Parvoviral myocarditis occasionally occurs in young dogs which are infected in utero or as neonates. Peracute disease may result in sudden death from heart failure in pups aged 3-8 weeks. Milder lesions may result in dilated cardiomyopathy and signs of congestive heart failure or arrythmias in older pups up to the age of 6 months. There is also experimental evidence to suggest that canine distemper virus can cause severe myocardial damage in very young pups.
Focal suppurative myocarditis may occur as a sequel to bacteraemia associated with bacterial endocarditis or pericarditis. Affected animals may show systemic signs (fever, weight loss and depression) and an arrhythmia is often evident on an ECG. Serial blood cultures should be performed in an animal showing appropriate clinical signs. Myocarditis has been reported in a dog which was seropositive for Borrelia burgdorferi.
Infection of the myocardium with Toxoplasma gondii occasionally occurs in immunosuppressed animals. Neospora caninum infection has been reported as a cause of myocarditis and sudden death in a dog. Trypanosoma cruzi infection (Chagas* disease) is associated with granulomatous myocarditis in young dogs in the southeastern United States.
Myocardial involvement has been reported with systemic mycotic infections, for example cryptococcosis, coccidioidosis and aspergillosis.
Traumatic myocarditis may be caused by penetrating wounds or blunt trauma for example after a road traffic accident. Myocardial ischaemia, haemorrhage or contusion may result in severe ventricular arrhythmias which may not be apparent until 12-48 h after the traumatic episode. Serious life-threatening arrhythmias require prompt and aggressive therapy; less severe arrhythmias associated with minimal haemodynamic changes may resolve spontaneously alter a few days.
Diagnosis of myocarditis
The diagnosis of myocarditis is often presumptive and based on the history and clinical and electrocardiographs findings. Infectious myocarditis should be suspected when persistent or intermittent pyrexia is accompanied by an arrhythmia and / or signs of congestive heart failure (congestive heart failure). In the absence of signs of congestive heart failure thoracic radiographs are often unremarkable. Serial blood cultures should be taken if possible during a pyrexic episode, and serological tests for specific diseases, for example canine parvovirus or toxoplasmosis, may also be indicated.
Treatment of myocarditis
Therapy should be directed toward the underlying disease process as well as management of congestive heart failure and any arrhythmia which may be present. A broad spectrum antibiotic should be used if an infectious cause is suspected; the administration of corticosteroids for their anti-inflammatory properties may also be justified.
Primary myocardial tumours are rare. Haemangiosarcoma involving the right atrium is the most common primary cardiac tumour with most cases occurring in older German shepherd dogs. Chemodectomas or heart base tumours (most are aortic body tumours rather than carotid body tumours) arise from the base of the aorta and / or pulmonary artery. They tend to be locally invasive and have a predilection for brachycephalic breeds such as boxers and Boston terriers. Metastatic tumours (for example lymph o ma or haemangiosarcoma) also may infiltrate the myocardium. The clinical signs of myocardial neoplasia vary depending on the location of the mass and degree of myocardial infiltration. Arrhythmias and atrioventricular conduction blocks are common; animals with pericardial involvement may develop a pericardial effusion resulting in cardiac tamponade and signs of right-sided congestive heart failure.
Confirmation of myocardial and pericardial neoplasia is best achieved by the use of echo-cardiograph y which may reveal echodense foci or masses within the myocardium.
The ventricular arrhythmias which are often associated with gastric dilatation-volvulus and acute pancreatitis may be the result of myocardial ischaemia and necrosis. The pathogenesis of these lesions is uncertain; myocardial depressant factors have been implicated.
Chronic administration of the anthracycline drug, doxorubicin, results m progressive myocardial degeneration with clinical signs which are similar to those of dilated cardiomyopathy. The acute effects of cardiotoxicity (reduced left ventricular filling and decreased cardiac output) may occasionally occur after initial therapy and are thought to be mediated by histamine and catecholamine release. Signs of chronic toxicity (left ventricular enlargement and congestive heart failure) may occur with median cumulative doses greater than 150 mg m-2 BSA. Left ventricular dilatation is associated with a marked decrease in myocardial contractility and arrhythmias (supraventrieular and ventricular arrhythmias as well as conduction abnormalities) are common. ECG changes may occur at cumulative doses less than 90 mg m : and may precede signs of congestive heart failure. Regular ECG and echocardiographic monitoring of patients receiving doxorubicin is essential therefore and therapy should be discontinued if abnormalities are noted.
Myocardial ischaemia, necrosis and infarction is not a major cause of death in dogs as it is in humans. Microscopic focal myocardial infarction has been associated with thrombotic diseases, for example bacterial endocarditis, following thromboembolic occlusion of the coronary artery. Similar microscopic infarcts and focal areas of myocardial necrosis and fibrosis may occur in older dogs with valvular endocardiosis although the significance of these Lesions is uncertain. The pathogenesis of these lesions is not known; one possibility is that they are caused by coronary vasoconstriction in response to increased levels of circulating catecholamines. Myocardial ischaemia may also occur as an important and sometimes life-threatening complication in dogs with acute gastric dilatation-volvulus and acute pancreatitis. Less frequently it has been reported with atheroselerosis in hypothyroid dogs which are hyper cholesterolacmic.