Feline Hypertrophic Cardiomyopathy

This section is dedicated to the loving memory Mickey, the Perfect Cat

Cardiomyopathy is the name applied to an abnormality of heart muscle function.  The heart's pumping ability is diminished, resulting in such signs as inability to exercise, fatigue, fainting, fluid collection in the lungs, abdomen, and limbs, or emboli (clots that arise in the heart and travel to the kidney, brain, or legs). Although some cats with cardiornyopathy do not develop clinical signs, others experience rapid progression of their disease or sudden death. The causes of cardiomyopathy include genetic predisposition, infections, toxic causes (drugs and chemical compounds), specific dietary insufficiencies, and unknown causes. Whereas some cases are entirely reversible, others are not and are treated with various levels of success.

Three major forms of cardiomyopathies occur in the canine and feline species. In dilated cardiomyopathy., the heart muscle is weak and flaccid (floppy). This condition is associated with a reduction in heart muscle function during contraction (systole) and a decrease in forward flow of blood. Subsequent upper heart chamber (left atrial) enlargement is associated with backup of blood and then fluid into the lungs (pulmonary edema).

Hypertrophic cardiomyopathy is a thickening of the lower heart muscle chambers (ventricles). The results are inappropriate heart function, obstruction of blood flow from the heart into the circulation, and enlargement of the upper heart chambers (atria). This abnormality is called diastolic dysfunction a condition -in which the heart fails to relax fully, fill, and then empty. The resulting backup of pressures into the lung is responsible for the clinical signs of respiratory distress. coughing, and systemic emboli (blood clots).

Unclassified or restrictive cardiomyopathies are unidentified disease conditions in which heart problems are associated with severely enlarged upper chambers and diminished pumping ability. The clinical signs resemble those of hypertrophic cardiomyopathy. Although not thickened, the ventricular muscle is dysfunctional and the heart is unable to fill and then pump adequately.

Cardiomyopathies are seen in both dogs and cats. The form in dogs is usually dilated, whereas hypertrophic and unclassified forms are identified most often in cats. The diagnosis of cardiomyopathy is based on a history of weakness, coughing, panting, fainting, or fluid collection around the lungs and in the abdominal cavity. Weight loss occurs, and seizures associated with fainting may occur. Emboli (clots) can result in blood vessel blockage, sudden lameness, and cold painful limbs. Clinical signs usually develop suddenly, often without apparent prior illness. In addition to these signs, the diagnosis depends on abnormalities found at the physical examination. Irregularities occur in the heart's rhythm and rate, and abnormal heart sounds (murmurs) are heard with the stethoscope. Radiographs (x-rays) of the chest show heart enlargement. Evaluation of the blood may identify complicating organ problems. The electrocardiogram can diagnose an irregular heart rhythm and substantiate heart enlargement. Ultrasound examination of the heart confirms the suspicion of cardiomyopathy. Dilatation of the heart cavity, poor contractility of the heart muscle, and left atrial enlargement occur with dilated cardiomyopathy. Thickening of the heart muscle, obstruction of the flow of blood into the circulation, and left atrial enlargement identify hypertrophic cardiomyopathy. Normal muscle thickness with disturbed function and enlarged left atrium indicates restrictive cardiomyopathy.

The prognosis for survival with cardiomyopathies varies from poor to good. Once cardiomyopathy has been recognized, much of the damage to the heart muscle has already occurred. The result is congestive heart failure, the signs and symptoms of which may be treated for a variable period of time (often cats live several years with proper treatment). Although the pet may enjoy a period of good health and comfort, the long-term prognosis continues to indicate that heart failure will recur. As a result, the pet will become less responsive to medical intervention. Surgery is not yet an option for any form of cardiomyopathy.

 This section is confined to hypertrophic cardiomyopathy since it it’s the most common cardiomyopathy found in cats.

