Max's House

Myocardial Diseases of the Cat

Wendy A. Ware, DVM, MS,
Diplomate, American College of Veterinary Internal Medicine (Cardiology)
Associate Professor,Departments of Veterinary Clinical Sciences and Biomedical Sciences
Attending Cardiologist Veterinary Teaching Hospital Iowa State University Ames, Iowa






Myocardial diseases that affect cats encompass a diverse collection of idiopathic and secondary diseases affecting the myocardium, and the spectrum of anatomic and pathophysiologic characteristics of these diseases is wide. Disease characterized by myocardial hypertrophy is most often seen clinically in cats and is discussed at length in this chapter. Myocardial disease with restrictive pathophysiologic condition is also common. Classic dilated cardiomyopathy is now rarely seen clinically in cats. The myocardial disease of some cats does not fit neatly into the categories of hypertrophic, dilated, or restrictive cardiomyopathy; rather, it is considered "indeterminate" or unclassified myocardial disease. Systemic thromboembolism is a troubling complication in cats with myocardial disease.



The cause of primary or idiopathic hypertrophic cardiomyopathy (HCM) in cats is unknown, although a genetic basis or predisposition is likely in some cases. The disease appears to be highly prevalent in certain bloodlines of several breeds. Most cases of HCM in people are familial, and several specific abnormalities of genes for myocardial proteins have been identified in different kindreds. In addition to mutations of genes that encode for myocardial contractile or regulatory proteins, postulated causes of the disease include an increased myocardial sensitivity to or excessive production of catecholamines; an abnormal hypertrophic response to myocardial ischemic, fibrosis, or trophic factors; a primary collagen abnormality; or abnormalities of the myocardial calciumhandling process. Some cats with HCM have high serum growth hormone concentrations.

Secondary Hypertrophic Myocardial Diseases

Myocardial hypertrophy develops as a compensatory response to certain identifiable stresses or disease; marked left ventricular wall and septal thickening and clinical heart failure can occur in some cats. Such cases are not considered idiopathic HCM. Secondary causes should be ruled out if left ventricular hypertrophy is identified.

Testing for hyperthyroidism is indicated in cats with myocardial hypertrophy that are 6 years of age or older. Hyperthyroidism alters cardiovascular function by its direct effects on the myocardium and through the interaction of heightened sympathetic nervous system activity and excess thyroid hormone on the heart and peripheral circulation. Cardiac effects of thyroid hormone include myocardial hypertrophy and enhanced heart rate and contractility. The metabolic acceleration accompanying hyperthyroidism creates a hyperdynamic circulatory state characterized by increased cardiac output, oxygen demand, blood volume, and heart rate. Systemic hypertension can result and further stimulate myocardial hypertrophy. Clinical cardiovascular signs often include a systolic murmur, hyperdynamic precordial and arterial impulses, tachycardia and arrhythmias, and evidence of left ventricular enlargement or hypertrophy, seen on electrocardiograms (ECGs), thoracic radiographs, or echocardiograms. Signs of congestive heart failure develop in an estimated 15% of hyperthyroid cats; most have normal to high fractional shortening, but a few have poor contractile function. Specific therapy, in addition to the antithyroid treatment, may be necessary to manage the cardiac complications of hyperthyroidism. -Blockers can temporarily control many of the adverse cardiac effects of excess thyroid hormone, especially tachyarrhythmias. Diltiazem is another alternative therapy. Treatment for congestive failure is the same as that described later for HCM. The rare hypodynamic (dilated) cardiac failure is treated in the same way as dilated cardiomyopathy. (-Blocker or other cardiac therapy is not a substitute for antithyroid treatment, however.

Left ventricular concentric hypertrophy is the expected response to increased ventricular systolic pressure (afterload). Systemic arterial hypertension  increases afterload because of high arterial pressure and resistance. Increased resistance to ventricular outflow also occurs in the presence of a fixed (e.g., congenital subaortic stenosis) or dynamic left ventricular outflow tract obstruction. The latter occurs in some cats with idiopathic HCM and is described later.

Cardiac hypertrophy also develops in cats with hypersomatotropism (acromegaly) as a result of growth hormone's trophic effects on the heart; congestive heart failure ensues in some of these cats. Increased myocardial thickness occasionally results from infiltrative myocardial disease, most notably from lymphoma.

Pathophysiology (Diastolic Dysfunction)

The myocardial thickening that occurs in HCM leads to increased ventricular stiffness and the development of relaxation abnormalities. Left ventricular filling is impaired and higher diastolic pressures are required when the ventricle is stiff and less distensible. Furthermore, the myocardial relaxation process may be prolonged and incomplete, especially if the myocardium becomes ischemic. Fibrosis and disorganized myocardial cell structure can also contribute to the development of abnormal ventricular stiffness. Because progressively higher filling pressures are required as the left ventricle becomes more stiff, left atrial and ventricular enddiastolic pressures rise. The atrium enlarges, sometimes markedly, but the left ventricular volume remains normal or decreased. A reduced ventricular volume results in a lower stroke volume and may contribute to the activation of the renin-angiotensin system and sympathetic nervous system. Geometric changes of the left ventricle and papillary muscles or abnormal (anterior) systolic motion of the mitral valve may prevent normal valve closure. The resulting mitral regurgitation exacer bates the increased left atrial volume and pressure and may lead to pulmonary congestion and edema. Higher heart rates further interfere with left ventricular filling, exacerbate myocardial ischemic, and promote venous congestion by shortening the diastolic filling period. Contractility, or systolic function, is usually normal in affected cats.

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Some cats also have dynamic left ventricular outflow obstruction during systole (i.e., those with functional subaortic stenosis or hypertrophic obstructive cardiomyopathy). In these cats, excessive and asymmetrical hypertrophy of the basilar interventricular septum may be evident on echocardiograms or at necropsy. Systolic outflow obstruction increases wall stress and myocardial oxygen demand and promotes myocardial ischemia. Mitral regurgitation is exacerbated by forces tending to pull the anterior leaflet toward the interventricular septum during ejection (for an M-mode echocardiogram of mitral systolic anterior motion. An audible ejection murmur is common in cats with outflow obstruction. About one fourth to one third of cats with HCM are thought to have asymmetrical septal hypertrophy.

