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急性 HIV 感染导致亚临床炎症性心肌病。

Acute HIV Infection Results in Subclinical Inflammatory Cardiomyopathy.

机构信息

Department of Dermatology, Medical University of Vienna, Austria.

Department of Laboratory Medicine, Medical University of Vienna, Austria.

出版信息

J Infect Dis. 2018 Jul 2;218(3):466-470. doi: 10.1093/infdis/jiy183.

DOI:10.1093/infdis/jiy183
PMID:29608697
Abstract

The impact of excess viral RNA on myocardial function and morphology in the setting of acute human immunodeficiency virus (HIV) infection remains unknown. In this study, 49 patients with acute HIV infection showed increased levels of N-terminal prohormone of brain natriuretic peptide, a surrogate of myocardial function, which decreased with viral suppression and normalization of systemic inflammation (79 pg/mL vs 28 pg/mL; P < .001). A comparable change was seen with levels of troponin T, a marker of morphologic myocardial damage (4.9 ng/L vs 1.5 ng/L; P < .001). In conclusion, we observed significant functional and morphological myocardial impairment during acute HIV infection, fueled by inflammatory activation and extensive viral replication, resulting in a reversible subclinical inflammatory cardiomyopathy.

摘要

在急性人类免疫缺陷病毒 (HIV) 感染的情况下,过量病毒 RNA 对心肌功能和形态的影响尚不清楚。在这项研究中,49 例急性 HIV 感染患者的脑钠肽前体 N 端水平升高,这是心肌功能的替代指标,随着病毒抑制和全身炎症的正常化,该水平降低(79pg/ml 比 28pg/ml;P<0.001)。肌钙蛋白 T 水平也出现了类似的变化,肌钙蛋白 T 是心肌形态损伤的标志物(4.9ng/L 比 1.5ng/L;P<0.001)。总之,我们观察到在急性 HIV 感染期间存在明显的功能性和形态性心肌损伤,其由炎症激活和广泛的病毒复制所驱动,导致可逆转的亚临床炎症性心肌病。

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