Abstract
BackgroundThe total QT interval comprises both ventricular depolarization and repolarization currents. Understanding how HIV serostatus and other risk factors influence specific QT interval subcomponents could improve our mechanistic understanding of arrhythmias.MethodsTwelve‐lead electrocardiograms (ECGs) were acquired in 774 HIV‐infected (HIV+) and 652 HIV‐uninfected (HIV−) men from the Multicenter AIDS Cohort Study. Individual QT subcomponent intervals were analyzed: R‐onset to R‐peak, R‐peak to R‐end, JT segment, T‐onset to T‐peak, and T‐peak to T‐end. Using multivariable linear regressions, we investigated associations between HIV serostatus and covariates, including serum concentrations of inflammatory biomarkers such as interleukin‐6 (IL‐6), and each QT subcomponent.ResultsAfter adjustment for demographics and risk factors, HIV+ versus HIV− men differed only in repolarization phase durations with longer T‐onset to T‐peak by 2.3 ms (95% CI 0–4.5, p < .05) and T‐peak to T‐end by 1.6 ms (95% CI 0.3–2.9, p < .05). Adjusting for inflammation attenuated the strength and significance of the relationship between HIV serostatus and repolarization. The highest tertile of IL‐6 was associated with a 7.3 ms (95% CI 3.2–11.5, p < .01) longer T‐onset to T‐peak. Age, race, body mass index, alcohol use, and left ventricular hypertrophy were each associated with up to 2.2–12.5 ms longer T‐wave subcomponents.ConclusionsHIV seropositivity, in combination with additional risk factors including increased systemic inflammation, is associated with longer T‐wave subcomponents. These findings could suggest mechanisms by which the ventricular repolarization phase is lengthened and thereby contribute to increased arrhythmic risk in men living with HIV.
Highlights
Lengthening of the electrocardiographic QT interval is associated with increased risk for sudden cardiac death (SCD) in the general population(Montanez, Ruskin, Hebert, Lamas, & Hennekens, 2004; Soliman et al, 2011; Straus et al, 2006) and atrial fibrillation in com‐ munity‐based cohorts(Mandyam et al, 2013; O'Neal et al, 2015) via shared potassium and sodium currents that impact both ventricular and atrial repolarization (Nerbonne & Kass, 2005)
We extended our QTc interval findings to investigate the relationship between specific QT subcomponent durations and human immunodeficiency virus (HIV) serostatus in our pre‐ viously described large cohort of HIV+ and HIV− men who have sex with men (MSM)
We extend our prior findings of an HIV‐associated increase in total QTc interval by reporting here that there is specific lengthening of the ventricular repolarization phase, as reflected by longer T‐wave subcomponent durations without significant changes in the other QT subcomponents
Summary
Lengthening of the electrocardiographic QT interval is associated with increased risk for sudden cardiac death (SCD) in the general population(Montanez, Ruskin, Hebert, Lamas, & Hennekens, 2004; Soliman et al, 2011; Straus et al, 2006) and atrial fibrillation in com‐ munity‐based cohorts(Mandyam et al, 2013; O'Neal et al, 2015) via shared potassium and sodium currents that impact both ventricular and atrial repolarization (Nerbonne & Kass, 2005). Longer T‐wave sub‐ components have been associated with atrial and ventricular ar‐ rhythmias and SCD in HIV‐uninfected (HIV−) cohorts (Goldenberg & Moss, 2017; Morin et al, 2012; O'Neal et al, 2017; Panikkath et al, 2011; Roberts et al, 2017; Rosenthal et al, 2015; Shimizu et al, 2002; Yamaguchi et al, 2003). Whether these associations occur in HIV‐infected (HIV+) persons is unknown. We investigated associations between HIV serostatus and covariates, in‐ cluding serum concentrations of inflammatory biomarkers such as interleukin‐6 (IL‐6), and each QT subcomponent.
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