AHA Scientific Sessions 2026 Abstract · Nov 2, 2026
Residual Cardiovascular Risk in People with HIV with Sustained Viral Suppression Without Viral Blips: A Propensity Score-Matched Retrospective Cohort Study
By Babapour G, Hsieh R, Chan E et al.
Background: People with HIV face 1.5- to 2-fold higher atherosclerotic cardiovascular disease (ASCVD) risk compared with the general population, even with effective antiretroviral therapy (ART). Whether this excess risk persists in people with HIV achieving sustained HIV-1 RNA ≤20 copies/mL without any viral blips (21–200 copies/mL) remains unknown. We examined cardiovascular outcomes in this cohort compared with healthcare-engaged controls without HIV. Methods: Using the TriNetX federated deidentified healthcare database, we identified adults ≥18 years with HIV on continuous ART (2015–2023) with sustained viral suppression (≤20 copies/mL on ≥ 2 measurements) and no viral blips, free of prior ASCVD events (including acute myocardial infarction [AMI], stroke, heart failure, and prior revascularization). The comparator cohort comprised adults without HIV who had serial lipid/HbA1c screening, ≥10 ambulatory visits spanning ≥1 year, and no prevalent ASCVD. Propensity score matching (1:1) was done on key covariates including demographics, comorbidities, and medications. The primary outcomes were all-cause mortality and major adverse cardiovascular events (MACE; AMI, cerebral infarction, and all-cause mortality). Secondary outcomes included stroke and AMI individually. Urinary tract infection (UTI) and acute upper respiratory infection (URI) served as negative control outcomes. Outcomes were assessed from 1 to 10 years post-index using Kaplan-Meier analysis with Cox proportional hazards regression. Results: After matching, cohorts were well-balanced (standardized mean difference < 0.1 for covariates; n=1,978 in each group). Adults with HIV had higher all-cause mortality (HR 1.80, 95% CI 1.20 –2.70, p=0.004) and MACE outcomes (HR 1.52, 95% CI 1.12–2.06, p=0.007). Stroke was similar between groups (HR 0.98, 95% CI 0.62–1.54, p=0.93). AMI events were too few for analysis. Both negative controls showed null results (UTI: HR 1.04, p=0.80; URI: HR 1.00, p=0.98). Conclusions: People with HIV with sustained viral suppression without viral blips had significantly higher all-cause mortality and composite MACE compared with healthcare-engaged controls, with MACE findings likely driven by all-cause mortality. These findings may suggest persistent residual cardiovascular risk despite durable viral suppression and highlight the need for further investigation and continued attention to cardiovascular prevention strategies in people with HIV.