April 7, 2003
The authors followed a series of 24 consecutive HIV-infected patients admitted for acute myocardial infarction (AMI) between 1998 and 2000. During hospitalization, the patients were examined for recurrent ischemia, congestive heart failure, arrhythmia and death. Post discharge, patients were followed up for an average of 15 months for reinfarction; recurrent angina; the need for any angioplasty, bypass surgery or target vessel revascularization for restenosis and stent thrombosis; HIV-related complications; and death. For comparison, the authors included a matched control group of 48 patients not HIV-infected. None of the patients in either group reported recent use of cocaine or anabolic steroids.
The HIV-infected patients with AMI were predominantly male (21; 88 percent), 47 ? 9 years of age. Twenty-two (92 percent) were receiving antiretroviral treatment; 17 (71 percent), protease inhibitors; and 13 (54 percent), lipid-lowering therapy. With aggressive therapy, the lipid profile was similar in HIV-infected patients treated with protease inhibitors and those who were not. The mean duration of the infection was 10.7 ? 4.4 years in patients with and 8.4 ? 4.2 years in patients without protease inhibitor treatment.
The authors found that AMI in HIV-infected patients is associated with a favorable in-hospital outcome, not unlike the outcome in the matched control patients. This is likely due to the young age of the patients and the absence of significant hemodynamic compromise. Although both the HIV-infected and matched control patients had relatively benign hospital courses, with no deaths or reinfarctions reported, after discharge, HIV-infected patients had a higher incidence of reinfarction (4/20; 20 percent) and rehospitalization for recurrent coronary event (9; 45 percent) than uninfected control patients in the approximately 15-month follow up. This study suggests that HIV infection is associated with an increased rate of restenosis after percutaneous coronary intervention. This association is particularly evident in patients with increased viral load, irrespective of protease inhibitor therapy.
Dyslipidemia associated with protease inhibitor therapy was considered as a significant factor for premature CAD in HIV-infected patients. The lipid profile of patients receiving protease inhibitors (71 percent) and lipid-lowering therapy (59 percent) was similar to the profile of HIV-infected patients not treated with protease inhibitors and control patients. Although the hyperlipidemia and insulin resistance associated with the use of protease inhibitors may contribute to the development of premature CAD, results of this study and others suggest that HIV infection is associated with CAD independent of the metabolic effects of antiretroviral therapy. This is supported by necropsy findings of premature atherosclerosis in a large percentage of HIV-positive patients not treated with protease inhibitors and in children who have died of AIDS.
The authors conclude that HIV-infected patients sustain AMI at a young age and have a benign in-hospital course. Although HIV-patients have a higher incidence of postdischarge coronary events, the intermediate-term mortality is low. Nevertheless, the major determinants of prognosis likely remain complications associated with HIV infection.
Archives of Internal Medicine
02.24.03; Vol. 163: P. 457-460; Shlomo Matezky, M.D; Michelle Domingo, B.A.; Saibal Kar, M.D.; Marko Noc, M.D., Ph.D.; Prediman K. Shah, M.D.; Sanjay Kaul, M.D., Eric Daar, M.D.; Bojan Cercek, M.D., Ph.D.