King Charles spaniel (CKCS). But based upon recent studies, it looks like cavaliers do not even have CM!

CM is defined as, "decreased caudal fossa volume with caudal descent of the cerebellum, and often the brainstem, into or though the foramen magnum." The caudal fossa is the cavity within the hind portion of the skull, also known as the occipital bone. The occipital bone contains the foramen magnum, which is the hole at the base of the skull.

The implication has been that the smaller caudal fossa volume within the occipital bone would force the cerebellum (the hindbrain) to squeeze through that hole, the foramen magnum, causing excessive pressure on the cerebrospinal fluid (CSF) and resulting in the production of a syrinx. The conclusion was that it was the smaller size of the hind-skull that was to blame for that squeeze play and the consequent syrinxes.

However, three veterinary research journal articles published in 2009 and 2010 point to evidence that cavaliers’ hind-skull volumes are not different from other small breeds, particularly those with short muzzles, and that the percentage of the volume of the caudal fossa to the volume of the total cranial cavity did not differ significantly between CKCSs with and without SM.

Instead, the oversized cerebellum may be the culprit. These studies also found that the volume of hindbrain was significantly greater for young -- 2-years and younger -- cavaliers with SM than older dogs -- 5 years and older -- without SM. They also found that increased hindbrain volume in CKCSs with SM, compared to that of the hind-skull, was directly correlated with the size of the dogs’ syrinxes.

If the 2009 and 2010 studies are on the right track, then we may have to either re-define "Chiari-like malformation" or use another term to describe the disorder, since the "malformation" may not be of the skull, but of the brain. A re-definition could be "increased cerebellar parenchyma volume with caudal descent of the cerebellum, and often the brainstem, into or though the foramen magnum."  But then, would that really be "Chiari-like", or just some other type of malformation?

So, indeed, the SM cavalier’s brain may be too large for its skull!

December 28, 2010:

CKCSC,USA's board reinstates a third of
the REAL MVD breeding protocol

Huh?In our October 7 Editorial, we called upon the CKCSC,USA's board of directors to reinstate the REAL mitral valve disease breeding protocol at their October meeting. Well, apparently they did a third of that. Recall, if you will, that at their April 2010 meeting, they dumped the real protocol, which their predecessors had unanimously approved in May 1998 when the protocol was introduced. See our September 7 Editorial ("CKCSC,USA Dumps MVD Breeding Protocol") politely pointing out their act of virtual insanity.

In April, the current board replaced the REAL protocol with an odious, worthless version, in which they stated: "The CKCSC,USA recommends that prior to breeding any Cavalier, the dog have a clear rating at two years of age from an auscultation by a board certified veterinary cardiologist."

In the face of an onslaught of justifiable criticism, the board met in October and tweaked their bogus breeding recommendation thusly:

"The CKCSC,USA recommends that prior to breeding any Cavalier, the dog should have a heart clearance from an auscultation by a board certified veterinary cardiologist that is consistent with prevailing cardiology protocols; however, the CKCSC,USA recommends a minimum of a cardiology clearance at age 2.5 years by a board certified cardiologist."

Say what???  I suppose we should be grateful for whatever crumbs the board chooses to throw our way, but really!!!  This October revision is only a miniscule improvement over their April abomination, and the bottom line is that, according to the researchers, it is still worthless. After all, whatever the CKCSC,USA board "recommends" is toothless at best. No breeders are bound by it, so why doesn't the board go all the way and actually reinstate the REAL MVD protocol that the Club stood by for the past twelve years until this board came along?

Why not add the other two-thirds of the REAL protocol?

• Do not breed any Cavalier under the age of 5 years, unless its parents' hearts were free of MVD murmurs by age 5 years.
• Do not breed any Cavalier who is diagnosed with an MVD murmur under the age of 5 years.

Come On, CKCSC,USA Board: MAN UP!!!  Show the world that your Club really does take early-onset MVD seriously, instead of showing your incredible pride and your heinous contempt for future generations of Cavalier King Charles spaniels.

October 7, 2010:

To CKCSC,USA's board:
Reinstate the REAL MVD breeding protocol!

Get Real!Dear CKCSC,USA board of directors:  Your next board meeting on October 14 is your chance to redeem yourselves. Reinstate the REAL MVD Breeding Protocol!

The Club’s 1998 board wisely endorsed the REAL protocol which the international research panel of heart specialists and geneticist drew up and urged all cavalier King Charles spaniel breeders to follow, at a minimum! They told us at the Club’s MVD Symposium in May 1998 that we could eliminate early-onset MVD in just a few generations if enough breeders faithfully followed it. Since then, we know that only a handful of cavalier breeders ever paid any attention to it, so twelve years after 1998, there has been no progress in ridding the breed of young cavaliers with bad hearts, suffering and dying all too soon. But that was no excuse for you to dump the REAL protocol at your April 2010 meeting!

In April, you had your chance to re-new the endorsement and urge all club members to follow the REAL protocol. Instead, you replaced it with a worthless recommendation to breed cavaliers "clear at 24 months", which no cardiologist or geneticist researcher has ever recommended. In fact, they told us in 1998 that breeding "clear-to-clear" has not worked and would not work!

You have ignored the research experts’ conclusions that, at a minimum:
(A) All four parents of the breeding pair be MVD-clear as of their 5th birthday;
(B) The breeding pair be at least 30 months old and MVD-clear at the time of breeding; and
(C) No cavalier be bred if diagnosed with an MVD murmur before its fifth birthday.