Feline Hypertrophic Cardiomyopathy

John D. Bonagura, D.V.M.,
Diplomate, American College of Veterinary Internal Medicine
(Cardiology and Internal Medicine); Professor, Section of Small
Animal Medicine, Department of Veterinary Clinical Sciences,
College of Veterinary Medicine, The Ohio State University

Hypertrophic cardiomyopathy is a common myocardial disorder of cats and is characterized by hypertrophy of the left ventricle. The cause of this hypertrophy is unknown, and while elevated growth hormone levels were observed in one study of cats with HCM and while acromegaly is associated with CHF, it seems more likely that the disease has a genetic basis, which is certainly the situation in many human patients with this condition. Recently, a description of HCM in a family of Maine coon cats has been reported. Other recognized causes of left ventricular hypertrophy, including systemic hypertension, hyperthyroidism, and subaortic stenosis, should be excluded before diagnosing HCM.

The left ventricular hypertrophy may be symmetric, involving the entire ventricle, or regional. Generally the left ventricular lumen is smaller than normal, encroached by the ventricular hypertrophy; however, occasional cats exhibit left ventricular Inminal dilation. The best recognized form of asymmetric hypertrophy is asymmetric septal hypertrophy, which is diagnosed when the ventricular septal-to-free wall thickness is 1.3: 1 or greater.  However, focal hypertrophy of the subaortic or midventricular ventricular septum and asymmetric left ventricular free wall hypertrophy have also been observed. The clinical significance of this heterogeneity is only beginning to be recognized.  Cats with asymmetric septal hypertrophy or with moderate to severe symmetric left ventricular hypertrophy may develop dynamic systolic left ventricular outflow tract gradients or what has been termed obstructive HCM.  Doppler studies in unanesthetized cats indicate that subaortic intraventricular pressure gradients do develop in some cats with HCM, and that these gradients are very labile, varying with sympathetic activity and heart rate.  This obstruction occurs after the onset of ejection, when the anterior leaflet of the mitral valve moves to contact the ventricular septum, and leads to systolic anterior motion of the septal mitral leaflet. The result is a dynamically narrowed left ventricular outflow tact with concomitant mitral regurgitation. The percent of cats affected by significant outflow tract gradients is unknown, but is probably less than 25 percent.

Pathology

The left ventricle is the chamber affected (Fig. 1), and hypertrophy of the free wall, septum, and papillary muscles typically occurs, with mild thickening of the mitral valve.  The heart weight-to-body weight ratio is increased.  A subaortic, fibrotic, contact lesion, where the septal mitral valve leaflet touches the ventricular septum, is occasionally observed at postmortem and is a marker for dynamic left ventricular outflow obstruction.  Multifocal areas of subendocardial myocardial fibrosis may be evident. The left atrium is both dilated and hypertrophied, a consequence of increased resistance to ventricular filling and mitral regurgitation. Pulmonary edema, attributed to left-sided CHF, develops in some cats. Secondary enlargement of the right ventricle and atrium is likely if pulmonary hypertension increases the right ventricular load. Lung edema combined with hepatic congestion, hydrothorax, and ascites are indicative of biventricular heart failure. Aortic thrombosis and an occasional left atrial ball thrombus are additional necropsy findings.

Fig. 1. Hearts obtained from two cats with hypertrophic cardiomyopathy. (A) The left ventricle is opened to demonstrate moderate hypertrophy of the left ventricular wall (W) and ventricular septum (S). Ao, aorta. (B) Severe hypertrophy is evident in this case. The left ventricular lumen is very small.

Histologic examination of the myocardium indicates hypertrophy and interstitial fibrosis. The ventricular myocytes are thickened, have large hyperchromatic nuclei, and demonstrate varying degrees of cellular disarray, degeneration, and myofibrillar lysis. Degeneration, interstitial fibrosis, and chondroid metaplasia are found in the AV node and central fibrous body. This may proceed to ossification of the AV conduction system. Electron microscopy findings have been described elsewhere. Coronary arteriosclerosis of intramural vessels is not uncommon and may be a factor in limiting myocardial perfusion.