Several factors probably contribute to the development of myocardial ischemia in this disease. These include a myocardial capillary density inadequate for the degree of hypertrophy, narrowing of intramural coronary arteries, decreased coronary artery perfusion pressure, and increased left ventricular filling pressure. Ischemia impairs early, active ventricular relaxation, which further increases the ventricular filling pressure. It is also thought to predispose to the development of lethal arrhythmias and possibly thoracic pain. Diastolic dysfunction and ischemia are exacerbated by increases in heart rate.

Pulmonary venous congestion and edema frequently result from increased left atrial pressure. Some cats with HCM also have pleural effusion. The effusion may be chylous, although a modified transudate is more common. It is thought that increased pulmonary venous and capillary pressures cause pulmonary vasoconstriction, increased pulmonary arterial pressure, and secondary right-sided heart failure. Accumulation of pleural effusion may also be promoted if pleural venous drainage into the pulmonary veins occurs in cats, as it does in people.

Thrombi may form within the dilated left atrium or other areas of the heart. Systemic thromboembolism results if portions are dislodged into the circulation. Moderate-to-severe left atrial enlargement and secondary blood stasis are considered risk factors for thromboembolism. This complication is discussed later.


Postmortem findings in cats with HCM consist of left ventricular free-wall and interventricular septal hypertrophy. The hypertrophy is symmetrical in most cats, but some have asymmetrical septal thickening, and a few have hypertrophy limited to the free wall or papillary muscles. The degree, of left atrial enlargement varies from mild to massive. `A thrombus is sometimes found within the left atrium or attached to a ventricular wall. The left ventricular lumen usually appears small. Focal or diffuse areas of fibrosis within the endocardium, conduction system, or myocardium and narrowing of small intramural coronary arteries may also be noted. Myocardial fiber disarray, common in people with HCM, is found in a minority of cats. Evidence of congestive heart failure or systemic thromboembolism may also be present.

Clinical Features

HCM has historically been most common in middle-age male cats, but clinical signs occur in cats in a wide range of ages. Cats with milder disease may be asymptomatic for years. This is not surprising, because there is also a wide range of clinical expression of the disease in people with HCM, even within the same kindred.

Symptomatic cats are most often presented for respiratory signs of variable severity or signs of thromboembolism. Respiratory signs include tachypnea, panting associated with activity, dyspnea, or, rarely, coughing (which can be misinterpreted as vomiting). Disease onset may seem acute in sedentary cats, even though pathologic changes have developed gradually. Occasionally lethargy or anorexia is the only evidence of disease. Some cats have syncope or sudden death in the absence of other signs. Stresses such as anesthesia, surgery, fluid administration, systemic illnesses (e.g., fever or anemia), and even boarding can precipitate heart failure in an otherwise compensated cat. Asymptomatic disease may be discovered by detecting a murmur or gallop sound on auscultation.

Systolic murmurs indicative of either mitral regurgitation or left ventricular outflow tract obstruction are common. A diastolic gallop sound (usually S4) may be heard, especially if heart failure is evident or imminent. Cardiac arrhythmias are not uncommon. Femoral pulses are usually strong, unless distal aortic thromboembolism has occurred. A vigorous precordial impulse is often palpable. Prominent lung sounds, pulmonary crackles, and sometimes cyanosis accompany severe pulmonary edema; pleural effusion usually attenuates ventral pulmonary sounds. The physical examination findings can be normal, especially if paroxysmal arrhythmias are the only disease manifestation.


Radiographic features of HCM include a prominent left atrium and variable left ventricular enlargement. The classic valentine-shaped appearance of the heart on dorsoventral or ventrodorsal views is not always present, although usually the point of the left ventricular apex is maintained. The cardiac silhouette appears normal in cats with mild HCM. Enlarged and tortuous pulmonary veins may be seen in the presence of chronically high left atrial and pulmonary venous pressures. Variable degrees of patchy interstitial or alveolar pulmonary edema develop in the setting of left-sided heart failure. The radiographic distribution of pulmonary edema is variable; a diffuse or focal distribution throughout the lung fields is common, in contrast to the perihilar distribution characteristic of cardiogenic pulmonary edema seen in dogs. The finding of pleural effusion suggests biventricular failure; hepatomegaly may also be noted in the setting of right-sided failure.


Most (about 60% to 70%) cats with HCM have ECG abnormalities. These commonly include criteria for left atrial and ventricular enlargement, supraventricular and/ or ventricular tachyarrhythmias, or a left anterior fascicular block pattern. Occasionally an atrioventricular (AV) conduction delay, complete AV block, or sinus bradycardia is found.


An echocardiogram is the best means of diagnosis because it is noninvasive. Echocardiography allows the differentiation of HCM from the now uncommon dilated cardiomyopathy and other myocardial disorders. Nonselective angiocardiography is an alternative method but poses a greater risk to the cat.

Cats with severe HCM have diastolic left ventricular wall or septal thicknesses of 8 mm or more, although the degree of hypertrophy is not necessarily correlated with the severity of clinical signs. Papillary muscle hypertrophy can be marked, and systolic left ventricular cavity obliteration is observed in some cats. The distribution of hypertrophy is variable (see earlier section on pathology); therefore the entire ventricle should be scanned. Use of two-dimensional-guided M-mode is important to ensure proper beam position. Standard M-mode views and measurements are obtained, but thickened areas outside these standard positions should also be measured. The diagnosis may be questionable in cats with mild or only focal thickening. 5 mm is considered the upper limit of normal for diastolic left ventricular wall and septal thicknesses. Left ventricular fractional shortening is generally normal to increased. Right ventricular enlargement and pericardial or pleural effusion are occasionally detected.

Cats with dynamic left ventricular outflow tract obstruction are often found to have systolic anterior motion of the mitral valve  or premature closure of the aortic valve leaflets on M-mode scans. Doppler modalities can demonstrate mitral regurgitation and left ventricular outflow turbulence, although optimal alignment with the maximal-velocity outflow jet is often difficult and it is easy to underestimate the systolic gradient. Left atrial enlargement may be mild to marked. Spontaneous contrast (swirling, smokey echos) is visible within the enlarged left atrium of some cats and is thought to result from blood cell aggregations. A thrombus is occasionally visualized within the left atrium, usually in the auricle.