Just last month, Sweden’s Dr. Clarence Kvart reported that the Swedish CKCS club’s "clear at 24 months" protocol has not reduced the percentage of cavaliers having MVD, and as a result, the Swedish club is considering making the REAL protocol mandatory!

Whatever your purpose in rejecting the REAL protocol, now is your opportunity to redeem yourselves. You owe it to the future generations of cavaliers. Remember, the next edition of Pedigreed Dogs Exposed is focusing on you!

September 10, 2010:

How self-absorbed can the CKCSC,USA board be?

Self-AbsorbedNow, after the editorial CKCSC,USA dumps MVD breeding protocol first appeared on September 7, the CKCSC,USA has added to its website an introduction to the announcement of the board's April 29, 2010 decision to reject its 1998 endorsement of the MVD breeding protocol. The introduction falsely states:

"The Board took a historic step and established minimal recommendations for conducting health tests ... where none had existed before."

This is a very odd attempt to revise the club's history. The club's 1998 endorsement of the MVD breeding protocol was indeed "historic". The only thing which is historic about the board's April 2010 decision is that it has replaced the MVD breeding protocol with a worthless "clear at 24 months" recommendation, which the research experts told the club back in 1998 would not work. 

In the face of the laser now shining brightly and critically upon the cavalier King Charles spaniel, beginning with the broadcast of Pedigree Dogs Exposed, one would expect the CKCSC,USA's board to take a giant step forward and, at the very least, re-new its recommendation of the MVD breeding protocol, if not make it mandatory for registering litters. Instead, the board in April of this year has pretended that it never had recommended the protocol at all, and then replaced it with nonsense. Why does the board now deny that it approved the MVD breeding protocol in 1998?

September 7, 2010:

CKCSC,USA dumps the MVD breeding protocol

With Stupid!Taking a giant step backwards from its May 1998 decision endorsing the MVD breeding protocol, the board of directors of the Cavalier King Charles Spaniel Club, USA rejected that protocol at its April 2010 meeting. Instead, its board approved a watered down, proven worthless "recommended guideline", calling for the breeding pair to have MVD-murmur-clear hearts at only 24 months.

It has been twelve years since the CKCSC,USA sponsored the "International Symposium on Chronic Cardiac Valve Disease (CVD) in the Cavalier King Charles Spaniel" in Atlanta, Georgia in May 1998. The club invited a panel of veterinary cardiologists from the USA and the UK -- Drs. Andrew Beardow, James Buchanan, Virginia Luis Fuentes, and Bruce Keene -- and the renowned canine geneticist, Lennart Swenson from Sweden. Before a packed theater of club members, the panel reported on the severity of the disease and its pervasiveness throughout the breed. They stated these conclusions:

• MVD is the leading cause of death in Cavaliers;
• It is a hereditary, genetic disorder;
• There has been no statistical improvement in Cavaliers' mitral valves in the eleven years since the first studies; and
• The disease can be decreased and the age of onset delayed by following guidelines of only breeding Cavaliers who are over the age of 2.5 years, have hearts free from MVD murmurs, and have parents whose hearts were MVD murmur-free at age 5 years. No Cavaliers should be bred which have murmurs before age 5 years.

The panelists then introduced:

MVD Breeding Protocol

That same weekend in May 1998, the CKCSC,USA's board endorsed the protocol and then sent a verbatim transcript of the symposium to all club members, with this statement:

Cavalier's Year of the Heart"In this 'Year of the Heart' in which the CKCSC,USA is instituting a number of programs geared toward the study and control of chronic cardiac valve disease, this symposium was organized to bring together international experts to present data and provide guidelines for breeders.
"We urge our members to follow their recommendations, and hope that we will attain our goal of bringing the prevalence, the age of onset, and the severity of the disease to the levels seen in other breeds of dogs."

The Club also mailed to its members annually, beginning in 1998, a Health Registry booklet, which included this set of MVD breeding guidelines:

Guidelines to Reduce the Incidence of Mitral Valve Disease

Even with these strong endorsements, only a handful of cavalier breeders have faithfully followed the MVD breeding protocol. As evidence of that lack of participation, in March 2009, eleven years after the protocol was introduced, cardiologist Simon Swift stated: "In the UK and the USA, about ½ of all cavaliers [still] have a murmur by the time they are 5 years old."

Purebred breed clubs -- of which indeed the CKCSC,USA is one -- are obliged to educate breed owners on the nuances of the breed and oversee the breed’s health and welfare. The leadership of breed clubs owe a fiduciary duty, not to the club's breeders, but to the breed, to assure that the dogs are protected from irresponsible breeding practices and from the creation of future litters of genetically damaged puppies. Since most all cavalier breeders in the club have failed to faithfully follow the MVD breeding protocol these past twelve years, the responsible thing for its board to do, to protect the breed, would be to re-affirm the importance that its breeders comply with the protocol.

But now we find, twelve years after endorsing the MVD breeding protocol, that instead of doing that responsible thing, the CKCSC,USA board has dumped it and instead has contrived this totally bogus guideline which has been proven to be a failure:

"The CKCSC,USA recommends that prior to breeding any Cavalier, the dog have 1) a clear rating at two years of age from an auscultation by a board certified veterinary cardiologist; ..."

This new worthless guideline ignores the research experts' conclusions that: (A) All four parents of the breeding pair be MVD-clear as of their 5th birthday; (B) The breeding pair be at least 30 months old and MVD-clear at the time of breeding; and (C) No cavalier be bred if diagnosed with an MVD murmur before its fifth birthday.

Sadly, the Club's board has effectively thumbed its collective nose at the heart-health of all future generations of CKCSC,USA cavalier King Charles spaniels.