Pathophysiology

The proposed pathophysiologyy of HCM is summarized in Figure 2 (Under construction). The principal abnormality occurs in diastole.  Hypertrophy and fibrosis decrease ventricular compliance and active ventricular relaxation is impaired; higher diastolic pressures must therefore be achieved in order to fill the left ventricle. This is evident at the catheterization table by the increased ventricular A wave and elevated ventricular end-diastolic pressures that are recorded in cats that have not been volume contracted by diuretics.  End-diastolic pressure was elevated to more than six times normal in cats in one study.  In addition to increased myocardial and chamber stiffness, it is likely that an imbalance between myocardial oxygen demand and supply may acutely decrease ventricular compliance. This may partially explain the frequent clinical observation that stress can precipitate pulmonary edema in a previously compensated cat with HCM. Increased sympathetic activity increases myocardial oxygen demand through various mechanisms, including elevating heart rate, augmenting contractility, and enhancing ventricular gradients and myocardial tension. Tachycardia also limits the time for coronary perfusion and ventricular filling. These changes, no doubt, have a negative impact on myocardial oxygen balance, and it is clear that myocardial hypoxia or ischemia can quickly impair ventricular relaxation.

Systolic hemodynamic abnormalities may also occur in cats with HCM. Left ventricular shortening fraction-typically normal to increased in cats with HCM-is decreased below 30 percent in about 5 to 10 percent of affected cats and when decreased is a negative predictor of survival.  Some cats develop severe regional left ventricular wall hypokinesis, perhaps as a consequence of a coronary embolus and myocardial infarction. Left ventricular outflow gradients, as well as intraventricular pressure gradients,  have been recorded in some cats; however, the overall importance of these findings is somewhat controversial in both cats and human patients . At a minimum, these gradients probably increase myocardial tension and reduce subendocardial perfusion. That mitral regurgitation is very common in cats with HCM is clear,  and this hemodynamic abnormality seems to be especially common when the ventricular septum is hypertrophied either symmetrically  or asymmetrically. The clinical significance of mitral regurgitation may be great, because this hemodynamic abnormality further increases left atrial size and pressure, predisposing to both CHF and to thromboembolism. In one study, increasing left atrial size was an independent predictor of decreased 3-month survival. The pathogenesis of mitral regurgitation in cats with HCM may be multifactorial. Geometric deformation of the left ventricle and mitral apparatus may predispose to incompetency throughout systole. It is also obvious from Doppler echocardiographic studies in unanesthetized cats that motion of the mitral valve into the left ventricular outflow tract is related to mid- to late systolic mitral regurgitation. This abnormal mitral motion is believed to represent a Venturi effect caused by early systolic ejection of blood at high velocity across the outflow tract. Similar Doppler studies in human patients have indicated a relationship between the magnitude of the outflow obstruction and the severity of' mitral regurgitation.

Congestive heart failure and systemic thromboembolism are the principal clinical consequences of' moderate to severe HCM. The pathogenesis of atrial thrombi is not established but is certainly related to the size of the left atrium and abnormal flow patterns within that chamber. Congestive heart failure can be traced to elevations of left atrial and pulmonary venous pressures that predispose the cat to pulmonary edema. Myocardial oxygen imbalance, as previously discussed, can suddenly potentiate diastolic dysfunction in the noncompliant left ventricle. Atrial arrhythmias, such as atrial fibrillation, diminish effective left atrial contraction and can cause florid pulmonary edema.  Stress, aortic thromboembolism, ketamine anesthesia, or inadvertent intravenous fluid loading are other conditions that may precipitate pulmonary edema. This is often a labile condition, for it is common for pulmonary edema to develop rapidly and to abate after 24 to 48 hours of diuretic therapy. However, progressive loss of ventricular compliance, chronic stiffening of the left atrium,  or progressive mitral regurgitation result in chronic pulmonary venous hypertension and leftsided CHF. Since the right ventricle must perfuse this hypertensive circulation and also contribute to left atrial and ventricular filling, right ventricular systolic pressure increases, often exceeding 50 mmHg.  Presumably, it is this increased pressure work that predisposes to biventricular failure and accounts for the hepatic congestion and pleural effusion often observed in some cats clinically and in necropsy studies.


Clinical Manifestations

There is an increased prevalence in young to middle-aged males cats at most centers,   but the clinician should never be surprised to diagnose HCM in cats younger than 1 year of age. The Persian breed may be predisposed,' although this has not always been confirmed. There may be a geographic bias in prevalence, with HCM being more frequently observed in the eastern portion of the United States. Perhaps this represents a genetic predisposition to this disease.

