Abstract Body

Cardiovascular disease (CVD) has emerged as an important co-morbidity in HIV-infected patients. The relative risk of CVD, including myocardial infarction and stroke, is increased in HIV patients compared to age and gender-matched non HIV patients. Although some traditional risks, including smoking, are increased in HIV-infected patients and should be targeted for treatment, very often this disease occurs in relatively young, asymptomatic patients with only modest increases in traditional risk scores. Epidemiological studies suggest unique patterns of CVD in HIV patients, for example younger HIV-infected women may be less protected from CVD than younger women in the general population. Recent studies suggest an emerging mechanistic paradigm in which persistent immune activation and inflammation may contribute to atherosclerotic disease in HIV patients. In the HIV population, this disease manifests itself as subclinical, primarily non-calcified, vulnerable plaque, at increased risk for rupture. Indeed studies show increased rates of sudden cardiac death in the HIV population, consistent with acute rupture of vulnerable plaque. Monocyte activation and trafficking into the arterial surface may contribute to an inflammatory pro-thrombotic local milieu, more amenable to buildup of plaques with lipid laden foam cells and a thin necrotic surface. Indeed, molecular imaging techniques, assessing metabolic indices, suggest increased activity at the arterial surface among HIV patients, in association with immune activation and high risk, low attenuation, positively remodeled plaque. Treatment options to prevent CVD in HIV patients are critically needed. Emerging data suggests that targeting inflammation and immune activation may be useful to reduce CVD risk in the HIV population and specific strategies targeting these pathways are now under investigation. Significant evidence suggests that statins may offer a number of benefits, potentially useful to lower CVD risk and prevent disease in the HIV population. Statins have been shown to reduce arterial inflammation, reduce monocyte activation and trafficking, and target key systemic inflammatory pathways. In addition, this class of agents reliably lowers LDL and thus may have advantages in reducing both traditional and nontraditional risk factors. Large scale NIH funded studies are now underway to test whether statins can safely prevent CVD in HV and the mechanisms by which this effect may occur.