Other causes of myocardial hypertrophy should be excluded before a diagnosis of HCM is made. Myocardial thickening can also result from infiltrative disease or fibrosis. A variation in myocardial echogenicity, wall irregularities, or enhanced endocardial brightness may be noted in such cases. Excess moderator bands appear as bright, linear echos within the left ventricular cavity.


The main goals of therapy are to facilitate ventricular filling, relieve congestion, control arrhythmias, minimize ischemia, and prevent thromboembolism. Ventricular filling is improved by slowing the heart rate and enhancing relaxation. Stress and activity level should be minimized.

Pulmonary edema is treated with furosemide; cats with severe respiratory distress are usually given the drug intramuscularly (IM) (2 mg/kg), because intravenous (IV) injection can be excessively stressful. If pleural effusion is suspected, thoracocentesis is performed expediently, with the cat in sternal position. Nitroglycerin ointment is often applied (q4-6h), although no studies of its efficacy in this situation have been done. Once initial medications have been given, the cat should be allowed to rest, preferably while receiving supplemental oxygen. The respiratory rate is noted initially, then every 30 minutes or so without disturbing the cat. Catheter placement, blood sampling, radiographs, and other tests and therapies should be delayed until the cat's condition is more stable. Airway suctioning and mechanical ventilation with positive end-expiratory pressure can be considered in extreme cases. The bronchodilating and mild diuretic effects of aminophylline may be helpful in cats with severe pulmonary edema, as long as the drug does not increase the heart rate. Acepromazine has been used to reduce anxiety and promote the peripheral redistribution of blood by its -adrenergic-blocking effects (0.05 to 0.2 mg/kg subcutaneously [SC]), but preexisting hypothermia can be exacerbated by peripheral vasodilation. Morphine should not be used in cats. Furosemide can be continued (1 mg/kg) in 1 to 2 hours and then q8-12h; diuretic therapy is guided by the animal's respiratory rate and effort. Excess diuresis should be avoided, because it could induce azotemia, anorexia, and electrolyte disturbances and because increased atrial pressure is required for left ventricular filling to be optimal.

Cautious fluid administration may be needed in some cats. Once pulmonary edema is controlled, furoscmidc is gradually reduced to the lowest dose and longest dosing interval at which it is effective, and given orally (PO).

Diltiazem or a -blocker is the foundation of longterm oral therapy. The decision to use one particular drug may be influenced by the specific abnormalities in the individual case or the response to medication. Diltiazem (1.75 to 2.5 mg/kg PO q8h) is well tolerated and effective in many cases. It promotes coronary vasodilation and enhances ventricular relaxation. The drug causes mild decreases in heart rate and contractility; it may also decrease systolic outflow gradients if peripheral vasodilation does not enhance ventricular shortening. It is generally less effective than the -blockers in decreasing heart rate. Calcium entry blockers that primarily have vasodilatory effects (e.g., nifedipine, nicardipine) can cause reflex tachycardia and worsen systolic outflow gradients; therefore they are not used for cats with HCM. Verapamil has a greater negative inotropic effect than diltiazem, and thus should be better for reducing ventricular outflow obstruction. However, it appears to have variable bioavailability, and toxic concentrations are easily reached in cats.

The -adrenergic blockers can produce greater decreases in heart rate than diltiazem can. They are also useful in controlling tachyarrhythmias and reducing systolic outflow obstruction and myocardial oxygen demand through their negative inotropic effects. These effects can be especially important in cats with severe outflow obstruction or paroxysmal arrhythmias. I favor atenolol over diltiazem for cats with these disease features. The reduction in heart rate and myocardial ischemia that results from P-blocker therapy may also indirectly alleviate left ventricular diastolic stiffness and enhance filling. However, there is no direct enhancemcnt of relaxation, and -blockers may even slow the relaxation process. If propranolol is used, its administration is usually delayed until after pulmonary edema is largely resolved; because propranolol is a nonselective R-blocker, an adverse effect of its use can be bronchoconstriction stemming from antagonism of airway (߲ receptors. This is not such a concern with more (,receptor-selective agents. Yet the advantages of slowing sinus tachycardia and minimizing ventricular arrhythmias may outweigh the risk of bronchospasm even with propranolol. Some cats do not tolerate propranolol well (e.g., lethargy, depressed appetite). In these cases, atenolol or another -blocker may be better tolerated instead, or diltiazem could be used.

In cats that respond well to long-term therapy with diltiazem or a -blocker, it may eventually be possible to discontinue furosemide therapy, although close monitoring for the occurrence of pulmonary edema is necessar1,. Occasionally a -blocker is added to diltiazem therapy (or vice versa), for example, to further control heart rate in cats with atrial fibrillation. However, care must be taken to prevent bradycardia or hypotension in animals receiving this combination.

Certain drugs are usually contraindicated in cats with 1 WM. These include digoxin and other positive inotropic agents, because they increase the myocardial oxygen demand and can worsen dynamic outflow tract obstruction. Any drug that accelerates the heart rate is- potentially detrimental, because tachycardia decreases filling time and predisposes to the development of myocardial ischemia. Arterial vasodilators can cause hypotension and reflex tachycardia, because cats with HCM have little preload reserve. Hypotcnsion can also exacerbate dynamic outflow obstruction. The angiotensin-converting enzyme inhibitors (ACEls) also have this potential; however, their vasodilating effects are usually mild. There is evidence that cnalapril (and other ACEls) may be beneficial in modulating neurohormonal activation, especially in eats with refractory heart failure.

Refractory pulmonary edema or pleural effusion can be difficult to manage. A severe pleural effusion should be treated by thoracocentesis. Various therapeutic strategies may also be useful, including increasing doses of furosemide (up to 4 mg/kg q8h), adding an A(TI, maximizing the dose of diltiazem or (3-blocker, or adding another diuretic, such as hydrochlorothiazide-spironolactonc. Frequent monitoring for the development of azotemia or electrolyte disturbances is warranted. Digoxin can also be considered for the treatment of refractory right-sided heart failure in the abscnce of outflow obstruction.