Many cats are clinically normal, and heart disease is detected by chance, usually from identification of a cardiac murmur or a gallop during a routine examination. Presenting clinical signs can include anorexia; reluctance to move, gagging, dyspnea, or tachypnea from CHF; hindlimb paresis from acute aortic thrombosis; and, uncommonly, syncope.   Sudden death, so common in human patients with this disease, is far less prominent in cats with HCM. Most symptomatic cats have an auscultable gallop rhythm or systolic murmur. The murmur is usually due to mitral regurgitation, and may vary with changes in heart rate, ventilation, or body position. A slower heart rate at the time of diagnosis (less than 200 beats/min) was a predictor of greater longevity in one study; however, it is likely that most of the cats presented with CHIF or with arterial thromboernboli had higher heart rates, so this would be expected. Moreover, occasional cats with CHF are actually bradycardic, perhaps from hypoxia. Audible crackles over the lung fields are suggestive of severe pulmonary edema, although many cats with pulmonary edema are simply tachypneic. Systemic blood pressure in cats with HCM is usually normal to slightly elevated. Laboratory tests are usually normal. Increased serium concentrations of potassium and skeletal muscle and liver enzymes may be observed secondary to aortic obstruction with secondary tissue injury. Renal function is usually normal unless renal infarction or dehydration have occurred.

Diagnosis

The diagnosis of HCM is best made by combining clinical features with results of echocardiography. Cats with the clinical findings of aortic thromboembolism or acute pulmonary edema with gallop rhythm or systolic murmur, valentine-shaped heart with prominent left auricle and pointed left apex, vigorous left apical impulse, and left axis deviation of the ECG are very likely to have idiopathic HCM. However, since other causes of myocardial hypertrophy, including congenital subaortic stenosis, systemic hypertension, and hyperthyroidism can cause these findings, clinical, radiographic, or ECG abnormalities cannot be relied on to render the diagnosis of HCM.

Radiography

Radiographic findings are quite variable.  most reports have emphasized the valentine-shaped heart, as visualized on the ventrodorsal radiographs.  This appearance is explained by the significant left atrial and auricular enlargement that occurs in conjunction with shifting of the cardiac apex toward the midline. It has also been stated that right atrial and ventricular enlargement contribute to the valentine shape; however, there are no angiographic or echocardiographic studies to indicate that this is a consistent finding. If present, right-sided cardiomegaly could be explained by the development of pulmonary hypertension secondary to left-sided heart disease. Pericardial effusion may produce a globoid silhouette. Pulmonary edema is typical of CHF in cats with HCM; however, pleural effusion also may develop, and is especially common in chronic cases or when atrial fibrillation ispresent.

Nonselective or selective angiocardiography, now supplanted by echocardiography, can be diagnostic since contrast studies can outline the left ventricular cavity.  Tortuous pulmonary veins, left atrial and auricular enlargement, and left ventricular hypertrophy are typical findings and distinguish this condition from dilated, intergrade, and restrictive cardiomyopathies. Often the hypertrophied papillary muscles protrude into the ventricular lumen, producing filling defects. Intraventricular obstruction is observed during systole in some cats with hypertrophic as well as restrictive forms of' cardiomyopathy and results in an absence of dye in the outflow tract or in the midventricular region. If the obstruction is persistent, it likely represents midventricular fibrosis or moderator band proliferation. Apical aneurysms have been observed in a small percentage of cats. The aorta is normal to large in diameter and well illuminated with contrast material. The circulation time is normal.

