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Feline Hypertrophic Cardiomyopathy

by Andrea Jensen
Fall 2007

Feline Hypertrophic Cardiomyopathy (HCM) is far and away the most common form of heart disease in the cat.  Diagnosis of HCM means that there is a primary disease process causing the myocytes of the heart to behave inappropriately, and leads to enlargement of the heart, primarily of the left ventricle (the main muscular chamber that pumps blood to the body).  Secondary hypertrophic diseases of the heart may be caused by hyperthyroidism or hypertension, and lead to signs that mimic HCM, but if addressed early may be reversible by treating the underlying condition.  Primary HCM is not reversible, and has been shown to have a genetic link, particularly in Main Coons.  Unfortunately, genotyping is not yet available.  It is not yet possible to isolate the gene that causes HCM in cats, but through studying family trees, it has been shown to be an autosomal dominant gene in some Main Coons and likely other breeds as well.

In cats, HCM presents with a high degree of phenotypic heterogeneity from patient to patient.  In all cases, the left ventricle develops concentric hypertrophy, but this is not always uniform or symmetric.  The areas that may be affected are the septum, the free wall of the ventricle, or only sections of either or both.  It is also possible that only the myocytes of the papillary muscles (which control the mitral valve) will be affected.  In all cases, diastolic (filling) function is compromised.  The result is a heart chamber that cannot receive as much blood as it needs to.  This is referred to as a decreased pre-load.  A decreased pre-load causes a decreased stroke volume.  In order to compensate for a decreased stroke volume and maintain an adequate total cardiac output, the heart must pump harder and faster to feed the body.  This basically results in a snowball effect, where the compensation mechanism actually reduces compliance and pre-load even more, while increasing the need for a higher stroke volume to feed the overworking heart itself.  The compensation mechanism is good for the patient in the short term, but in the long run will usually snowball into a congestive heart failure if left untreated.  Approximately 10% of HCM patients progress to a "burnout" phase where the left ventricle "quits" and dilates (causing systolic dysfunction), but the vast majority will show such extensive thickening in an effort to pump harder that it stiffens and can no longer stretch to receive the blood from the atrium.  The backup of blood in the atrium can cause blood stasis, which allows for clot formation and possible thromboembolism, leading to sudden paralysis or death.  Backup in the lungs under high pressure has no where to go but leak out of the vessels, causing pulmonary edema.  The prognosis of the HCM patient is as varied as the phenotypic presentations, and the treatment can be complex.

One type of HCM that should be mentioned briefly, before discussing treatment, is Hypertrophic Obstructive Cardiomyopathy (HOCM).  This form of HCM shows both diastolic and systolic dysfunction, and occurs when the myocytes that hypertrophy reduce the diameter of the outflow tract dynamically or statically.  When this happens, stroke volume is reduced because the heart is trying to push the blood out a smaller hole.  The result is the same.  The heart must pump harder and faster to bring total cardiac output up to feed the body as well as feed the heart itself that has ever increasing oxygen demand as its workload increases.

Treatment of asymptomatic patients with HCM is controversial.  Many veterinarians and researchers have concluded that it is important to diagnose HCM early through echocardiography, EKG, and blood troponin levels, and treat the patient with cardioprotective drugs.  Since the first sign of HCM in approximately 30% of cats is sudden death, this opinion is gaining popularity.  In the obstructive form, HOCM, the beta blocker atenolol has been widely accepted as the drug of choice.  Atenolol specifically inhibits sympathetic activation of the receptors in the heart that directly increase contractility and heart rate.  This is the same receptor that is over stimulated in hyperthyroid patients, so atenolol is a good choice for HCM, HOCM, and also secondary hypertrophy caused by hyperthyroidism.  Especially important in HOCM, atenolol reduces dynamic outflow obstruction.  In all hypertrophic disorders, the use of atenolol slows the snowball effect of excessive hypertrophy and thickening of the heart, and prolongs the time it takes to reach congestive heart failure.  After administration of beta blockers, peripheral blood pressure decreases, which reduces the afterload the heart must overcome with each stroke, increases ejection fraction, and serves as a less damaging compensatory mechanism to increase cardiac output.  Finally, atenolol reduces the oxygen demand of the myocytes by decreasing heart rate and contractility, which decreases the need for a high cardiac output to deliver oxygen.  All beta blockers are considered to be cardioprotective, because they protect the heart muscle itself from injurious effects of the sympathetic nervous system on the heart.  However, beta blockers should NEVER be given to a patient that is suffering from congestive heart failure until the edema and effusion have been controlled, first.

