Polygenic Risk Scores Indicate Subclinical Coronary Artery Disease Risk in HIV

Among patients with HIV infection, a combination of nongenetic and genetic factors were found to be significantly predictive of coronary artery disease (CAD) risk. These study findings were published in Clinical Infectious Diseases.

Data for this study were sourced from the Swiss HIV cohort study, which included patients with HIV infection from Switzerland. Researchers sought to determine predictors for coronary artery calcification and subclinical CAD by evaluating genetic and nongenetic characteristics. Subclinical CAD was defined as the presence of soft, mixed, or high-risk plaque on coronary computed tomography angiography.

Among 345 participants included in the analysis, the median age was 53 (range, 50.5-55) years, 89% (range, 85%-95.3%) were men, 96% had virologically-suppressed HIV infection, and 8.9% to 11.6% had a family history of CAD. Coronary artery calcification was noted in 127 patients and subclinical CAD was noted in 172.

Compared with HIV-positive patients without coronary artery calcification (n=124) or subclinical CAD (n=173), both genetic and non-genetic risk factors were more prevalent among those with coronary artery calcification and subclinical CAD (all P <.01).

Patients with CAD-associated polygenic risk scores in the fifth quintile were more likely to have subclinical CAD (odds ratio [OR], 2.06; 95% CI, 1.02-4.15) and coronary artery calcification (OR, 2.99; 95% CI, 1.30-6.1). Dyslipidemia also was associated with subclinical CAD (OR, 2.08; 95% CI, 1.34-3.21) and coronary artery calcification (OR, 1.68; 95% CI, 1.01-2.79), with similar findings noted for recent abacavir exposure in regard to both subclinical CAD (OR, 3.05; 95% CI, 1.70-5.46) and coronary artery calcification (OR, 2.25; 95% CI, 1.14-4.43).

The best predictive model was the combined non-genetic and polygenic risk score for CAD model, which predicted 18.6% of the subclinical CAD variability, 27.2% of the coronary artery calcium score variability, and 35.3% of the acute CAD event variability. These rates compared with 3.1%, 4.2%, and 6.0% for CAD-associated polygenic risk scores; 7.8%, 6.5%, and 16.9% for HIV-related factors; 10.0%, 19.1%, and 15.0% for traditional risk factors; and 16.2%, 23.9%, and 30.5% for traditional factors and HIV-related factors, respectively.

These data may not be generalizable as the source population comprised only patients of European ancestry.

According to the researchers, “The integration of genetic, traditional, HIV-related, and antiretroviral CAD risk factors helps explain the interindividual variation and provides the best prediction of individual risk of subclinical and clinical CAD in PWLH [patients living with HIV.”

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