Rabbit Dilated Cardiomyopathy
Viruses have long been recognized as important etiologic agents of heart disease in man and experimental animals1. Epidemiologic evidence suggests that between 2–5% of a virus-infected population experiences some degree of cardiac involvement2. Virus infection may result in degeneration and necrosis of myocytes by direct cytotoxicity and cause myocarditis, or inflammation of the heart muscle3. Myocarditis may progress to arrhythmias, conduction disturbances, circulatory collapse and/or acute congestive (dilated) cardiomyopathy4. Clinically, dilated cardiomyopathy is diagnosed by an increase in the heart weight, heart weigh/body weight weight ratios, enlargement of the left and/or right ventricular cavities, thinning/hypertrophy of the ventricular walls, and low ejection fractions. In humans particularly ominous signs of dilated cardiomyopathy include the presence of pulmonary edema, pleural effusion, and congestion of the lungs and liver 4,5. The incidence of idiopathic dilated cardiomyopathy is estimated between 3–5 cases/100,000 population/year and accounts for about 30% of all heart disease related deaths in some areas of the world6. The mechanism(s) by which virus infection progresses to myocarditis and dilated cardiomyopathy is unclear.
KeywordsDilate Cardiomyopathy Ventricular Wall Ventricular Dilation Heart Weight Uninfected Control
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