Angiotensin Converting Enzyme Inhibitors (ACEI's), such as enalapril, are also considered to be cardioprotective.  This class of drugs is indicated in patients suffering from congestive heart failure (CHF), and may also be helpful in asymptomatic patients (still controversial).  When treating CHF cats, enalapril is usually combined with the diuretic furosemide to clear edema or effusion.  The mechanism of action of ACEI's is to inhibit the formation of angiotensin II, which is a step in a multistage pathway called the renin-angiotensin-aldosterone system or RAAS.  The general effects of RAAS are to vasoconsrict (increase blood pressure and increase renal blood flow), increase stimulation of the sympathetic nervous system (increase heart rate), increase aldosterone release (antidiuretic effects to increase blood volume and blood pressure), and increases fibrin formation (clots and scar tissue in the heart).  By inhibiting this pathway, the result is a reduction in all of the above.  Lowered arterial blood pressure, lowered fluid retention (especially when combined with a diuretic), lowered sympathetic stimulation, and reduced fibrosis of the heart occur with the use of enalapril.  The reduced fibrosis of the heart is especially useful in reducing excessive stiffening of the chamber walls.  Fibrosis that has already occurred is not reversible, but the progression may be slowed.  There are contraindications for the use of ACEI's, however.  Some patients are dependent on RAAS to maintain renal blood flow and glomerular filtration, and may be thrown into an ACEI induced renal failure.  ACEI's have a valuable use in a high proportion of patients, but should be used cautiously for this reason.

For a patient that presents with acute CHF, the initial in hospital therapy is to reduce stress and avoid unnecessary procedures while allowing three important treatments to work.  Furosemide (diuretic) reduces pulmonary edema, oxygen therapy reduces the need for high cardiac output, and nitroglycerin is used as a powerful vasodilator to reduce hypertension.  This triple combination is commonly used to stabilize a patient with acute CHF due to HCM.  Mild sedation is often used to decrease stress and heart rate.  Once the patient is stabilized, then chronic treatment protocols can be determined.  At this point, it is complex because of the phenotypic variations from patient to patient.  There is no single home care regimen that is appropriate for each cat.  Furosemide and ACEI's are very common, but both have indications and contraindications, and both must be monitored carefully to avoid overdose effects.  Atenolol is widely accepted as a helpful therapy in HCM and HOCM once CHF has been controlled with furosemide and enalapril, but not in cats with concurrent renal failure because atenolol is primarily cleared by the kidney.  In cats that suffer from thromboemboli, aspririn or clipidogrel are often used, but must be used cautiously and sparingly, and may not be mixed with many other medications.  Aspirin should never be given to a cat without a prescription, in any case.  A calcium channel blocker such as diltiazem may be selected to increase diastolic function (increase relaxation).  If the disease has progressed to the point that the atrium is so dilated that it cannot pump and force blood into the resistant ventricle, then a positive inotropic drug such as digoxin may be necessary, in spite of the fact that positive inotropes increase contractility and are not cardioprotective.  Patients that have advanced in this way have an uncertain prognosis.

Chronic treatment of HCM and CHF is complex and varied depending on the specific signs exhibited by the patient, and by the specific findings on advanced diagnostics, especially doppler echocardiography.  Treatment of the asymptomatic cat is controversial, but once any signs begin, it is widely accepted that cardioprotective drugs such as beta blockers and ACE inhibitors have cardioprotective effects.  All treatments must be carefully tailored to the specific signs and symptoms of each patient, and all treatments must be monitored and titrated to effect.

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