HIV and coronary arterial remodeling from the Multicenter AIDS Cohort Study (MACS)

Abstract

Objective Positive remodeling (PR), a coronary artery characteristic associated with risk for myocardial infarction (MI), may be more prevalent in HIV-infected (HIV+) people. We evaluated the prevalence of PR using coronary CT angiography (CCTA) in HIV+ and HIV-uninfected (HIV−) men. Methods/Results Men enrolled in the Multicenter AIDS Cohort Study underwent CCTA if they were 40–70 years, had normal kidney function and no history of coronary revascularization. Multivariable logistic regression models were used to estimate the odds ratio (OR) of PR by HIV serostatus, adjusting for demographics and coronary artery disease (CAD) risk factors. Analysis of PR among atherosclerotic segments further adjusted for plaque type and stenosis. The prevalence of PR was 8.4% versus 12.1% (p=0.10) for HIV− and HIV+ men, respectively. After demographic adjustment, HIV+ men had twice the odds of PR [OR 2.01(95% CI 1.20–3.38)], which persisted after CAD risk factor adjustment [1.76(1.00–3.10)]. Higher systolic blood pressure, total cholesterol, diabetes medication use, older age, segment number with plaque present, mixed and non-calcified plaque, and stenosis>50%, were associated with increased odds of PR, while higher HDL cholesterol, higher nadir CD4 count, and black race were associated with lower PR odds. Among atherosclerotic segments, the association between HIV infection and PR persisted, but was not statistically significantly. Conclusion HIV+ men have more positively remodeled arterial segments, which may be due to more coronary segments with atherosclerosis or HIV-related immunosuppression. Further studies are needed to evaluate whether PR contributes to higher rates of MI in HIV+ individuals.

Association of High-Sensitivity Troponin with Cardiac CT Angiography Evidence of Myocardial and Coronary Disease in a Primary Prevention Cohort of Men: Results from MACS

“…Asymptomatic HIV-infected persons also have an increased prevalence of subclinical atherosclerosis with more calcified and, particularly more noncalcified coronary artery plaque compared with HIV-uninfected individuals (14). In addition, HIV-infected persons appear to have a higher prevalence of vulnerable plaque that is associated with increased risk of CVD events (29).…”

Sex Differences in Select Non-communicable HIV-Associated Comorbidities: Exploring the Role of Systemic Immune Activation/Inflammation

“…Activated immune cells also contribute to plaque remodeling, promoting the development of high-risk morphology plaque features which predispose to atherothrombosis(8). In studies focused on MLHIV, systemic markers of monocyte activation have been related to arterial inflammation(9, 10), subclinical carotid and coronary artery atherosclerosis(11–14), and pathologically remodeled coronary atherosclerotic plaque(15, 16). Studies focused predominantly on WLHIV have revealed relationships between systemic immune markers and carotid atherosclerosis(17–19), as well as the percent of non-calcified coronary atherosclerotic plaque(6).…”

Cardiovascular disease risk among women living with HIV in North America and Europe

“…Activated immune cells (particularly monocytes-turned-macrophages, but also T cells and other types of immune cells) participate meaningfully in atherosclerotic plaque formation and pathologic plaque remodeling(20). Several physiology studies performed in all-male or predominantly male (>90% male) cohorts have revealed relationships between systemic markers of monocyte activation (sCD163, sCD14) and surrogates of atherosclerotic cardiovascular disease (ASCVD) risk including subclinical carotid artery atherosclerosis(21), aortic inflammation(22) (23), subclinical coronary atherosclerotic plaque(24) (25) (26), and pathologically remodeled coronary atherosclerotic plaque(27) (28). Separate physiology studies among WLHIV have confirmed parallel relationships between systemic immune activation markers and ASCVD risk surrogates, including subclinical carotid atherosclerosis(29) (30) (31) and the percent of non-calcified coronary atherosclerotic plaque(32).…”