Echocardiography

M-mode and 2D echocardiography, and now Doppler studies, are the studies most often used to substantiate the diagnosis and are increasingly available to practicing veterinarians. Reduced left ventricular internal diastolic dimension with increased diastolic and systolic thicknesses of the ventricular and septal walls are characteristic of HCM.. The left atrium is dilated (usually greater than 15 mm) in most cases, although the magnitude of enlargement probably depends on numerous factors, including myocardial relaxation, global left ventricular chamber stiffness, mitral valve function, and the degree of ventricular interstitial fibrosis. The finite ventricular wall value that characterizes hypertrophy in all cats has not been determined; however, in my experience, if the technical quality of the echo is high, the papillary muscle echoes are excluded, and the endocardial edges are clearly delineated, a left ventricular wall greater than 5.5 mm by M-mode echo or greater than 6 mm by 2D echo is diagnostic of left ventricular hypertrophy. In equivocal cases, the clinician should also consider the weight of the cat, the relative wall thickness--to-internal Iuminal dimension, and the size of the left atrium as well as the clinical examination, ECG, and radiographs. Simply inspecting the 2D echo for hypertrophy can be very misleading in a cat; particularly if the echocardiographer is inexperienced or if the cat is volume depleted due to dehydration. I have observed many cats with typical clinical and radiographic features of HCM that have ventricular wall measurements barely exceeding 5 mm by M-mode echocardiography, a finding reported by others.  Two-dimensional echocardiographic studies also contribute to the diagnosis by demonstrating hypertrophy of the papillary muscles and heterogeneous hypertrophy of the ventricular septum or left ventricular walls."' Left ventricular fractional shortening as measured by echocardiography is normal to increased in more than 90 percent of affected cats, indicating preserved global left ventricular contractility. Despite a normal to exaggerated shortening fraction, the systolic thickening percentage of the ventricular septum and left ventricular free wall, and the aortic root systolic excursion may be decreased. Reduced left ventricular shortening fraction,  left ventricular dilation, or regional left ventricular wall-motion abnormalities are infrequent findings, with the latter probably indicating rnyocarditis or previous coronary embolism and myocardial infarction. A small pericardial effusion is commonly observed; infrequently, the effusion is quite large.

Hemodynamic abnormalities in the left ventricular outflow tract may be obvious from the 2D and Doppler echocardiography. Doppler studies usually demonstrate slightly to markedly increased systolic RBC velocity in the left ventricular outflow tract. Color-coded Doppler studies will demonstrate high velocity and turbulent flow in moderate to severe cases of outflow obstruction. Careful 2D or M-mode studies of cats with increased outflow velocities often demonstrate systolic anterior motion of the mitral valve and narrowing of the outflow tract; however, the magnitude of systolic anterior motion varies widely, ranging from subtle to severe. Mitral regurgitation is another common hemodynamic abnormality observed by Doppler echocardiography. The jet is characteristically eccentric originating from the anterior (septal) mitral leaflet and projecting sinistrad toward the caudodorsal left atrium. Color M-mode studies, which allow accurate timing of hemodynamic events, often demonstrate that the mitral regurgitant jet does not begin until blood has first been ejected into the aorta, reflecting the importance of systolic anterior motion in the pathogenesis of mitral regurgitation in some cats. My experience with Doppler echocardiography in cats with moderate to severe HCM is quite similar to that reported in humans with this disease.

Electrocardiography

The ECG may be normal or abnormal in cats with HCM.  Atrial dilation is suggested by increased amplitude or duration P waves, but this is not a sensitive test for atrial dilation. Left ventricular hypertrophy is suggested by increased amplitude QRS complexes in leads 2 and aVF or by left axis deviation with increased amplitude R waves in leads I and aVL . A marked left cranial axis deviation has been said to indicate left anterior fascicular block  and to be suggestive of' HCM. Other conduction disturbances have been reported, and almost 50 percent of the cats in one survey' had some form of conduction disturbance. Sinus tachycardia and premature atrial and ventricular complexes are often observed in cats with HCM. Atrial fibrillation is more common in this form. of' disease, as compared with the dilated form.  Ventricular arrhythmias have been recognized by routine ECG and with Holter monitoring; however, the overall incidence of rhythm disturbances in this disease is unknown.

Treatment

Initial therapy for CHF in cats with HCM is outlined in Tables 1 and Table 2 (tables underconstruction) summarizes
the clinical pharmacology of those drugs used in chronic management of this condition. As opposed to the cat with dilated cardiomyopathy, inotropic support is not recommended for therapy for HCM, and arterial vasodilators may be relatively contraindicated for the subgroup of cats with obstructive cardiomyopathy. Emergency therapy for acute pulmonary edema includes intravenous or intramuscular furosemide (initially using high doses to ensure diuresis), oxygen, and topical nitroglycerin ointment. The use of an intravenous ß-blocker or calcium channel blocker in this setting of acute pulmonary edema may gain popularity in the future, but there is scant evidence to recommend such treatments.