Long-term therapy may also include a drug to decrease the likelihood of thromboembolism. Although aspirin (25 mg/kg PO every 3 days) has been used traditionally for this purpose, some cats may benefit more from warfarin. Exercise and dietary sodium restriction are also recommended.

There is some debate about whether (and how) asymptomatic cats with HCM should be treated. It is unclear whether disease progression can be slowed or survival prolonged. Nevertheless, some cats show an increased activity level or improved "attitude" after they start to receive diltiazem or a -blocker on the basis of echocardiographic or ECG abnormalities, even when the owners had not previously noted a problem.


A major complication of hyperrophc and other forms of cardiomyopathy in cats is arterial thromboembolism. Atrial fibrillation and other tachyarrhythmias further impair diastolic filling and exacerbate venous congestion; the loss of the atrial "kick" and the rapid heart rate associated with atrial fibrillation are especially detrimental. Ventricular tachycardia or other arrhythmias may lead to syncope or sudden death. Refractory biventricular failure is another serious complication that may develop.


The prognosis for cats with HCM depends on several factors, including their response to therapy and whether thromboembolic events occur, the disease progresses, and/or arrhythmias develop. The prognosis can be good for asymptomatic cats with only mild to moderate left ventricular hypertrophy and atrial enlargement. However, cats with more severe hypertrophy and left atrial enlargement are thought to be at greater risk for heart failure, thromboembolism, and sudden death. Cats with congestive failure have variable outcomes: some do very well for several years. The prognosis is worse if there is atrial fibrillation or refractory right-sided heart failure. The prognosis is generally poor for cats presented with congestive failure and thromboembolism (median survival of about 2 months), although some do well if congestive signs can be controlled and infarction of vital organs has not occurred. Recurrence of thromboembolism is common.



Etiology and Pathophysiology

Restrictive cardiomyopathy (RCM) is associated with extensive endocardial, subendocardial, or myocardial fibrosis. The etiology is not clear but could be multifactorial. The disease may be a sequela of endomyocarditis or represent the end-stage of myocardial failure and infarction stemming from HCM. Severe perivascular and interstitial fibrosis and intramural coronary artery narrowing are reportedly typical histologic findings. Occasionally, secondary RCM results from neoplastic (e.g., lymphoma) or other infiltrative or infectious diseases. Restrictive cardiomyopathy shares characteristics of both hypertrophic and dilated cardiomyopathies; it has sometimes been called intermediate or intergrade cardiomyopathy, as has the myocardial disease encountered in some cats that do not clearly have a restrictive pathophysiologic condition.

A major abnormality appears to be impaired diastolic filling secondary to left ventricular fibrosis, although there is much variation in this syndrome and it is difficult to document clinically. Most affected cats have mildly reduced contractility, but this may progress with time as more functional myocardium is lost. Regional left ventricular dysfunction can occur, and systolic function can be very poor in some cats (these cardiomyopathies are perhaps better called unclassified rather than restrictive). Mitral regurgitation may be present but is usually mild. Yet, massive left atrial enlargement is often seen; markedly increased left ventricular wall stiffness resulting from the fibrosis is thought to be the main cause. Arrhythmias, ventricular dilatation, or ischcmia also contributes to the development of diastolic dysfunction. Chronic elevation of left heart filling pressures in combination with compensatory neurohormonal activation leads to left-sided or biventricular failure.

A prominent pathologic feature is marked atrial enlargement and hypertrophy. The left ventricle shows variable dilation, with or without hypertrophy, which can be regional. Endomyocardial fibrosis may be focal or widespread, with extensive scarring that deforms the ventricle. The mitral valve apparatus and papillary muscles may be distorted and fused to surrounding structures. 'thrombi arc commonly found within the left atrium, left ventricle, or systemic vasculature. Histopathologic changes include endocardial and myocardial fibrosis, hypertrophied myocytes, areas of myocardial degeneration, and necrosis. Excess moderator bands are found in some cats, but their role in the development of myocardial disease and congestive heart failure is unclear. They may represent a congenital anomaly, because they have been identified in young kittens as well as old cats.

Clinical Features and Diagnosis

RCM appears most often in middle-age or older cats. The clinical signs are variable but usually reflect the presence of left- or right-sided congestive heart failure, or both.

Signs are often precipitated by stress or concurrent disease that increases demands on the cardiovascular system and are likely to develop or worsen suddenly. Thromboembolic events are common and thought to be secondary to marked left atrial enlargement and blood stasis. Inactivity, poor appetite, vomiting, and weightloss may be part of the cat's recent history. Sometimes asymptomatic disease is discovered by the finding of auscultation abnormalities or radiographic evidence of cardiomegaly.

Common physical examination findings in cats with RCM include a gallop sound, a systolic murmur of mitral or tricuspid regurgitation, or arrhythmias. Abnormal pulmonary sounds can accompany pulmonary edema or a pleural effusion. Femoral arterial pulses are normal or slightly weak. Jugular vein distention and pulsation can often be detected in the setting of right-sided heart failure. Signs of distal aortic (or other) thromboembolism may be the reason for presentation.

Diagnostic test results are often similar to those in cats with HCM. Radiographs show left atrial enlargement that can be massive and left ventricular or generalized heart enlargement. Dilated, tortuous proximal pulmonary veins may be noted; infiltrates of pulmonary edema or a pleural effusion and sometimes hepatomegaly are seen in cats with heart failure. The ECG is often abnormal; wide QRS complexes, tall R waves, evidence of intraventricular conduction disturbances, wide P waves, and atrial tachyarrhythmias or fibrillation are common.

