Preclinical atherosclerosis due to HIV infection:

Cardiovascular morbidity and HIV

Preclinical atherosclerosis due to HIV infection:

Cardiovascular disease is an increasing cause of morbidity and mortality in HIV-infected patients. However, it is controversial whether HIV infection contributes to accelerated atherosclerosis independent of traditional cardiovascular disease risk factors. In a cross-sectional study of HIV-infected participants and controls without pre-existing cardiovascular disease from the study of Fat Redistribution and Metabolic Change in HIV Infection (FRAM) and the Multi-Ethnic Study of Atherosclerosis (MESA), preclinical atherosclerosis was assessed by carotid intima-medial thickness measurements in the internal/bulb and common regions in HIV-infected participants and controls after adjusting for traditional cardiovascular disease risk factors. For internal carotid, mean intima-medial thickness was 1.17 +/- 0.50 mm for HIV-infected participants and 1.06 +/- 0.58 mm for controls (P < style="text-decoration: underline;">After multivariable adjustment for demographic characteristics, the mean difference of HIV-infected participants vs. controls was 0.188 mm [95% confidence interval (CI) 0.113-0.263, P <>. Further adjustment for traditional cardiovascular disease risk factors modestly attenuated the HIV association (0.148 mm, 95% CI 0.072-0.224, P = 0.0001). For the common carotid, HIV infection was independently associated with greater intima-medial thickness (0.033 mm, 95% CI 0.010-0.056, P = 0.005). The association of HIV infection with intima-medial thickness was similar to that of smoking, which was also associated with greater intima-medial thickness (internal 0.173 mm, common 0.020 mm). Even after adjustment for traditional cardiovascular disease risk factors, HIV infection was accompanied by more extensive atherosclerosis measured by intima-medial thickness The stronger association of HIV infection with intima-medial thickness in the internal/bulb region compared with the common carotid may explain previous discrepancies in the literature. The association of HIV infection with intima-medial thickness was similar to that of traditional cardiovascular disease risk factors, such as smoking.

Although HIV infection and its therapies are associated with increases in several traditional cardiovascular disease risk factors, such as decreased high-density lipoprotein (HDL cholesterol is the good one), increased non-HDL cholesterol, and diabetes, this study of carotid wall thickness suggests that HIV infection itself confers an additional effect equivalent to a 5- to 9-year increase in age. These data suggest that women are more affected – for them the effects of HIV infection on the risk of atherosclerosis are greater than those of smoking.