Recommendations for chronic management are much more difficult. The need for treatment, and the form of therapy to prescribe for long-term care, probably vary depending on the type and severity of disease. One retrospective study has reviewed the median survival of cats without clinical signs versus those with CHF or thromboembolism. The reported median survival for cats asymptomatic at the time of diagnosis was over 5 years; whereas, cats with CHF had a median survival of about 3 months. Thromboembolism, as expected, carried a very poor chance of long-term survival. While more detailed subgroup analyses of affected cats would be needed to provide greater prognostic information, this survey does demonstrate that many asymptomatic cats will live for years; however, the impact of prophylactic treatment versus no therapy cannot be determined from these data. Moreover, while it is reasonable to assume that cats with CHF have a significantly shorter median survival, the retrospective nature of the study prevents assessment of the effectiveness of therapy for heart failure. In my experience, these data understate the effectiveness of currently available therapy. With optimal treatment, many cats with HCM can live for more than 1 year after an initial bout of CHF.

There is only one published prospective study that critically evaluates medical therapy in a smal number of cats with HCM, and there are no studies that compare different treatment regimens in a sufficient number of cats. Bright and associates  reported excellent responses to treatment with the calcium channel blocker, diltiazem, administered at dosages ranging from 1.75 to 2.4 mg/kg PO q8h. The cats treated in their study had very severe left ventricular hypertrophy based on the reported echocardiographic data (diastolic wall thickness averaged 9 mm), and it is difficult to know whether these cats are representative of most cats with this disease. Nonetheless, the data from this study strongly support the use of diltiazern in the management of cats with severe left ventricular hypertrophy and CHF. Improved ventricular relaxation was evident based on echocardiographic indices of relaxation and are similar to data reported in humans with HCM treated with diltiazem.  Other potential benefits of diltiazern in these cats could have included improved coronary perfusion from vasodilation, reduced myocardial oxygen demand from the negative inotropic effect and mild negative chronotropic effect of the drug  and, although not studied, the attenuation of ventricular pressure gradients. Another important finding of this study was apparent regression of left ventricular hypertrophy and reduction in left atrial size in the diltiazem-treated cats that occurred after 6 months of therapy. Whether similar results could be obtained with other treatments such as an ACE inhibitor or a ß-blocker and diuretic is unknown; however, in my experience in treating cats with ß-blockers, regression of left ventricular hypertrophy has never been a prominent result of such therapy. While the total number of cats treated in this study was relatively small, the results were impressive and indicate a significant therapeutic potential for diltiazem or related compounds.

ß-Adrenergic blockers have been used for many years in the management of human and feline HCM. When given in proper dosages, ß-blockers are more effective than diltiazern for slowing heart rate (the daily dosage usually can be titrated using heart rate), and these drugs exert potentially favorable effects by blocking sympathomimetic activity, reducing myocardial oxygen demand, increasing the time available for ventricular filling and for coronary perfusion, and relieving dynamic outflow obstruction.  When long-acting ß-blockers such as atenolol are prescribed, once-daily treatment appears to effectively block ß-adrenoceptors, and this convenience is clearly preferred by pet owners. Unfortunately, there are no clinical studies that demonstrate the efficacy of ß-blockers once CHF has developed, and ß-blockers without intrinsic sympathomimetic activity may not favorably influence ventricular relaxation,  although the entire issue is very complicated  and cannot be discussed without considering all the interrelated factors that influence diastolic function. One should avoid the use of B-adrenergic blockers in the setting of uncontrolled pulmonary edema or aortic thrombosis, because reduction of myocardial contractility, bronchospasm, and blockage of ß-2-vasodilating receptors could theoretically occur.