Echocardiographic features include marked left (and sometimes right) atrial enlargement, variable left ventricular free-wall and septal thickening, and often normal to somewhat depressed wall motion (fractional shortening usually exceeding 25%). Some cats have marked regional wall dysfunction, especially of the left ventricular free wall, which significantly depresses fractional shortening. Mild left ventricular dilation (a more than 18-mm diastolic dimension) is often evident, although parts of the ventricle can be hypertrophied, irregular, or focally thinned. Hyperechoic areas of fibrosis may appear to constrict portions of the ventricular lumen. Extraneous intraluminal echos representing excess moderator bands are occasionally seen. Right ventricular dilation is frequently identified. Sometimes an intracardiac thrombus is found, usually in the left auricle or atrium, but occasionally in the left ventricle. Doppler evaluation may show mitral or tricuspid regurgitation. Nonselective angiocardiography will reveal the same anatomic findings and highlight the distended and tortuous pulmonary veins.

The clinicopathologic findings are nonspecific. Pleural effusions usually consist of modified transudate or chyle. The plasma taurine concentration is low in some affected cats and should be measured if decreased contractility is identified.

Treatment and Prognosis

Therapy for acute heart failure is the same as that described for cats with HCM and involves the use of furosemide, oxygen, nitroglycerin, and thoracocentesis for the treatment of pleural effusion.  Long-term therapy for heart failure includes furosemide, as needed; the resting respiratory rate, activity level, and radiographic findings are used to monitor efficacy. Enalapril is also used, starting with very low doses and increasing to the usual maintenance dose of 0.25 to 0.5 mg/kg/day. Twice-daily administration can be helpful in refractory cases. Ideally, blood pressure is monitored when initiating or adjusting ACEI therapy. Creatinine or the blood urea nitrogen and electrolyte concentrations are measured periodically. The doses of furosemide or enalapril, or both, should be reduced if hypotension or azotemia occurs. Cats with considerably reduced systolic function are also given digoxin (see Table 3-8). An attempt is usually made to prevent thromboembolism using aspirin or warfarin, and a low-sodium diet is fed, if accepted.

Refractory heart failure with pleural effusion is difficult to manage. Besides doing a thoracocentesis, dosages of enalapril or furosemide can be increased cautiously; hydrochlorothiazide and spironolactone (2 to 3 mg/kg of the combination daily) can be added to the regimen, or nitroglycerin ointment can be added. Diltiazem can also be used, although its value in the face of significant fibrosis is controversial.

Diltiazem and -blockers could be detrimental because of their negative inotropic effects; however, they may be helpful in slowing heart rate in the presence of atrial fibrillation. Ventricular premature complexes are common in cats with RCM. If they are frequent or associated with syncope, a -blocker or procainamide may be helpful, although potential negative inotropic drug effects are of concern.

The overall prognosis for cats with RCM is guarded to poor, although some cats live well for more than a year. Thromboembolism and refractory pleural effusion commonly occur and worsen the prognosis.




In the late 1980s taurine deficiency was discovered to be a major cause of dilated cardiomyopathy (DCM) in cats. The taurine content of commercial feline diets has since been increased, and clinical DCM is now uncommon in cats. Because DCM does not develop in all cats fed taurine-deficient diets, factors other than a simple deficiency of this essential amino acid are thought to be involved and include genetic factors and a possible link with potassium depletion. Despite the presence of low plasma taurine concentrations in most cats with DCM, there may actually be no significant difference in the myocardial taurine concentrations in these cats compared with those in cats with other forms of heart disease.

Secondary dilated myocardial disease.  DCM in sonic cats may be the end stage of another myocardial metabolic derangement, toxicity, or infection. Doxorubicin causes characteristic myocardial histologic lesions in cats as well as dogs; however, this species appears fairly resistant to clinical dilated myocardial failure. Some cats show echocardiographic changes consistent with DCM after receiving cumulative doses of 170 to 240 mg/m.


The pathophysiologic features of DCM in cats are similar to those in dogs. The hallmark is poor myocardial contractility. Usually all cardiac chambers are dilated; AV valve insufficiency occurs secondary to chamber enlargement and papillary muscle atrophy. As cardiac output decreases, compensatory neurohormonal mechanisms are activated, leading to an increased cardiac volume and clinical manifestations of left- or right-sided congestive heart failure, or both. Arrhythmias and pleural effusion are common in cats with DCM.

Clinical Features and Diagnosis

DCM historically has occurred in cats of all ages, with no breed or gender predilection. Clinical signs are frequently vague and include the acute onset of anorexia, lethargy, or dyspnea, or a combination of these. Subtle evidence of poor ventricular function is found in conjunction with signs of respiratory compromise. Increased respiratory effort, depression, dehydration, and hypothermia are frequent findings. Jugular venous distention, an attenuated precordial impulse, weak femoral pulses, a gallop sound (usually S3), and a left or right apical systolic murmur (of mitral or tricuspid regurgitation) are common. Bradycardia and arrhythmias occur often, although many cats have a normal sinus rhythm. Increased lung sounds and pulmonary crackles can be auscultated in some cats, or pleural effusion may muffle ventral lung sounds. There may also be clinical signs of arterial thromboembolism.

Generalized cardiomegaly with rounding of the cardiac apex is a common radiographic finding. Pleural effusion is common and tends to obscure the heart shadow and coexisting evidence of pulmonary edema or venous congestion. Hepatomegaly and occasionally ascites may be detected. A left ventricular enlargement pattern, AV conduction disturbances, and arrhythmias are frequent ECG findings.

Definitive diagnosis is best made on the basis of the echocardiographic findings. These are analogous to those in dogs with DCM. A thrombus may be identified within the left atrium. Nonselective angiocardiography is a more risky alternative to echocardiography, as it is for the diagnostic evaluation of other cardiomyopathies. Characteristic angiographic features include generalized chamber enlargement, atrophied papillary muscles, a decreased aortic diameter, and a slow circulation time. Complications of the procedure, especially in cats with poor myocardial function or decompensated heart failure, include vomiting and aspiration, arrhythmias, and cardiac arrest.

The pleural effusion in cats with DCM is usually a mortified transudate, although true chylous effusions occur. Prerenal azotemia, mild increases in liver enzyme activities, and a stress leukogram are other common clinicopathologic findings. High serum muscle enzyme activities, an abnormal blood clotting profile, and disseminated intravascular coagulation can occur in association with thromboembolism.

