Clinical Guide > Comorbidities and Complications > CHD

Coronary Heart Disease Risk

Author: Marshall Glesby, MD
January 2011

Chapter Contents


Epidemiologic studies suggest that the incidence of myocardial infarction or hospitalization for coronary heart disease (CHD) is increased up to two- to threefold in HIV-infected individuals compared with age-matched controls without HIV infection. This increased risk of ischemic events likely is attributable to a higher prevalence of certain CHD risk factors that are independent of HIV status, such as smoking, as well as to both HIV infection and antiretroviral (ARV) medications. These various factors may interact in ways that are complex and incompletely understood.

Among the traditional CHD risk factors, dyslipidemia is common among persons with HIV infection, and can be caused both by HIV itself (e.g., resulting in low high-density lipoprotein [HDL] cholesterol) and by ARV therapy (ART); see chapter Dyslipidemia. Insulin resistance and diabetes also appear to be more prevalent in HIV-infected patients. (See chapter Insulin Resistance, Hyperglycemia, and Diabetes on Antiretroviral Therapy.) Visceral fat accumulation, a poorly understood complication of HIV or ART, also may contribute to CHD risk in certain patients (see chapter Abnormalities of Body-Fat Distribution).

A number of studies suggest that inflammation and immune activation owing to uncontrolled HIV infection also likely contribute to atherosclerosis. For example, in the Strategic Management of Antiretroviral Therapy (SMART) study, CHD events were more common in patients on intermittent ART than in those on continuous ART, possibly because of adverse effects of intermittent HIV viremia on inflammation, coagulation, and lipid parameters. There is even preliminary evidence that so-called elite controllers--patients with undetectable HIV viremia and preserved CD4 counts in the absence of ART--have increased carotid intima-medial thickness (a marker of atherosclerotic burden) compared with HIV-uninfected subjects, after adjusting for other CHD risk factors. Limited data also suggest that initiation of ART leads to improvement of endothelial dysfunction (an early marker of atherosclerosis that is predictive of future CHD events) and to improvement in markers of inflammation and immune activation. Taken together, these observations suggest that earlier initiation of ART could reduce CHD risk.

On the other hand, even patients with virologic suppression on ART appear to have higher levels of various physiologic markers of cardiovascular risk than the HIV-uninfected persons, perhaps owing to persistent immune activation. Additionally, exposure to ARVs has been linked to risk of myocardial infarction in large cohort studies such as the D:A:D study. In particular, the risk has been associated with use of ARV regimens that are based on protease inhibitors (PIs) rather than nonnucleoside reverse transcriptase inhibitors (NNRTIs). The risk is attributable in part to adverse changes in lipid profiles, but there appears to be additional risk associated with PIs that is not accounted for by changes in lipids; this remains poorly understood. Among the nucleoside reverse transcriptase inhibitors (NRTIs), abacavir and didanosine have been associated with increased risk of myocardial infarction in some but not all studies. The mechanism of this potentially increased risk has not been determined.

S: Subjective

Clinicians should ask all patients about CHD, CHD risk equivalents, and CHD risk factors. Assess the following during the history:

O: Objective

Perform a physical examination to include the following:

A: Assessment

P: Plan

Patient Education