Sunday, July 24, 2011
Notes from July 2011 St. Louis AVMA Conference-HCM
These are papers from the July 2011 St. Louis AVMA conference. I’ve edited them to delete some of the vet only jargon and for space considerations. If you see (…) that means that information has been deleted due to these considerations. The ones listed here include HCM, and other heart related papers, treatments, papers on x-rays and echos, thrombosis, kidney disease, idiopathic cystitis, pain management, anesthesia and cardiac disease, supplements and other hazards for pets, and some other basic information I hope is helpful.
My note-regarding the paper below, in class she said that there is a wide range and a non-cohesive approach to treating HCM among vets. There isn’t much data available on treatments and what slows the progression of the disease. Many vets follow human studies to gain more knowledge of the disease. There is research on a drug in this or that study but not regarding one total approach. Part of the problem (aside from financing a study) is that each pet presents with different side effects of the disease which requires an individual approach to the issue. But due to a lack of research, many doctors hesitate to use multiple drugs and multiple approaches. 8% or less of cats have HCM. More males than females will get the disease. There are breeds that will get it more, such as Maine Coon and Ragdoll. The average age of detection is 6-16 years. Half of the cats have no symptoms but are diagnosed due to other unrelated issues-before a dental or surgical procedure for example. Or others become sick from medications given for other illnesses, such as steroids, and CHF kicks in. Usually lethargy and difficult breathing is what owners notice in the cats. Up to 34% of cats have heart murmurs but not HCM. Most cats that will get HCM are born with a gene that will cause HCM. Others will get it due to having another disease which brings on the condition or brings on CHF. Sometimes the onset of the disease is greatly delayed for unknown reasons. But if the cat has the gene, the disease will eventually form. A good and inexpensive diagnostic tool is the x-ray. If an owner cannot yet afford an echo, an x-ray will show if the heart is enlarged. If the heart is enlarged, then an echo is needed. But if the heart is not enlarged and the cat does not present with other symptoms, then carefully monitor in the future with more x-rays until an echo is warranted. She discussed in class (but not in the paper below) how to measure the heart via x-ray. It’s too complicated for me to explain but has something to do with measuring the size of the heart in relation to the vertebrae by taking different mathematical measurements at different axis points on the x-ray to determine how much of the chest cavity the heart is taking up. If it is up to 8 or less vertebrae there is not an enlarged heart yet. If it is 9 or more, than an echo is warranted, the heart is enlarged, and treatment must begin. More doctors need to be aware of this as do owners of pets. However, having an HCM cat, I understand the necessity of getting an echo and will always recommend one for those cats who are presenting with HCM related side effects (such as lethargy, breathing difficulty, etc.) The only study she cited that showed which drug actually worked for HCM was the study regarding lasik. All other drugs have had either no feline studies or have not shown to work for all cats. But she said that certain things must be treated-tachycardia, left atrial enlargement, and severe dynamic stenosis. She gives ace inhibitor such as enalapril. Beta blockers such as atelenol in human studies have proven effective and she gives it to cats to treat tachycardia. She agreed (in a Q&A) with an audience member that vitamins were needed.
There is a school doing a genetic study in cats. If you want to find out more, call 909-513-8279 or go to www.cvm.ncsu.edu/vhc/csds/vcgl/index.html
Feline Hypertrophic Cardiomyopathy Update
Meg M Sleeper VMD, DACVIM (Cardiology)
Associate Professor of Cardiology; University of Pennsylvania School of Veterinary Medicine
Hypertrophic cardiomyopathy (HCM) is a primary myocardial disease that affects left
ventricular (LV) myocardium and is characterized by mild to severe thickening (concentric
hypertrophy) of the LV wall (septum and/or free wall) and papillary muscles. The thickening
may be global or regional. In feline HCM, the LV papillary muscles are consistently enlarged.