Plasma taurine quantification is offered by several commercial laboratories. In the event this is desired, specific instructions should be obtained from the laboratory regarding sample collection and mailing. Plasma taurine concentrations are influenced by the amount of taurine in the diet, the type of diet, and the time of sampling in relation to eating; however, a plasma taurine concentration of 20 nmol/ml or less in a cat with DCM is considered diagnostic for taurine deficiency. Cats with a plasma taurine concentration of less than 60 nmol/ml probably should receive taurine supplementation or have their diet changed Results may be more consistent if whole blood samples rather than plasma samples are used for taurine determinations.

Treatment and Prognosis

The goals of treatment are to increase cardiac output and improve pulmonary function, as for dogs with DCM. Pleural fluid is removed by thoracocentesis. Furosemide is given to promote diuresis, as described earlier for HCM. The venodilator nitroglycerin may be helpful in cats with severe pulmonary edema. Vasodilators (e.g., hydralazine or an ACEI) can help maximize cardiac output, although with the risk of hypotension. Blood pressure, hydration, renal function, electrolyte balance, and peripheral perfusion should be monitored closely. Hypothermia is common in cats with decompensated DCM, so external warming should be provided, as needed. Once pulmonary edema is controlled, furosemide is tapered to the lowest effective PO dosage.

Positive inotropic support is indicated. Dobutamine or dopamine administered by constant rate infusion can be used for critical cases. Adverse effects of dobutamine can include seizures or tachycardia; if they occur, the infusion rate should be decreased by 50% or the drug discontinued. The adverse effects of dopamine usually occur at higher doses; they include tachycardia and increased peripheral vascular resistance resulting from the a-adrenergic effects of the drug. Dopaminergic effects may cause renal blood flow to increase at low infusion rates. IV digoxin has also been used initially in cats with decompensated DCM. Amrinone (see p. 66) is a positive inotropic agent with peripheral vasodilating properties, although the dose for cats is not well established. Digoxin PO is the positive inotropic drug of choice for maintenance therapy. Digoxin tablets arc usually used, because many cats dislike the taste of digoxin elixir. Toxicity can easily occur, especially if other drugs are being used concurrently; therefore periodic evaluation of serum digoxin concentration is recommended.

Furosemide and vasodilating agents can reduce cardiac filling and predispose to the development of cardio-genic shock in cats with DCM. Half-strength saline solution with 2.5% dextrose or other low-sodium fluids can be given IV at 20 to 35 ml/kg/day in several divided doses or by constant rate infusion; potassium supplementation may be needed. Fluid can be administered SC if necessary, although the absorption of the fluids from the extravascular space may be impaired.

Long-term treatment for cats that survive acute heart failure includes oral furosemide, an ACEI, digoxin, aspirin (or warfarin), and taurine supplementation or a high-taurine diet. Taurine supplementation, at a dosage of 250 to 500 mg PO g12h, should be instituted as soon as possible in cats with low or unmeasured plasma taurine concentrations. Taurine is available in 500-mg capsules from health food stores. Because clinical improvement generally does not begin until after 1 to 2 weeks of taurine supplementation, supportive cardiac care is vital. Aspirin or warfarin therapy is usually instituted to reduce the risk of thromboembolism.

Echocardiographic evidence of improved systolic function is seen in most cats within 6 weeks of initiation of taurine supplementation. Drug therapy may become unnecessary in some cats after 6 to 12 weeks, although it is advised that the resolution of pleural effusion and pulmonary edema be confirmed radiographically before weaning the cat from medications. When echocardiographic measures of systolic function are at or near normal, the amount of taurine supplementation can be decreased and therapy eventually discontinued, as long as the cat eats a diet known to support adequate plasma taurine concentrations (e.g., most name-brand commercial foods). Dry diets with 1000 to 1200 mg of taurine per kilogram of dry weight and canned diets with 2000 to 2500 mg of taurine per kilogram of dry weight are thought to maintain normal plasma taurine concentrations in adult cats. Reevaluation of the plasma taurine concentration 2 to 4 weeks after supplement discontinuation is also advised.

Taurine-deficient cats that survive a month after initial diagnosis often can be weaned from all or most medications, except for taurine. These cats appear to have about a 50% chance for 1-year survival. The prognosis for cats not supplemented with taurine or those that are do not respond to taurine is guarded to poor. Thromboembolism in a cat with DCM is a grave sign.


Inflammation of the myocardium and adjacent structures also occurs in cats. Congestive heart failure or fatal arrhythmias may result from severe, widespread myocarditis. Cats with focal myocardial inflammation may remain asymptomatic. Acute and chronic cases of suspected viral myocarditis have been described. Although a viral cause is rarely documented, feline coronavirus has been shown to cause pericarditisepicarditis. Endomyocarditis found during histopathologic examination has occurred mostly in young cats. Acute death with signs of pulmonary edema lasting for 1 to 2 days, or without these signs, is the most common presentation. Histopathologic characteristics of acute endomyocarditis include focal or diffuse lymphocytic, plasmacytic, and histiocytic infiltrates with a few neutrophils. Degenerative and lyric changes are seen in adjacent myocytes. Chronic endomyocarditis has been associated with a minimal inflammatory response but much myocardial degeneration and fibrosis. It is speculated that RCM represents the end stage of nonfatal endomyocarditis. Therapy involves the management of congestive signs and arrhythmias and other supportive care.

Bacterial myocarditis may result from sepsis or from bacterial endocarditis or pericarditis, as it does in dogs. Myocarditis caused by Toxoplasma gondii also occurs occasionally, usually in immunosuppressed cats as part of a generalized disease process. Traumatic myocarditis is infrequently recognized in cats.


Thromboembolism can occur with any form of feline cardiomyopathy. Thrombosis and embolization result from circulatory stasis, altered blood coagulability, local tissue or blood vessel injury, or a combination of these. Poor intracardiac blood flow, especially within the left atrium, may result in blood stasis and clot formation. Hypercoagulability has been demonstrated in cats with thromboembolic disease, in which platelets are known to be quite reactive. Disseminated intravascular coagulation also may develop in cats with thromboembolism. Changes in cardiac endothelial surfaces secondary to the cardiomyopathy could induce platelet adhesion, leading to activation of the coagulation cascade.

