Cardiovascular risk in postmenopausal women living with HIV.

OBJECTIVE: To compare cardiovascular risk and subclinical atherosclerosis between postmenopausal women living with human immunodeficiency virus (WLH) and HIV-negative women, and to identify determinants of carotid plaque, with particular focus on menopausal timing and antiretroviral exposure. METHODS: This analytical cross-sectional study included 200 age-matched postmenopausal women (45-60 y; 100 WLH and 100 HIV-negative controls) in Manaus, Brazil. All participants had ≥12 months of amenorrhea. Cardiometabolic parameters, lifestyle factors, and carotid ultrasonography (carotid intima-media thickness [cIMT] and plaque) were assessed. Ten-year cardiovascular risk was estimated using the Framingham score (all participants) and the D:A:D R10 score (WLH only). Comparisons between WLH and HIV-negative women included demographic, metabolic, lifestyle, imaging, and cardiovascular risk variables. Multivariable logistic regression models using carotid plaque as the dependent variable included covariates with P<0.20 in univariate analyses. A separate model restricted to WLH additionally evaluated HIV-related clinical characteristics and cumulative antiretroviral exposure variables. The discriminative performance of Framingham and D:A:D R10 scores for carotid plaque detection were assessed using receiver operating characteristic curve analysis. RESULTS: WLH exhibited a more adverse cardiometabolic profile, including lower HDL-C, higher triglycerides, higher fasting glucose, greater metabolic syndrome prevalence (55% vs. 36%; P=0.007), and markedly higher physical inactivity (81% vs. 57%; P<0.001). Framingham risk scores were significantly higher in WLH (mean 10.5±6.9 vs. 7.5±4.8; P=0.007), with nearly half classified as high risk. Carotid plaque prevalence was significantly greater among WLH (12% vs. 3%; P=0.017), despite similar cIMT between groups. In adjusted models, HIV infection remained independently associated with plaque (odds ratio [OR]=4.65; 95% confidence interval [CI]=1.06-20.4), and older age at menopause was protective (OR=0.92 per year delay; 95% CI=0.85-0.99). Within WLH, longer non-nucleoside reverse transcriptase inhibitor (NNRTIs) exposure was independently associated with lower odds of plaque (OR=0.63 per year; P=0.005), with a protective trend observed for INSTI. For discrimination of carotid plaque, D:A:D R10 demonstrated higher area under the curve than Framingham (0.69 vs. 0.60), although the difference was not statistically significant (P=0.146). CONCLUSIONS: Among postmenopausal women, HIV infection was independently associated with a higher prevalence of carotid plaque, despite similar cIMT values between groups. Earlier menopause appeared to act as a cardiovascular risk amplifier in WLH. Although D:A:D R10 showed a trend toward better discrimination of carotid plaque than Framingham, further studies are needed to determine the optimal cardiovascular risk stratification strategy for WLH.