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Association of prior tuberculosis with cardiovascular status in perinatally HIV-1-infected adolescents.

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posted on 2024-11-18, 12:58 authored by Itai M Magodoro, Carlos Eduardo Guerrero-Chalela, Emma Carkeek, Nana Akua Asafu-Agyei, Nomawethu Jele, Lisa J Frigati, Landon Myer, Jennifer Jao, Mpiko Ntsekhe, Katalin A Wilkinson, Robert J Wilkinson, Heather Zar, Ntobeko Ntusi
BACKGROUND: Whether, and how, co-occurring HIV-1 infection (HIV) and tuberculosis (TB) impact cardiovascular status, especially in adolescents with perinatally acquired HIV (APHIV), have not been examined. We hypothesised that APHIV with previous TB disease have worse cardiac efficiency than APHIV without TB, which is mediated by increased inflammation and disordered cardiometabolism. METHODS: APHIV in Cape Town, South Africa, completed 3T cardiovascular magnetic resonance examination and high sensitivity C reactive protein (hsCRP), fasting plasma glucose (FPG), low-density lipoprotein (LDL) and triglyceride measurement. Ventriculoarterial coupling (VAC) was estimated as the ratio of arterial elastance (Ea) to ventricular end-systolic elastance (Ees). Regression models were applied to estimate cross-sectional associations between Ea/Ees ratio and TB status, with decomposition of these associations into direct and mediated effects of hsCRP, FPG and dyslipidaemia, if any, attempted. RESULTS: We enrolled 43 APHIV with prior TB and 23 without TB of mean (SD) age 15.0 (1.5) and 15.4 (1.7) years, respectively. Prior TB was associated with lower Ea/Ees ratio (0.59 (0.56 to 0.64)) than no TB (0.66 (0.62 to 0.70)), which corresponded to an adjusted mean difference -0.06 (-0.12 to 0.01) (p=0.048). However, previous TB was not associated with increased hsCRP, FPG, LDL or triglycerides nor were hsCRP, FPG, LDL and triglycerides associated with Ea/Ees ruling out their mediated effects in the association between TB and cardiac efficiency. CONCLUSIONS: Previous TB in APHIV is associated with comparatively reduced cardiac efficiency, related to altered VAC. The clinical significance of these findings requires further study, including a wider range of biomarkers of specific immune pathways.

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Crick (Grant ID: CC2112, Grant title: Wilkinson CC2112)

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