Objective HIV-infected (HIV+) individuals may be at increased risk for sudden arrhythmic cardiac death. Some studies have reported an association between HIV infection and prolongation of the electrocardiographic QT interval, a measure of ventricular repolarisation, which could potentiate ventricular arrhythmias. We aimed to assess whether HIV+ men have longer QT intervals than HIV-uninfected (HIV−) men and to determine factors associated with QT duration.
Methods We performed resting 12-lead ECGs in 774 HIV+ and 652 HIV− men in the Multicenter AIDS Cohort Study (MACS). We used multivariable linear and logistic regression analyses to assess associations between HIV serostatus and Framingham corrected QT interval (QTc), after accounting for potential confounders. We also determined associations among QTc interval and HIV-related factors in HIV+ men. In a subgroup of participants, levels of serum markers of inflammation were also assessed.
Results After adjusting for demographics and risk factors, QTc was 4.0 ms longer in HIV+ than HIV− men (p<0.001). Use of antiretroviral therapy (ART), specific ART drug class use and other HIV-specific risk factors were not associated with longer QTc. Among the subgroup with inflammatory biomarker measurements, higher interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1) and B-cell activating factor levels were independently associated with longer QTc and their inclusion partially attenuated the HIV effect.
Conclusions HIV+ men had longer QTc, which was associated with higher levels of systemic inflammatory factors. This longer QTc may contribute to the increased risk for sudden arrhythmic cardiac death in some HIV+ individuals.
- cardiac risk factors and prevention
- inflammatory markers
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Funding The MACS is funded primarily by the National Institute of Allergy and Infectious Diseases, with additional cofunding from the National Cancer Institute, the National Institute on Drug Abuse and the National Institute of Mental Health. Targeted supplemental funding for specific projects, including this one, was also provided by the National Heart, Lung, and Blood Institute and the National Institute on Deafness and Communication Disorders. Some of the biomarker data were derived from RO1 HL095129 (Post). MACS data collection is also supported by UL1-TR001079 (JHU ICTR) from the National Center for Advancing Translational Sciences (NCATS) a component of the National Institutes of Health (NIH) and NIH Roadmap for Medical Research. The contents of this publication are solely the responsibility of the authors and do not represent the official views of the National Institutes of Health (NIH), Johns Hopkins ICTR or NCATS. The MACS website is located at http://aidscohortstudy.org/.
Competing interests FJP is on the speaker’s bureau for Gilead Sciences, Janssen Pharmaceuticals, Merck & Co, Inc and Bristol‐Myers Squibb. MJB has received grants from General Electric Company. TTB has served as a consultant to Gilead Sciences, Merck, Theratechnologies and EMD-Serono.
Patient consent Not required.
Ethics approval Johns Hopkins Bloomberg School of Public Health IRB.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement No additional unpublished data available.
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