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Predictors of electrocardiographic QT interval prolongation in men with HIV
Katherine C Wu1, Long Zhang2, Sabina A Haberlen2
1Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Insights
HIV-infected men have longer QT intervals, a heart rhythm measure, compared to HIV-negative men. This finding may explain increased sudden cardiac death risk in HIV+ individuals.
Area of Science:
- Cardiology
- Infectious Diseases
- Public Health
Background:
- HIV infection is linked to increased risk of sudden arrhythmic cardiac death.
- Prolongation of the electrocardiographic QT interval (QTc) in HIV+ individuals may potentiate ventricular arrhythmias.
Purpose of the Study:
- To assess if HIV+ men have longer QT intervals than HIV-uninfected (HIV-) men.
- To identify factors associated with QT duration in HIV+ men.
Main Methods:
- Resting 12-lead ECGs were performed on 774 HIV+ and 652 HIV- men.
- Multivariable regression analyses assessed associations between HIV serostatus and QTc.
- Inflammatory biomarker levels were assessed in a subgroup.
Main Results:
- HIV+ men had a 4.0 ms longer QTc interval compared to HIV- men after adjustments.
- Antiretroviral therapy (ART) use was not associated with longer QTc.
- Higher levels of IL-6, ICAM-1, and B-cell activating factor were independently associated with longer QTc in HIV+ men.
Conclusions:
- HIV+ men exhibit longer QTc intervals, linked to elevated systemic inflammation.
- This prolonged QTc may contribute to the heightened risk of sudden arrhythmic cardiac death in HIV+ individuals.
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.
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