HIV-positive patients sustain acute myocardial infarction at a young age and have a benign in-hospital course

Reported series of patients have suggested that HIV-positive patients are at an increased risk of coronary artery disease (CAD), linked to the hyperlipidemia and insulin resistance associated with protease-inhibitor therapy. However, necropsy studies had demonstrated premature CAD in HIV-positive patients prior to the advent of protease inhibitors. Little data exist regarding the course of acute coronary events in HIV-positive patients.

The authors followed a series of 24 consecutive HIV-positive patients admitted for acute myocardial infarction (AMI) between 1998 and 2000. During hospitalisation, 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 revascularisation for restenosis and stent thrombosis; HIV-related complications; and death. For comparison, the authors included a matched control group of 48 HIV-negative patients. None of the patients in either group reported recent use of cocaine or anabolic steroids.

The HIV-positive 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- positive 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-positive 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 haemodynamic compromise. Although both the HIV-positive and matched control patients had relatively benign hospital courses, with no deaths or reinfarctions reported, after discharge, HIV-positive patients had a higher incidence of reinfarction (4/20; 20%) and rehospitalisation for recurrent coronary event (9; 45%) than HIV-negative 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.

The HIV-positive patients had lower low-density lipoprotein cholesterol and lower high-density lipoprotein values than HIV-negative patients. Otherwise, there were no significant differences in risk factors for CAD, ST-segment-elevation AMI, and AMI localisation between HIV-positive patients and control patients.

Dyslipidaemia associated with protease inhibitor therapy was considered as a significant factor for premature CAD in HIV-positive patients. The lipid profile of patients receiving protease inhibitors (71%) and lipid-lowering therapy (59%) was similar to the profile of HIV-positive 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-positive patients sustain AMI at a young age and have a benign in-hospital course. Although HIV-patients have a higher incidence of post-discharge coronary events, the intermediate-term mortality is low. Nevertheless, the major determinants of prognosis likely remain complications associated with HIV infection.

Source: CDC HIV/STD/TB Prevention News Update


Matetzky S, Domingo M, Kar S et al. Acute myocardial infarction in human immunodeficiency virus-infected patients. Arch Intern Med 2003 Feb 24;163(4):457-60


This is a small cohort, but it is interesting to put the relevance of MI into perspective.

Unfortunately because of the design of the cohort studies with a lack of an HIV-negative control, and the often unknown individual duration of the HIV-infection, current cohort studies like D:A:D or HOPS are unable to assess the influence of HIV-infection itself on CVD. A possible approach would be to match the HIV+ patients with individuals from the WHO MONICA project to have at least an HIV-negative control.

Links to other websites are current at date of posting but not maintained.