ABSTRACT
The acquired immunodeficiency syndrome (AIDS) is induced by the human immunodeficiency virus (HIV-1) and represents a multiorgan disease (1-3). A major feature of the disease is the progressive loss of CD4+ T-cells with lymphadenopathy, thymic atrophy, and destruction of the architecture of lymphoid organs. Other significant AIDS-related phenotypes include lung disease (lymphocytic interstitial pneumonitis) (4,5), renal disease (interstitial nephritis, segmental glomerulosclerosis) (6-8), wasting (9,10), peripheral (11) and central (12-15) neurodegenerative diseases, hematological disorders (16), and cardiac disease. Such cardiac disease is now recognized as a relatively frequent complication of HIV-1 infection and is characterized by a progressive dilated cardiomyopathy sometimes accompanied by compensatory cardiac hypertrophy and functional loss. A variety of histopathological lesions have been observed in hearts of HIV-1 infected individuals, the most common being cardiomyocyte necrosis, often with fibrosis. Mononuclear cell infiltration is often observed with these lesions but may be absent. Several reviews have appeared on the clinical and pathological aspects of the AIDS-associated cardiomyopathy (17-25).