The diagnosis is one of exclusion. Several possible secondary causes of LV concentric
hypertrophy exist in cats including systemic arterial hypertension, hyperthyroidism and aortic
stenosis. When LV hypertrophy is caused by any of these diseases, the cardiac abnormality is
not called HCM since it is not cardiomyopathy (primary heart muscle disease). Some patients
with HCM will demonstrate dynamic left ventricular outflow obstruction (most often systolic
anterior motion (SAM) of the mitral valve). Historically, cats with HCM and SAM have been
diagnosed with hypertrophic obstructive cardiomyopathy (HOCM), however some veterinary
cardiologists have suggested that veterinarians should follow the human cardiology lead and
simply use the term “HCM” regardless of the presence of SAM.
A male predilection for HCM is commonly reported…The genetic cause of HCM in Maine Coon cats and Ragdoll cats has been determined. Numerous other breeds also have HCM as a prevalent problem, including,
Persians, American and British Shorthairs, Siberians, Norwegian Forest Cats, and Turkish
Vans. Most HCM is diagnosed in mixed breed cats (domestic short hair, domestic long hair)…In Maine Coon cats a typical scenario is for a cat to have no evidence of HCM during the first 2-5 years of life and then to develop the maximum stage of its HCM (mild to severe HCM) over a year or more. Cats that only develop mild to moderate HCM
usually have no clinical sequelae to their disease (although a small percentage may die
suddenly). Cats that develop severe disease may go on to have severe sequelae (i.e., heart
failure, sudden death, systemic thromboembolism) within a short period while others may
stabilize for a remarkably long time. Cats with HCM may have no clinical evidence of the
disease, many have auscultatory abnormalities (murmur and/or gallop), some are presented
due to signs of congestive heart failure (tachypnea and/or dyspnea), and some are presented
because of systemic thromboembolic disease. Since household cats are generally sedentary,
owners usually do not notice that they are having respiratory difficulty until it is advanced. At
that time, the onset of the disease commonly appears to be acute to the owner, whereas the
disease actually has been present for years and the heart failure gradually worsening for
weeks. Cats with mild to moderate HCM may never develop clinical signs and may live normal
lives. In others, the left ventricular wall may thicken further and complications may develop
when they are older and develop a complicating disease such as systemic hypertension or
HCM almost always causes diastolic dysfunction rather than systolic dysfunction. When LV
hypertrophy is severe, it is common for the LV wall thickness to be twice the normal thickness
(increased from 3-5 mm up to 7-10 mm…Left heart failure is manifested as either pulmonary edema or pleural effusion in cats. SAM of the mitral valve is common in cats with HCM. However, SAM comes and goes depending on the contractile state of the heart so it is likely that SAM can be provoked in many cats that do not have SAM at rest
by just taking them to see a veterinarian and it is also likely that many cats that have SAM in a
veterinary clinic do not have it when asleep…
The diagnosis of HCM is almost always made using echocardiography. Cats with severe HCM
have severe papillary muscle hypertrophy, a markedly thickened LV wall (7-10 mm), and often,
but not always, an enlarged left atrium. The hypertrophy can be global, affecting all areas of
the LV wall or can be more regional, symmetrical or asymmetrical. Because it can be regional,
HCM is a diagnosis that should be made by examining several different two-dimensional
echocardiographic views and measuring wall thickness in diastole from the thickest region or
regions. M-mode echocardiography may miss regional thickening unless it is guided by the
two-dimensional view and so should never be used without two-dimensional guidance, if at all…Color flow Doppler echocardiography can be used to demonstrate the two turbulent jets originating from the LVOT--one regurgitating back into the left atrium (mitral regurgitation) and the other projecting into the aorta that is typical of SAM.
Spectral Doppler is used to determine the pressure gradient across the region of dynamic
subaortic stenosis to characterize the severity of the SAM although it can be quite labile.
Diastolic dysfunction in cats with severe HCM has been documented using tissue Doppler
imaging (TDI) and measures of transmitral flow and relaxation time.
