Coronary Disease in Patients with HIV Infection


HIV-infected individuals are at increased risk for noncalcified coronary plaques, with lower nadir CD4-cell counts and longer antiretroviral therapy duration being associated with coronary artery stenosis >50%.


Several studies have noted increased risk for coronary artery disease (CAD) and myocardial infarction in HIV-infected patients. This increase has been attributed to direct effects — or metabolic complications — of antiretroviral therapy (ART), factors associated with the virus itself (including chronic immune activation), or both. Surrogate markers of atherosclerotic disease have been used to further characterize this risk in HIV-infected patients.

Now, as part of the large, prospective Multicenter AIDS Cohort Study (MACS), researchers have used noncontrast cardiac computed tomography (CT) to measure coronary artery calcium (CAC) and CT angiography to assess plaque extent and characteristics. A total of 618 HIV-infected and 383 HIV-uninfected men who have sex with men underwent cardiac CT; 759 of the participants without contraindications to CT angiography also underwent this procedure. Data on CAD risk factors and HIV clinical variables were obtained from records for previous MACS visits.

In multivariate analyses adjusted for age, race, CT scanning center, cohort, and established CAD risk factors, the prevalence and extent of CAC were similar between HIV-infected and uninfected men. However, HIV-infected men had a significantly greater prevalence of plaque in any coronary segment and of noncalcified plaque, and a significantly greater extent of noncalcified plaque. In the HIV-infected group, lower nadir CD4-cell counts and longer ART duration were associated with coronary artery stenosis >50%.


Noncalcified plaque represents an early stage of plaque formation. Compared with calcified plaque, it may be more prone to rupture, the first step in the development of an acute coronary syndrome. The finding that HIV-infected individuals are at increased risk for noncalcified plaque suggests that the pathophysiology of plaque formation or progression may differ in this population. This study confirms similar observations in smaller ones, which have also shown an association between the presence of noncalcified plaque and markers of immune activation such as soluble CD163. These findings open the door for studies to further address the mechanisms leading to the increased risk for cardiac events in HIV-infected individuals, and to identify preventive strategies.

Dr. Armstrong is Medical Director of the Infectious Diseases Program at Grady Health System and Associate Professor of Infectious Diseases at Emory University School of Medicine, Atlanta. She reports no conflicts of interest.


  1. Post WS et al. Associations between HIV infection and subclinical coronary atherosclerosis. Ann Intern Med 2014 Apr 1160:458. (

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