Abstract

Background: Human immunodeficiency virus (HIV) is associated with elevated risks for heart failure (HF). No studies to our knowledge have evaluated physician-adjudicated etiologies of HF (e.g., ischemic vs. non-ischemic) for HIV-infected persons in the modern ART era. Hypothesis: We hypothesize that non-ischemic etiologies of HF will comprise a greater proportion of overall HF for HIV-infected than uninfected persons. Methods: We performed a nested study of a cohort of HIV-infected and uninfected persons frequency-matched on age, sex, race, zip code of residence, and clinic location receiving care at an urban medical center between 1/1/2000 and 1/1/2018. Two trained MDs independently reviewed clinical notes, imaging and laboratory studies to determine contributing etiologies of HF for 128 patients (75 HIV-infected, 53 uninfected) with physician-adjudicated HF. Laboratory and imaging data as well as clinical notes from clinical care were used to classify etiologies of HF. HF was considered ischemic in etiology based on any prior angiogram demonstrating ≥70% epicardial coronary stenosis, stress testing consistent with ischemia, and/or documented previous myocardial infarction. Non-ischemic heart failure etiologies were subtyped based on pre-specified criteria as valvular, inflammatory, drug induced, hypertensive, infiltrative, hypertrophic, dilated, tachycardia induced, pulmonary hypertension, acute pulmonary embolism, stress cardiomyopathy (Takotsubo), renal volume overload, cirrhotic volume overload, or unspecified. More than one etiology of HF was possible if criteria were met for multiple etiologies. Results: Age at HF onset, sex, and race of HIV-infected vs. uninfected persons with HF were similar. Diabetes was less common among HIV-infected (30.7%) vs. uninfected (54.7%; p = 0.01) persons with HF. There were no significant differences in the proportion of HIV-infected vs. uninfected persons with ischemic vs. non-ischemic etiology of HF. Within non-ischemic HF, drug/toxin-induced cardiomyopathy was more common among HIV-infected (17.3%) than uninfected (5.7%) persons (p= 0.049). The left ventricular ejection fraction (LVEF) at HF diagnosis was significantly lower for HIV-infected (37.6% ± 16.4%) than uninfected (44.9% ± 18.3%; p =0.02) persons. The difference was apparent among persons with non-ischemic etiologies (38.0% ± 16.7% vs. 47.9% ± 17.8% for HIV-infected vs. uninfected; p=0.01), but not for those with ischemic etiologies of HF (37.1% ± 15.9% vs. 38.3% ± 18.3% for HIV-infected vs. uninfected; p=0.83). Conclusions: HIV-infected persons with HF had lower LVEF at HF diagnosis and were more likely to have toxin/drug-induced HF etiology than uninfected persons with HF. Future studies are needed to understand etiologies of and prognosis HF among HIV-infected persons to inform prevention and treatment.

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