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Pathogenesis and biomarkers of cardiovascular disease in HIV-infected patients

Author
Judith S Currier, MD
Section Editor
John G Bartlett, MD
Deputy Editor
Allyson Bloom, MD

INTRODUCTION

As patients are living longer with HIV, cardiovascular disease has emerged as an important cause of morbidity and mortality among infected patients. Even with effective antiretroviral therapy, HIV-infected patients have a higher risk of myocardial infarction and cardiovascular death than age-matched uninfected controls. Although an increased prevalence of traditional risk factors, such as dyslipidemia and smoking, among HIV-infected patients likely contributes to this increased cardiovascular morbidity, growing evidence suggests that HIV infection and treatment are more directly linked to atherogenesis, endothelial dysfunction, and coagulation abnormalities, likely through inflammation and immune dysregulation.

Measures of subclinical cardiovascular disease and the pathogenesis of atherosclerosis in HIV-infected patients are discussed here. The epidemiology of cardiovascular morbidity and traditional risk factors and the management of dyslipidemia and cardiovascular risk in HIV-infected patients are discussed elsewhere. (See "Epidemiology of cardiovascular disease and risk factors in HIV-infected patients" and "Management of cardiovascular risk (including dyslipidemia) in the HIV-infected patient".)

SUBCLINICAL ATHEROSCLEROSIS

Cardiovascular disease has emerged as an important cause of death in HIV-infected patients, as illustrated by clinical studies evaluating such hard endpoints as stroke or myocardial infarctions (see "Epidemiology of cardiovascular disease and risk factors in HIV-infected patients"). However, HIV patients are generally young and thus have overall low short-term cardiovascular risk and few events. Therefore, many clinical studies rely upon surrogate markers to indirectly assess the burden of cardiovascular disease. These studies have generally demonstrated an increased prevalence of subclinical atherosclerosis in HIV-infected compared with HIV-uninfected individuals. Such measurements include intima media thickening (IMT) and intraluminal arterial plaque as assessed by ultrasound and evaluation of coronary artery calcification and plaque by computed tomography (CT). These measurements have been moderately associated with coronary atherosclerosis and the future risk of a cardiovascular event in studies of HIV-uninfected adults [1]. (See "Overview of the possible risk factors for cardiovascular disease", section on 'Arterial intima-media thickness' and "Overview of the possible risk factors for cardiovascular disease", section on 'Coronary artery calcification'.)

Evidence of increased subclinical atherosclerosis among HIV-infected elite controllers compared with uninfected controls has also been observed, suggesting that an increased risk of atherosclerosis can occur in the absence of antiretroviral therapy, detectable viremia, or overt immunodeficiency [2,3].

Intima media thickening — Most, but not all studies of IMT of the carotid artery and coronary arteries in asymptomatic adults have found an increase in measurement with HIV infection [2,4-13]. In a meta-analysis of observational studies evaluating subclinical atherosclerosis in HIV-infected patients, the following observations were noted [4]:

                   

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Literature review current through: Nov 2016. | This topic last updated: Wed Aug 05 00:00:00 GMT+00:00 2015.
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