Review of Cardiovascular Disease in HIV-Infected Women

Abstract

Rates of coronary heart disease (CHD) are over twice as high in younger HIV-infected patients compared to uninfected patients, but most of these studies were conducted in men or in predominantly male cohorts. In the general population, the death rate from CHD has decreased among men, but continues to increase in women. It is unclear if the same increased rate of deaths due to CHD exist in HIV-infected women, and whether rates or risk of CHD differ between HIV-infected men and women, and between seropositive and seronegative women. We reviewed the literature on the rates of cardiovascular events and surrogate measures of atherosclerosis or CHD risk in HIV-infected women. We also reviewed rates of metabolic disease and other markers of inflammation and immune activation that could contribute to increased cardiovascular risk. We found that HIV-infected women have increased rates of acute myocardial infarctions and ischemic strokes compared to HIV-uninfected women and likely HIV-infected men despite women being projected to have lower CHD risk based on Framingham risk scores. Studies assessing CHD risk by measuring anatomical or physiological measures of subclinical atherosclerosis have reported mixed results, and there are no well-validated risk assessment tools or surrogate measures of subclinical CHD among HIV-infected patients to help identify high-risk women for targeting intensive preventive measures. Potential explanations for the increased rates of CHD and subclinical atherosclerosis may be partly explained by increased levels of inflammation and immune activation in HIV-infected women despite virological suppression on antiretroviral therapy. It appears unlikely that disproportionate representation of traditional CHD risk factors and metabolic indices among HIV-infected women can explain well the observed increased rates of CHD. Future studies that include large numbers of HIV-infected women with extended follow-up periods using surrogate measure of CVD and investigating pathogenic mechanisms underlying these observations are urgently needed.