Both diltiazern and ß-adrenoceptor blockers are useful in the chronic management of cats with HCM. In cats without clinical signs, and with only mild ventricular hypertrophy (less than 7 mm by M-mode echo) and mild left atrial enlargement, or in cats with substantial left ventricular outflow gradients (greater than 50 mmHg by Doppler), the vet should discuss the potential benefits of both classes of drugs with the owner. While the potential to cause regression of left ventricular hypertrophy might suggest consideration of diltiazern therapy even in these minimally affected cats, in most mild, asymptomatic cases, some vets prescribe once-daily atenolol to reduce the resting heart rate to less than 150 beats/min and act as a cardioprotective medication. This therapy is well tolerated, convenient, and many cats have lived uneventually for years receiving this medication (or an equivalent dose of propranolol q8h). Diltiazem is preferred when left ventricular hypertrophy is moderate to severe, the left atrium is significantly enlarged (e.g., greater than 18 mm by M-mode echo), or the cat has experienced CHF. In such cases, diltiazem may be prescribe based on the experience of Bright et al.  If the resting heart rate is not well controlled (less than 200 beats/min) with diltiazem, or if significant left ventricular outflow obstruction is identified by 2D or Doppler echocardiography and persists following diltiazern therapy, both a ß-blocker and diltiazern are prescribed. A similar approach has been used in human patients.

Furosemide is an effective drug for both acute and chronic management of pulmonary edema in cats with HCM. Frequently, the daily dosage can be markedly reduced after acute pulmonary edema has been resolved. The smallest effective dosage should be chosen to avoid hypokalemia, azotemia, and excessive volume contraction that can further reduce left ventricular diastolic volume. In advanced cases, furosemide every 8 to 12 hours may be needed. If pulmonary edema becomes refractory to combination therapy of furosemide and diltiazem, or if pleural effusion develops, enalapril is added taking great care with the initial doses to avoid precipitating hypotension or renal failure. Future studies may indicate an early use of ACE inhibitors, particularly if they are shown to act locally at the myocardial level to reduce hypertrophy and improve ventricular relaxation.  When prescribing any combination drug therapy, the clinician must be particularly mindful of drug-induced hypotension, which can cause weakness, renal failure, and decreased coronary perfusion. Accordingly, the periodic measurement of heart rate (maintain a rate of 120 to 160 beats/min) and systolic arterial blood pressure (maintain systolic pressures above 100 mmHg) is essential, especially when initiating new therapy. The simplest method to monitor systolic aterial blood pressure is by the indirect and economical Doppler method.

Other cardiac drugs are used infrequently in cats with this disorder. Digoxin is generally not prescribed for cats with HCM unless there are other indications for its use such as atrial fibrillation with a rapid ventricular response. In the case of atrial fibrillation, combining digoxin with either a B-blocker or a calcium channel blocker will be more effective for controlling ventricular rate response than either drug alone. Potent arterial vasodilators like hydralazine may worsen outflow tract obstruction by reducing the ventricular afterload and increasing the shortening of the hypertrophic septum. Verapamil and amiodarone,  drugs frequently used in human patients with HCM, have not been adequately evaluated in cats, although preliminary experience with verapamil has been discouraging.

Prognosis

Although there are no prospective data indicating the precise prognostic factors that influence survival, retrospective studies and clinical experience indicate that the survival for clinically healthy cats affected with this disease is good, with many cats living for years without difficulty.  Often cats with MCM remain asymptomatic unless their condition is complicated by severe left atrial enlargement, progressive myocardial failure,  aortic thrombosis, atrial fibrillation, hyperthyroidism, anemia, fever, renal failure, tranquilizers or anesthesia, or fluid infusions. When the precipitating cause is reversible, the cat may stabilize spontaneously following the management of acute pulmonary edema. Median survival of cats with CHF or aortic thromboembolism was quite short in one report  ; however, it was not possible to assess the type and intensity of therapy or follow-up employed. With optimal care, many cats with CHF survive with a good quality of life for more than 1 year. When HCM is associated with aortic thrombosis, severe mitral regurgitation, atrial fibrillation, or biventricular heart failure with pleural effusion or chylothorax, the prognosis is guarded to poor.

Related Subjects
(Under Construction)

Aortic thrombolism
Congestive Heart Failure
Diltiazem therapy
ß-adrenoceptor blockers
Furosemide
Current Research

References

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