ABSTRACT
With the increasing life spans of patients infected with the AIDS virus, morbidity and mortality associated with a plethora of cardiovascular complications is becoming more obvious in this population (1,2). HIV infection itself has been associated with the development of dilated cardiomyopathy, pericardial effusions, and vasculopathy. However, recent reports on the appearance of premature atherosclerosis in young patients have raised serious concerns regarding the role of viral and other factors in atherogenesis (1-5). In addition, highly active antiretroviral therapy (HAART) used for the treatment of HIV infection has been associated with dyslipidemia and lipodystrophy, which can further accentuate the development of atherosclerosis (2). Cocaine abuse, which is becoming alarmingly common, has also been associated with the development of atherosclerosis but may also synergize with HIV infection in causing endothelial injury. In the individual patient who is infected with HIV and is abusing cocaine, accelerated development of coronary disease is very likely. Table 1 lists the roles of HIV infection, HAART, and cocaine in the genesis of vascular disease. The molecular mechanisms underlying these complicated interactions are reviewed in this chapter.
