Key result
Virally suppressed HIV is linked to ~1-point higher myocardial ECV fraction versus uninfected controls.
Why the study?
Heart failure is a prominent cardiovascular disease manifestation in sub-Saharan Africa, and the authors aimed to characterize myocardial fibrosis among persons with HIV in South Africa.
Does treated HIV infection increase myocardial fibrosis assessed by CMR ECV in individuals without known cardiovascular disease compared to uninfected controls?
Cross-Sectional (n=229)
Blind assessment of CMR images
No
Does treated HIV infection increase myocardial fibrosis assessed by CMR ECV in individuals without known cardiovascular disease compared to uninfected controls?
Virally suppressed persons with HIV in South Africa exhibit greater subclinical myocardial fibrosis than uninfected controls, highlighting a potential mechanism for increased heart failure risk in this population.
Answers are grounded in this paper and cite their sources.
May signal elevated HF risk in treated HIV; leaves open whether fibrosis predicts outcomes or merits targeted screening.
BACKGROUND: Heart failure is a prominent cardiovascular disease (CVD) manifestation in sub-Sarahan Africa. Myocardial fibrosis is a central feature of heart failure that we aimed to characterize among persons with human immunodeficiency virus (PWH) in South Africa. METHODS: Cardiovascular magnetic resonance (CMR) imaging was performed among PWH with viral suppression and uninfected controls, both free of known CVD. Plasma levels of N-terminal pro B-type natriuretic peptide (NT-proBNP) were measured. Comparisons by human immunodeficiency virus (HIV) status were made using linear and logistic regression, adjusted for age, sex, and hypertension. RESULTS: One hundred thirty-four PWH and 95 uninfected persons completed CMR imaging; age was 50 and 49 years, with 63% and 67% female, respectively. Compared with controls, PWH had greater myocardial fibrosis by extracellular volume fraction ([ECV] absolute difference, 1.2%; 95% confidence interval [CI], 0.1-2.3). In subgroup analyses, the effect of HIV status on ECV was more prominent among women. Women (vs controls) were also more likely to have elevated NT-proBNP levels (>125 pg/mL; odds ratio, 2.4; 95% CI, 1.0-6.0). Among all PWH, an elevated NT-proBNP level was associated with higher ECV (3.4% higher; 95% CI, 1.3-5.5). CONCLUSIONS: Human immunodeficiency virus disease may contribute to myocardial fibrosis, with an effect more prominent among women. Research is needed to understand heart failure risk among PWH within sub-Saharan Africa.
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Shuldiner et al. (2020) conducted a cross-sectional in Human Immunodeficiency Virus (HIV) and Myocardial Fibrosis (n=229). Human immunodeficiency virus (HIV) infection vs. HIV-uninfected controls was evaluated on Myocardial extracellular volume fraction (ECV) (absolute difference 1.2%, 95% CI 0.1-2.3, p=0.04). Compared to uninfected controls, persons with virally suppressed HIV on ART had greater myocardial fibrosis as measured by extracellular volume fraction.
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