Adverse Cardiac Phenotypes More Likely in Women With vs Without HIV

Women with HIV infection with low CD4⁺ T-cell counts were found to be at increased risk for isolated left ventricular diastolic dysfunction (LVDD), left atrial enlargement (LAE), left ventricular hypertrophy (LVH), and elevated tricuspid regurgitation velocity (TRV) compared with women without HIV infection. These study findings were published in Clinical Infectious Diseases.

Data for this study were sourced from the Women’s Interagency HIV Study, which was a multicenter study that enrolled women living in the United States between 1994 and 1995, 2001 and 2002, 2011 and 2012, and 2013 and 2015. For this study, women who were either positive for HIV infection (n=1163) or at risk for HIV infection (controls; n=491) were evaluated to identify associations between HIV-specific risk factors and adverse cardiac phenotypes. The analysis used clinical-, laboratory-, and echocardiography-based findings obtained between 2014 and 2019.

Among women in the positive HIV (median age, 53 [IQR, 46-58] years) and control cohorts (median age, 51 [IQR, 43-58] years), 8.9% and 5.1% were White (P =.028), the median BMI was 30.7 (IQR, 26.0-37.6) and 32.0 (IQR, 26.6-37.9) kg/m², 36.9% and 43.2% were current smokers (P =.016), 7.2% and 10.8% were heavy alcohol users (P =.016), 54.3% and 60.5% had a history of heroin or cocaine use (P =.019), and 22.0% and 16.1% had a history of hepatitis C virus (HCV) seropositivity (P =.006), respectively.

Of women in the positive HIV and control cohorts, left ventricular systolic dysfunction (LVSD) was observed among 5.4% and 3.5%, isolated LVDD in 6.5% and 8.0%, LAE in 22.4% and 25.9%, and LVH in 4.6% and 5.1%, respectively. Further analysis of women in the positive HIV vs control cohorts showed mild or moderate aortic valve regurgitation among 5.7% vs 4.9%, mild or moderate aortic valve stenosis among 0.4% vs 0.4%, mild or moderate mitral valve regurgitation among 20.0% vs 21.5%, mild or moderate tricuspid valve regurgitation among 40.4% vs 39.9%, and minimal pericardial effusion among 3.1% vs 4.3%.

Additional analyses were performed after adjustments for age, study site, race/ethnicity, echocardiography interpreter, BMI, smoking status, estimated glomerular filtration rate. Adjustments also were made for previous alcohol, injection drug, and heroin or cocaine use, as well as a history of HCV infection, hypertension, diabetes, dyslipidemia, myocardial infarction, and heart failure. Results showed that women in the positive HIV cohort with undetectable viral loads were at increased risk for LVSD (relative risk [RR], 1.87; P =.048) and isolated LVDD (RR, 0.53; P =.050) compared with those in the control cohort. Women in the positive HIV cohort with low CD4⁺ T-cell counts (<200 cells/mm³) also were at increased risk for LVH (RR, 4.13; P <.001), peak TRV of more than 2.8 m/s (RR, 2.48; P =.007), and LAE (RR, 1.52; P =.028); those with high CD4⁺ T-cell counts (³500 cells/mm³) were found to be at decreased isolated LVDD risk (RR, 0.65; P =.043).

In the fully adjusted model, no significant associations were observed between adverse cardiac phenotypes and the duration of ART.

No clinically meaningful different results were noted in sensitivity analyses that were adjusted on the basis of menopausal status.

This study was limited by significant baseline and sample size differences observed between the 2 patient cohorts.

“Together, the present results contribute novel information regarding the cardiovascular consequences of HIV infection in women receiving contemporary ART,” the researchers concluded.

Disclosure: Multiple authors declared affiliations with industry. Please see the original reference for a full list of disclosures.