The most common site of embolization is the distal aortic trifurcation ("saddle thrombus"), noted in more than 90% of cats with thromboembolic disease. Thromboemboli can also lodge within a brachial artery, various organs, and the heart itself. Vasoactive substances that impair the development of collateral circulation are released after thromboembolization. Experimental ligation of the distal aorta does not result in the clinical syndrome seen in cats with thromboembolic disease, however. Instead an ischemic neuromyopathy results from the thromboembolus and the resulting impaired collateral circulation. Nerve conduction failure, ischemic damage to nerve sheaths, and wallerian-type degeneration cause peripheral nerve dysfunction; pathologic changes also occur in the associated muscle tissue.

Clinical Features and Diagnosis

Middle-age male cats appear to be at highest risk for thromboembolism. The clinical signs occur acutely and are usually dramatic. Often there is no history of cardiac disease. The clinical findings depend on the area embolized. For example, acute distal aortic embolization is manifested by paresis in the hindlimbs. The femoral pulses are absent, the limbs cool, the nailbeds cyanotic, and the affected muscles firm and painful. The cat is usually able to flex and extend the hips but drags the lower legs; sensation to the lower legs is poor. One side may show greater neurologic deficits than the other; occasionally only distal embolization of one limb occurs, resulting in paresis of the lower limb alone. Embolization of a brachial artery causes forelimb monoparesis; intermittent claudication occurs occasionally. Thromboembolism of the renal, mesenteric, or pulmonary arterial circulation may result in failure of these organs and death.

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Respiratory distress, a cardiac murmur, or an arrhythmia is often noted at presentation.  Azotemia may result from dehydration, poor cardiac output related to the cardiomyopathy, embolization of the renal arteries, or a combination of these. Skeletal muscle damage and necrosis are accompanied by elevations of alanine aminotransferase and aspartate aminotransferase activities, beginning within 12 hours of the thromboembolic event and peaking by 36 hours. Widespread muscle injury causes lactate dehydrogenase and creatine kinase activities to be increased soon after the event; elevations in these enzyme activities may persist for weeks. Metabolic acidosis, disseminated intravascular coagulation, and hyperkalemia may also be present secondary to ischemic muscle damage and reperfusion. Stress hyperglycemia is also common.

Echocardiography delineates the type of myocardial disease and may reveal the presence of an intracardiac thrombus. Most cats have significant left atrial enlargement. If echocardiography is unavailable, nonselective angiocardiography can be done to define the nature of the cardiac disease and allow the anatomic location and extent of the embolus to be determined; however, angiocardiography should be delayed until the animal's condition is stabilized. The finding of no palpable femoral pulses, in conjunction with other physical examination, auscultatory, and plain thoracic radiographic findings, is often diagnostic. However, a cardiac murmur, gallop sound, or arrhythmia is an inconsistent finding, and a minority of affected cats have no radiographic evidence of cardiomegaly. Other causes of acute posterior paresis to be considered include intervertebral disc disease, spinal neoplasia (e.g., lymphoma), trauma, fibrocartilaginous infarction, diabetic neuropathy, and myasthenia gravis.

Treatment and Prognosis

The goals of treatment are to manage the congestive heart failure (if present), provide supportive care, and prevent extension of the embolus and formation of additional thrombi. The treatment of heart failure is outlined in preceding paragraphs (HCM) Digoxin is not used unless DCM is identified. Propranolol is also avoided because its -blocking effects may leave vascular a -adrenergic receptors unopposed and lead to peripheral vasoconstriction. In addition, propranolol has no antithrombotic effects at clinical doses.

The therapy for the thromboembolism is somewhat controversial, and there is no proven best treatment. At a minimum, supportive care should be given to allow time for the establishment of collateral circulation (2 to 5 days). The conditions of some cats improve with or despite specific therapy. An analgesic is recommended because this is a painful condition. Torbutrol (0.15 to 0.2 mg/kg IM into the cranial lumbar area or SC q8h) has been recommended, especially for the first 24 to 36 hours after the embolic event. Acepromazine has been advocated for its a-adrenergic receptor-blocking effects (0.05 to 0.3 mg/kg SC q8h); however, it has not been documented to improve collateral flow and it, as well as other vasodilators such as hydralazine, could worsen cardiac function by causing hypotension or exacerbating a preexisting outflow tract obstruction.

Sodium heparin (initial dose of 200 ItJ/kg IV, then 150 to 200 ILJ/kg SC q8h) is frequently administered for 2 to 4 days in an attempt to prevent further thrombus formation. Heparin is a cofactor for antithrombin 111; the antithrombin III-heparin complex neutralizes factors IX, X, XI, XII, and thrombin (factor II), thereby preventing further coagulation. Existing thromboemboli are not affected. SC doses are adjusted to prolong the animal's activated coagulation time from 1.5 to 2.5 times the pretreatment level. As expected, however, bleeding can be a major complication of therapy. If this occurs, protamine sulfate may be given, but care must be taken because an overdose of protamine can paradoxically cause irreversible hemorrhage. Dosage guidelines for protamine sulfate are as follows: 1 mg/100 U of heparin is given if the heparin was given within the previous 60 minutes; 0.5 mg/100 U of heparin is given if the heparin was given more than 1 but less than 2 hours earlier; and 0.25 mg/100 U of heparin is given if more than 2 hours have elapsed since heparin was administered.

