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ventricular hypokinesis, and decreased fractional shortening. It is possible that cardiomyopathy
and myocarditis are immunologic phenomenon resulting from HIV-containing lymphocytes in
cardiac muscle.[896] Cytokine elaboration by inflammatory cells may contribute as well, since
increased levels of both tumor necrosis factor-alpha and inducible nitric oxide synthase have
been found in patients with HIV-associated cardiomyopathy. The incidence of HIV-related
cardiomyopathy has decreased significantly since the advent of ART.[902]
Cardiac myocytes have also been shown to be a direct target for HIV infection, which
may result in cardiomyopathy. A proposed autoimmune mechanism for myocardial damage is
based upon the observation that autoantibodies to myosin and cell B receptor can be detected in
HIV-infected patients with cardiomyopathy. This may occur when HIV alters myocardial cell
surface proteins to elicit an immune reaction. A possible mechanism for an autoimmune
contribution to myocardial damage is hypergammaglobulinemia with immune complex
formation.[896]

DRUG TOXICITY.-- A number of pharmacologic agents may induce significant cardiac
arrhythmias. These include amphotericin B, pentamidine, and interferon alfa. Bradycardia is
seen in children treated with amphotericin B. Doxorubicin can produce cardiomyopathy.
Interferon alfa administered as part of prolonged antiretroviral therapy may also lead to a dilated
cardiomyopathy, as well as ischemia, and congestive heart failure. Zidovudine can produce
mitochondrial changes in striated muscle. Cocaine use in patients with a history of drug abuse
may lead to myocarditis, contraction band necrosis, and cardiomyopathy.[896]
The antiretroviral drug abacavir is associated with an increased risk for cardiovascular
disease and heart failure. Recent tenofovir use is associated with heart failure.[903]

ENDOCARDITIS.-- Debilitation of patients with AIDS, particularly in the terminal
course, may predispose to the formation of non-bacterial thrombotic endocarditis (marantic
endocarditis). This is the most common form of endocarditis with AIDS and may be seen in
about 5% of persons dying with AIDS at autopsy, most of them older than age 50. Such
marantic valvular vegetations can occur on any valve and are probably agonal, although
occasional infarcts in spleen, kidney, or cerebrum may result from pre mortem
embolization.[896]
Persons with HIV infection whose risk is injection drug use (IDU) have an increased risk
for infective endocarditis compared to HIV seronegative IDUs. Over 90% of cases of infective
endocarditis with HIV infection occur in IDUs. Staphylococcus aureus is the most common
pathogen, followed by Streptococcus, viridans group. Other agents may include Salmonella
species, Aspergillus, and Pseudallescheria boydii. The tricuspid valve is the most commonly
affected valve, in over half of cases, but left sided valvular disease occurs in 45% of cases, and
multiple valves are involved in 18%. Pulmonic valve infection is rare. The mortality rate is
higher with multiple valve involvement and with lower CD4 counts. Most patients have a
coexisting pneumonia or meningitis.[896,904]

ATHEROSCLEROSIS.-- Coronary artery disease may be seen in a specific setting in
AIDS. The pattern of risk factors, pathologic lesions, location of lesions, and plaque
composition is similar to atherosclerosis in HIV-negative patients.[905] Persons with HIV
infection on antiretroviral therapy (ART) area at increased risk because the syndrome of HIV
lipodystrophy and because of endothelial dysfunction from viremia, which promote