The myocardium is affected by a variety of disease processes including the primary muscle disorders such as dilated cardiomyopathy and hypertrophic cardiomyopathy, degenerative and inflammatory diseases, neoplasia, and infarction. The myocardium is also sensitive to toxin exposure, including adriamycin, oleander, and fluoroacetate (1080). Myocarditis occurs in all species and may be caused by viral, bacterial, parasitic, and protozoal infection. Canine parvovirus, encephalomyocarditis virus, and equine infectious anemia are viruses with a propensity to cause myocarditis. Myocardial degeneration occurs in lambs, calves, and foals with white muscle disease, and in pigs with mulberry heart disease or hepatosis dietetica. Mineral deficiencies can also result in myocardial degeneration, including iron, selenium, and copper.

Dilated Cardiomyopathy (DCM) is an acquired disease characterized by the progressive loss of cardiac contractility of unknown cause. Several forms of secondary dilated cardiomyopathy exist (cause known) such as taurine deficiency (cats), adriamycin-induced, parvoviral-induced, and post-partrum. As cardiac contractile function is progressively lost, there is a decrease in cardiac output. Increased blood volume and pressure within the chambers causes them to dilate, most dramatically evident in the left atrium and left ventricle. In response to the poor contractility and decreased cardiac output, the sympathetic nervous system and the renin-angiotensin-aldosterone axis are activated. As with degenerative valve disease, these compensatory mechanisms are initially beneficial, however their chronic activation becomes deleterious. Constant stimulation of the heart by the sympathetic nervous system causes ventricular arrhythmias and myocyte death, while constant activation of the renin-angiotensin-aldosterone axis causes excessive vasoconstriction and retention of sodium and water. The majority of cases exhibit signs of left-sided congestive heart failure, although right-sided signs (ascites) can occur.

This disease is common is large breed dogs, and very rare in small breed dogs (exception being English cocker spaniel). Doberman pinschers, great Danes, German shepherds, and labrador retrievers are particularly at risk. The disease is typically seen in middle-aged dogs, with males affected more than females. Once common in cats, the incidence of dilated cardiomyopathy has dropped dramatically since the 1985 discovery that taurine deficiency was responsible for a majority of cases. Since that time, taurine levels have been increased to acceptable levels in all commercial cat foods. Most cases today are not taurine responsive and reflect a primary (or idiopathic) disease. In cats, there is no breed predilection for dilated cardiomyopathy.

Most often, dogs and cats are presented with signs that have developed acutely. These include exercise intolerance, inappetance, weight loss, cough, weakness and syncope. Dogs with predominately right-sided failure usually have a more chronic course, with signs including weakness, exercise intolerance, and ascites. A soft systolic murmur is present in most cases and is best heard at the left cardiac apex. In addition, a third heart sound or gallop is also frequently present, especially in cats.

A complete blood count, serum chemistry profile, and urinalysis are usually within normal limits. Radiographically, there is mild to marked generalized cardiomegaly. If heart failure is present there will be an increase in the interstitial densities and enlargement of the pulmonary veins. Echocardiography is the ideal test to definitively diagnose DCM. There is a dramatic loss of cardiac contractility (reported as a low fractional shortening). Cardiac chambers are dilated especially the left atrium and left ventricle. There are no significant valvular lesions, although mitral insufficiency may develop as the cardiac dilatation separates the mitral valve leaflets. Electrocardiographically, the rhythm in most cases is normal sinus rhythm to sinus tachycardia. Ventricular premature complexes are common, especially in Doberman pinschers and boxers. Atrial premature complexes and atrial fibrillation are also common. There may be electrocardiographic evidence of left atrial enlargement (p-mitrale or widened P waves) and left ventricular enlargement (tall and wide R-waves). Conduction disturbances such as left bundle branch block are uncommon. The occurrence of one or more VPCs in a presumed healthy Doberman pinscher is highly suggestive of occult DCM.