More aggressive thrombolysic therapy has proved problematic, even if instituted within 8 hours of the thromboembolic event and closely monitored. Specifically, 90,000 IU of streptokinase (Streptase; HoechstRoussel, Somerville, NJ, and Kabikinase; SmithKline Beecham, Philadelphia, PA) has been infused IV during the first hour, then 45,000 IU/hr is given for a total of to 8 hours. However, the mortality in these cats is very high. Acute hyperkalemia (secondary to thrombolysis and reperfusion) and other complications are thought to be responsible for causing death. Streptokinase therapy should not even be considered if heparin has already been administered, (because of the risk for excess hemorrhage); if the cat is anuric; or if the serum potassium concentration and the ECG cannot be monitored continuously. Streptokinase works by nonspecifically enhancing the production of plasmin, causing generalized clot lysis with the potential for excess bleeding; intraurterial administration close to the clot probably would have greater positive effects. Tissue plasminogen activator (TPA; Activase, Genentech San Francisco, CA) has a higher specificity of action against fibrin within thrombi, with a low affinity for circulating plasminogen. A dose of 0.25 to 1 mg/kg/hr up to a total of 1 to 10 mg/kg IV has been used. However, this also has yielded disappointing results in the few cats evaluated. Although evidence of reperfusion was found, the mortality rate during therapy was high. The cause of death in most cats was related to reperfusion (hyperkalemia, metabolic acidosis), although congestive heart failure and arrhythmias were also involved.

Other supportive therapy includes maintaining normal body temperature, treating dehydration, monitoring renal function and the serum potassium concentration daily, and general nursing care. Surgical removal of the clot is not advised (except, perhaps, for a suprarenal thrombus). The surgical risk is high in most cases because of the presence of decompensated heart failure, arrhythmias, disseminated intravascular coagulation, and hypothermia. Furthermore significant neuromuscular ischemic injury has probably already occurred by the time surgery is performed, thus further reducing the likelihood for a good outcome. Clot removal using an embolectomy catheter has not been very effective in cats either.

If concurrent congestive heart failure can be controlled, function should begin to return in the affected limbs within 7 to 14 days. Some cats become clinically normal within 1 to 2 months, although residual deficits may persist for a variable length of time. In general, the prognosis is guarded. About two thirds of affected cats die or are euthanized soon after the thromboembolic event. Some cats survive well for more than a year, although repeated events are common and worsen the long-term prognosis. Significant embolization of the kidneys, intestines, or other organs carries a grave prognosis.

Prevention of Thromboembolism

No current therapeutic strategy has been found to consistently prevent thromboembolism. The risk of thromboembolism is thought to be greater in cats with marked left atrial enlargement, echocardiographic evidence of intracardiac spontaneous contrast ("swirling smoke"), or visible intracardiac thrombi, and in those with a prior thromboembolic event.

Aspirin has been observed to inhibit platelet aggregation and improve collateral circulation in experimental aortic thrombosis at a dose of 10 to 25 mg/kg (1.25 grains/cat) administered every third day, PO. The drug acts by irreversibly inhibiting the enzyme cyclooxygenase, thereby reducing thromboxane AZ synthesis and subsequent platelet aggregation, serotonin release, and vasoconstriction. However, the optimal dose of aspirin that can inhibit thromboxane A2 production but minimally affect prostacyclin synthesis by the vascular endothelium is not yet established. Prostacyclin causes vasodilation and inhibits platelet aggregation. Although aspirin has been used widely with generally little risk, it does not consistently prevent initial or recurrent thromboembolism. Diltiazem given at clinical doses also does not appear to have significant platelet-inhibiting effects.

Long-term therapy with warfarin (Coumadin; DuPont, Wilmington, DE), given PO, is becoming more widely used in cats that survive an acute thromboembolic event or are otherwise presumed to be at high risk for thromboembolism. It may afford better protection than aspirin, but thromboembolism can still recur. Furthermore, warfarin has a greater potential for causing serious adverse effects, even in animals that are closely monitored. Warfarin works by inhibiting the formation of vitamin K-dependent clotting factors (II, VII, IX, and X) as well as the anticoagulant proteins C and S. A transient hypercoagulable state occurs after the initiation of therapy until the levels of factors IX and X decrease. Studies regarding this phenomenon in animals are not available, but heparin is usually given for the first 2 to 5 days of warfarin therapy. The pharmacokinetics of warfarin in cats is not well documented; in people, the bioavailability varies with different drug preparations and elimination is mainly by hepatic metabolism. Many drug interactions with warfarin are observed in people.

Monitoring of the patient is very important because of the potentially wide variability in dose response and the risk of bleeding. It is prudent to hospitalize the patient during the initiation of therapy. A baseline coaguhtion profile and platelet count should be obtained. Aspirin, if previously being given, should be discontinued. An initial dose of 0.1 mg/kg/day (or a quarter to half of a 1-mg warfarin tablet) is given PO. Heparin (100 IU/kg S(: q8h) is administered for 3 to 4 days. It is preferable to keep the medication administration and blood sampling times consistent. The prothrombin time (PT) is evaluated daily (at least 2 hours after warfarin dosing) for 5 to 6 days initially. The PT can then be evaluated at progressively increasing time intervals (e.g., twice a week, then once a week, then every month to 2 months) as long as the cat's condition appears stable. Use of the same brand of warfarin may provide more consistent results.

The initial warfarin dose is adjusted to maintain a desirable PT. Variable recommendations for this exist; a PT value from 1.3 to 2 times the baseline value at 8 to 10 hours after dosing may be used. A more precise method is the standardized PT represented by the international normalization ratio (INR). This method has been recommended to eliminate the problems posed by variations in commercial PT assays. The INR is calculated by dividing the animal's PT by the control IvT and raising the quo to the power of the international sensitivity index (ISO of the thromboplastin used in the assay, or INR = (animal P'f/control PT)ISI. The ISI is provided with each batch of thromboplastin manufactured. Extrapolation from data in humans would indicate that an INR of 2 to 3 is as effective as higher values, with less chance for bleeding. However, it may be difficult to achieve fine dose adjustments in cats because of the size of commercial drug tablets.

If the P'f or INK is excessively increased, warfarin should be discontinued and vitamin K administered (1 to 2 mg/kg/day PO or SC). If the PT is still prolonged after 3 days, vitamin K treatment is continued until the PT is normal and the packed cell volume is stable. Some cats with significant bleeding need fresh blood transfusions. Warfarin can be resumed at half the original dose, along with heparin, which is given for several days.

The combination of aspirin and warfarin has been used in some cats judged to be at very high risk for thromboembolism. However, preliminary experience indicates that the combination is no more effective than either alone in preventing recurrent thromboembolism.

Additional Reading
Arterial Thromboembolism - Philip Fox
Hyperthrophic Cardiomyopathy (John Bonagia)

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