Cardiovascular Pathology in AIDS

Abstract

The heart is not the most frequent site for opportunistic infectious or neoplastic processes in patients with AIDS (table 1). However, cardiovascular pathologic findings may occur in up to 40% of AIDS patients at autopsy [2-4]. Cardiac lesions are the immediate cause of death in 1-3% of AIDS patients [5]. The most common significant manifestations of cardiac disease, which can occur at any stage of HIV infection and can lead to death, include cardiomyopathy, dysrhythmias and pericardial effusion with tamponade [6]. Clinical cardiac findings may be present in a fourth to three fourths of adult AIDS patients and may be accompanied by findings that include chest pain, tachycardia, electrocardiographic changes including various arrhythmias, effusions and congestive heart failure. There may be mild cardiomegaly on chest roentgenograms [7]. The prevalence of HIV-related cardiac disease appears to be decreasing with the use of highly active antiretroviral therapy (HAART) [8]. Overall, deaths from cardiovascular diseases in patients dying of AIDS increased slightly from 1987 to 1999, as advances in antiretroviral therapy reduced deaths due to HIV infection after 1995 and the proportion of deaths caused by other conditions increased [9]. Atherosclerosis Many persons with HIV infection are in the third to fifth decades of life when cardiovascular complications from atherosclerosis are not as frequent as in older persons. Atherosclerotic cardiovascular disease leading to ischemia and myocardial infarction (fig. 1) can and does occur in HIV-infected patients, particularly as the numbers of HIV-infected persons on HAART rise and as the population of long-term survivors from AIDS increases. In one autopsy study, 39% of men and 21% of women dying of AIDS had significant atherosclerosis [4].

Cardiovascular complications in the acquired immunodeficiency syndrome

“…Lymphocytes, along with fewer macrophages, are distributed diffusely as single cells or in small clusters. Autopsy studies of AIDS patients who died of acute left ventricular dysfunction, almost in variably show a marked inflammatory infiltrate 11,12 . However, mild and focal mononuclear infil trates are frequently observed in the hearts of AIDS patients, irrespective of the presence of cardiac symptoms 11,12 .…”

“…Autopsy studies of AIDS patients who died of acute left ventricular dysfunction, almost in variably show a marked inflammatory infiltrate 11,12 . However, mild and focal mononuclear infil trates are frequently observed in the hearts of AIDS patients, irrespective of the presence of cardiac symptoms 11,12 . The intracardiac conduction sys tem is sometimes affected in AIDS patients, gen erally as a complication of myocarditis.…”

“…The most common oppor tunistic infectious agent associated with myocar ditis in AIDS is Toxoplasma gondii, observed as often as 12% in one autopsy series of deaths from AIDS between 1987 and 1991 12 . There may be regional differences in the incidence of Toxoplasma gondii myocarditis, perhaps because the natural reservoir of organisms persists more easily in hu mid environments.…”

“…Toxoplasma gondii can produce fairly variable inflammation along with myocardial fiber necrosis. The three microscopic patterns of involvement by Toxoplasma gondii include acute diffuse myocarditis, focal myocardi tis, and presence of organisms without significant inflammation or necrosis 10,12 .In Toxoplasma myocarditis, true Toxoplasma gondii extracellular cysts, or pseudocysts within myocardial fibers, both of which contain the small 2-µ-sized bradyzoites, are often difficult to find, even if inflammation is exten sive. Immunohistochemical staining may reveal free tachyzoites, organisms that are found outside of cysts.…”

“…Immunohistochemical staining may reveal free tachyzoites, organisms that are found outside of cysts. Otherwise, with rou tine hematoxylin and eosin staining, it is difficult to distinguish these free tachyzoites from fragments of inflam matory cells or myocytes that have undergone necrosis within the areas of inflammation 10,12 .…”