Abstract
Highly active antiretroviral therapy (HAART) has significantly improved outcomes in patients with human immunodeficiency virus (HIV) and may provide cardioprotective effects; however, its long-term impact on HIV-associated cardiomyopathy remains uncertain. Although short-term benefits have been reported, potential cardiovascular toxicity, particularly from protease inhibitors, warrants further investigation. This retrospective study evaluated HIV-infected patients with cardiomyopathy treated at five community hospitals in Michigan from 2015 to the present, examining changes in left ventricular ejection fraction (EF) following HAART therapy. Baseline EF measurements were obtained at or near the initiation of HAART, when available, although the exact timing varied across patients. EF changes were categorized as increased, unchanged, or decreased using a <10% threshold, consistent with the known interobserver variability of echocardiographic EF measurement. In this cohort, HAART exposure was not uniform, as treatment regimens, durations of therapy, and viral suppression statuses varied due to the retrospective nature of the study. Due to the limited availability of uniformly collected covariates, multivariable adjustment was not feasible, and the high exclusion rate resulting from missing treatment or follow-up imaging data introduces potential selection bias. Of 125 patients identified, 50 met the inclusion criteria, while the remaining 75 were excluded due to incomplete data. Among the included patients, 44% (n = 22) demonstrated a decrease in EF, 28% (n = 14) showed an increase, and 28% (n = 14) had no significant change. Patients with decreased EF were older than those with increased EF (55.5 ± 10.3 vs. 47.9 ± 10.5 years; p = 0.04). When patients with decreased and unchanged EF were combined, age remained significantly higher compared with the increased EF group (p = 0.03), suggesting age as an important determinant of EF trajectory during HAART therapy. Gender and ethnic distributions did not differ significantly across EF groups. Males comprised 59% of the decreased EF group and 78.6% of both the unchanged and increased EF groups (p = 0.32). African American patients represented 77.3%, 63.4%, and 85.7% of the decreased, unchanged, and increased EF groups, respectively (p = 0.36). Alcohol use and chronic kidney disease were not significantly associated with EF changes (p = 0.84 and p = 0.43). These findings identify age as a key factor influencing left ventricular EF changes in patients with HIV-associated cardiomyopathy receiving HAART. The absence of a control group, heterogeneity in HAART exposure, and incomplete comorbidity data limit causal interpretation. Larger controlled studies are needed to clarify the long-term cardiac effects of HAART and to determine how patient-level factors modify EF trajectories over time.