Predictors of electrocardiographic QT interval prolongation in men with HIV

Katherine Chih-Ching Wu, Long Zhang, Sabina Haberlen, Hiroshi Ashikaga, Todd T Brown, Matthew J. Budoff, Gypsyamber D'Souza, Lawrence A. Kingsley, Frank J. Palella, Joseph Bernard Margolick, Otoniel Martínez-Maza, Elsayed Z. Soliman, Wendy S Post

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
JournalHeart
DOIs
StateAccepted/In press - Jan 1 2018

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HIV
Sudden Cardiac Death
Biomarkers
B-Cell Activating Factor
Intercellular Adhesion Molecule-1
HIV Infections
Cardiac Arrhythmias
Linear Models
Interleukin-6
Electrocardiography
Acquired Immunodeficiency Syndrome
Cohort Studies
Logistic Models
Regression Analysis
Demography
Inflammation
Drug Therapy

Keywords

  • cardiac risk factors and prevention
  • electrocardiography
  • inflammatory markers

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Predictors of electrocardiographic QT interval prolongation in men with HIV. / Wu, Katherine Chih-Ching; Zhang, Long; Haberlen, Sabina; Ashikaga, Hiroshi; Brown, Todd T; Budoff, Matthew J.; D'Souza, Gypsyamber; Kingsley, Lawrence A.; Palella, Frank J.; Margolick, Joseph Bernard; Martínez-Maza, Otoniel; Soliman, Elsayed Z.; Post, Wendy S.

In: Heart, 01.01.2018.

Research output: Contribution to journalArticle

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abstract = "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.",
keywords = "cardiac risk factors and prevention, electrocardiography, inflammatory markers",
author = "Wu, {Katherine Chih-Ching} and Long Zhang and Sabina Haberlen and Hiroshi Ashikaga and Brown, {Todd T} and Budoff, {Matthew J.} and Gypsyamber D'Souza and Kingsley, {Lawrence A.} and Palella, {Frank J.} and Margolick, {Joseph Bernard} and Otoniel Mart{\'i}nez-Maza and Soliman, {Elsayed Z.} and Post, {Wendy S}",
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T1 - Predictors of electrocardiographic QT interval prolongation in men with HIV

AU - Wu, Katherine Chih-Ching

AU - Zhang, Long

AU - Haberlen, Sabina

AU - Ashikaga, Hiroshi

AU - Brown, Todd T

AU - Budoff, Matthew J.

AU - D'Souza, Gypsyamber

AU - Kingsley, Lawrence A.

AU - Palella, Frank J.

AU - Margolick, Joseph Bernard

AU - Martínez-Maza, Otoniel

AU - Soliman, Elsayed Z.

AU - Post, Wendy S

PY - 2018/1/1

Y1 - 2018/1/1

N2 - 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.

AB - 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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KW - electrocardiography

KW - inflammatory markers

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