There currently is no evidence that any drug alters the natural history of hypertrophic
cardiomyopathy (HCM) in cats until they are in heart failure. Diltiazem, atenolol, ACE inhibitors
and, possibly, spironolactone are commonly administered by veterinarians to cats with mild to
severe HCM that are not in heart failure on an empirical basis in the hope that they will slow
the progression of the disease. Beta blockers are effective for reducing severe SAM that is
some times observed in clinical situations. Atenolol is a specific β1-adrenergic blocking drug
that usually needs to be administered twice a day, often at a total dose of 6.25 to 12.5 mg PO
q12h. Cats that present in left heart failure primarily have clinical signs referable to pulmonary edema
and/or pleural effusion. Consequently, therapy is generally aimed at decreasing left atrial and
pulmonary venous pressures in these cats and physically removing pleural effusion. In some
cats with severe heart failure, clinical evidence of hypoperfusion (low-output heart failure) may
be apparent in addition to the signs of CHF (e.g., cold extremities, total body hypothermia).
Pulmonary edema is primarily treated with diuretics (almost exclusively with furosemide)
acutely. Pleurocentesis is most effective for treating cats with severe pleural effusion.
Furosemide is usually helpful at slowing effusion reaccumulation but repeated pleuracenteses
are often needed to keep signs of heart failure in check.
Cats that present with respiratory distress suspected of having heart failure secondary to HCM
need to be placed in an oxygen enriched environment. If possible the cat should be initially
evaluated by doing a cursory physical examination, taking care not to stress the patient during
this or any other procedure since stress exacerbates dyspnea and arrhythmias and may lead
to death. A butterfly catheter should be used to perform thoracentesis on both sides of the
chest to look for pleural effusion as soon as possible…If fluid is identified, it should be removed.
If none is identified, a lateral thoracic radiograph to identify
pulmonary edema may be taken with the veterinarian present to ensure that the cat is not
stressed. Cats present in respiratory distress due to a number of respiratory and thoracic cavity diseases
in addition to heart failure. Differentiation between left heart failure and respiratory failure may
be difficult…if differentiation is difficult, assessment of left atrial size via
radiography or echocardiography is one of the most useful diagnostic tests available.
Furosemide should initially be administered IV or IM to the cat in severe respiratory distress
due to pulmonary edema…Dosing must be reduced sharply once the resting respiratory rate starts to decrease to avoid severe dehydration. Nitroglycerin paste might be beneficial in cats with severe pulmonary edema secondary to feline HCM…no studies have examined any effects of this drug in this species and its efficacy is
suspect…the medication is safe and this author recommends 1/8 "-1/4" of a 2% paste
administered to the inguinal region every 4-6 hours for the first 12-24 hours as long as
furosemide is being administered…cat should be left to rest quietly in an oxygen enriched environment.
Care should be taken not to distress the cat. A baseline measurement of the respiratory rate and assessment of respiratory character should be taken when the cat is resting and every 30 minutes. Furosemide administration should be continued until the respiratory rate starts to decrease (a consistent decrease of the respiratory rate from
70 to 90 breaths/minute into the 50 to 60 breaths/minute range is a general guide)…the furosemide dose and
dosage frequency should be curtailed sharply. In some cats sedation with acepromazine (0.04-
0.1 mg/kg subQ) may help by producing anxiolysis…
Preliminary evidence from a recent placebo-controlled and blinded clinical trial suggests that
enalapril, diltiazem and beta blockers produce little to no benefit when compared to furosemide
alone in cats with heart failure due to HCM. This study has only been presented in abstract
form, however this author continues to recommend use of an ACE inhibitor such as enalapril in
cats in heart failure and receiving furosemide therapy. This author uses atenolol and/or
diltiazem in this population of cats (HCM cats with congestive heart failure) only if heart rate
control is indicated or concurrent hyperthyroidism is present. Pimobendan is contraindicated in
cats with HCM…The owner should be taught how to count the sleeping
respiratory rate at home and instructed to keep a daily written log of the respiratory rate. This is
highly beneficial for making decisions regarding dosage adjustment in individual patients.
Normal sleeping respiratory rate in a cat is usually in the 15-30 breaths/minute range but the
pattern is as important (i.e. a gradual increasing of the respiratory rate over several days).