Therapy centers on controlling the congestive state (diuretics), improving contractility (digoxin, dobutamine), and reducing cardiac stress (vasodilators). Occasional cases will benefit from L-carnitine, taurine, or Coenzyme Q10 (CoMal Q10) supplementation. When congestive heart failure is severe, diuretic therapy should be aggressive. The typical dose of furosemide in this setting is 4-6 mg/kg IV. A repeat dose will be required 4 hours later. Oxygen supplementation should also be provided, either through an oxygen cage or by nasal insulflation. Nitroglycerin ointment is also indicated. A combination dobutamine and sodium nitroprusside infusion is often very beneficial in these cases. As the pulmonary edema resolves, oral furosemide replaces IV, while oxygen therapy and nitroglycerin are continued. Treatment with digoxin should also be initiated - the dose for a large breed dog is 0.22 mg/m2 (body surface area) twice daily. Vasodilator therapy is definitely indicated in these dogs. Enalapril is the preferred drug and should be administered twice daily (0.5 mg/kg BID). Other ACE inhibitors, such as captopril and benazepril can be used, but are not approved for use in the dog. L-carnitine will help a very small subset of dogs. The limitation is that an L-carnitine deficient dog cannot be identified without an endomyocardial biopsy. Also, the supplement is expensive and may be cost prohibitive. Coenzyme Q10 supplementation has resulted in significant improvements in humans with DCM, and trials are underway investigating its efficacy in dogs with DCM. The recommended dose is 30 mg TID. Fish oil administration was recently shown to reduce the severity of cardiac cachexia in Dobermans with DCM. Antiarrhythmic therapy is also frequently indicated, especially for Doberman pinschers and boxers. Routine or preferably continuous ambulatory electrocardiography is indicated to determine the type and frequency of the arrhythmia and the effect of the antiarrhythmic agent. Procainamide, propranolol, and tocainide are most commonly used. The prognosis is guarded to poor for most dogs. The prognosis is worst in Doberman pinschers, with most dying within 2 months of diagnosis. The prognosis is better for dogs exhibiting predominately right-sided failure, with some surviving for 1-2 years.

The most common cardiomyopathy in cats is hypertrophic cardiomyopathy (HCM). This disease is characterized by left ventricular hypertrophy in the absence of a precipitating cause, such as hypertension, or aortic stenosis, and is typically seen in middle aged cats. Although contractility is not significantly impaired, the hypertrophic ventricular walls lose compliance and resist filling during diastole (diastolic failure). This increases pressure within the left atrium causing this chamber to dilate and pressure to be transmitted to the pulmonary veins causing pulmonary edema. Stasis of blood often occurs in markedly dilated left atria predisposing affected cats to aortic thromboembolism.

Middle-aged male cats are primarily affected and often develop acute dyspnea, collapse, or rear limb paresis. Abnormal heart sounds are frequently present and include soft to prominent heart murmurs and gallop rhythms. Increased bronchovesicular sounds and rales are suggestive of pulmonary edema. Pulses may be weak, normal, or absent if thormboembolic disease is present.
Radiographically, there is pronounced left atrial enlargement and variable left ventricular enlargement. Evidence of pulmonary edema is frequently present, and pleural effusion is occasionally encountered. Echocardiography is the test of choice and allows confirm ation of the disease, and need for additional therapy, e.g. anticoagulant therapy is most beneficial in cats with severe left atrial enlargement. Contractility is usually within normal limits or excessive. A variety of electrocardiographic abnormalities may be present including atrial premature complexes, ventricular premature complexes, ventricular tachycardia, and left anterior fascicular block.

Treatment must control pulmonary edema, improve diastolic function, and reduce the incidence of systemic thromboembolism.
Furosemide and nitroglycerin are indicated when acute pulmonary edema is present. Diltiazem (7.5 mg TID), a calcium channel blocker, is the drug of choice by many for improving diastolic function. Vasodilators are occasionally used. Recently, enalapril has been demonstrated to reduce left ventricular hypertrophy and left atrial enlargement in affected cats. Either aspirin (10 mg/kg every third day) or warfarin (0.2 mg - 0.5 mg daily) are used to reduce the chance of thrombus formation.

Myocardial diseases are infrequently reported in horses. Streptococcus is the most common bacterial cause of myocarditis.
Salmonella, Clostridium, the viral agents Equine influenza and equine infectious anemia, Borrelia burgdorferi and Strongylosis have also been incriminated. Vitamin E and selenium deficiency are known to cause myocardial necrosis. Cardiac toxins include ionophore antibiotics such as monensin and salinomycin, cantharidin (blister beetle toxicosis), Cryptostegia grandiflora (rubber vine poisoning), and Eupatorium rugosum (white snake root poisoning). These diseases cause typical signs of congestive heart failure - exercise intolerance, tachycardia, and tachypnea. In the horse, signs of right-sided heart failure are common and include ascites, venous congestion, and jugular pulsations. A murmur of mitral or tricuspid regurgitation is usually audible as well as an irregular rhythm. Atrial fibrillation is common, and ventricular or atrial premature complexes may also be seen. Echocardiography reveals chamber dilation and poor contractility with essentially normal valves. A complete blood count often demonstrates a neutrophilic leukocytosis and hyperfibrinogenemia. Elevations in cardiac isoenzymes (creatine kinase and LDH) are often present.

Treatment should be aimed at improving cardiac contractility, relieving congestion, and reducing vasoconstriction. Digoxin and dobutamine are used most commonly to improve contractility. Furosemide is indicated to control signs of pulmonary edema.
Corticosteroids are often used when cardiac isoenzymes are increased and a viral infection is deemed unlikely.