BACKGROUND: A higher prevalence of QT prolongation has been reported among human immunodeficiency virus (HIV)-infected patients. Previous studies have demonstrated that QT dispersion is a better predictor of serious ventricular tachyarrhythmia and cardiac mortality than corrected QT (QTc) interval. However, data of QT dispersion in HIV-infected patients receiving a combined antiretroviral therapy (cART) is limited. We sought to assess QTc interval and QT dispersion in HIV-infected patients receiving cART. The association between QT parameters and heart rate variability (HRV) was also examined. METHODS: Ninety-one HIV-infected patients receiving cART (male = 33, mean age = 44 ± 10 years) and 70 HIV-seronegative subjects (male = 25, mean age = 44 ± 8 years) were enrolled in the study. In a resting 12-lead electrocardiogram, QT interval was measured by the tangent method in all leads with well-defined T waves. The QT dispersion was defined as the difference between maximum and minimum QTc intervals in any of 12 leads. RESULTS: The baseline characteristics were not different between the two groups. We demonstrated the significantly longer mean QTc interval (420 ± 21 vs. 409 ± 21 ms, P < 0.001), and greater QT dispersion in HIV-infected group compared to the control group (85 ± 29 vs. 55 ± 23 ms, P < 0.001). Among the HIV-infected patients, those who had lower CD4 lymphocyte count (<350 cells/mm(3)) tended to have greater QT dispersion (92 ± 28 vs. 81 ± 29 ms, P = 0.098). There were no associations between QT parameters and either HRV or cART regimens. CONCLUSIONS: HIV-infected patients receiving cART were associated with prolonged QTc interval and increased QT dispersion, independent of autonomic dysfunction and antiretroviral drugs, which may have led to the potentially higher risk of ventricular arrhythmia and cardiac mortality.
BACKGROUND: A higher prevalence of QT prolongation has been reported among human immunodeficiency virus (HIV)-infectedpatients. Previous studies have demonstrated that QT dispersion is a better predictor of serious ventricular tachyarrhythmia and cardiac mortality than corrected QT (QTc) interval. However, data of QT dispersion in HIV-infectedpatients receiving a combined antiretroviral therapy (cART) is limited. We sought to assess QTc interval and QT dispersion in HIV-infectedpatients receiving cART. The association between QT parameters and heart rate variability (HRV) was also examined. METHODS: Ninety-one HIV-infectedpatients receiving cART (male = 33, mean age = 44 ± 10 years) and 70 HIV-seronegative subjects (male = 25, mean age = 44 ± 8 years) were enrolled in the study. In a resting 12-lead electrocardiogram, QT interval was measured by the tangent method in all leads with well-defined T waves. The QT dispersion was defined as the difference between maximum and minimum QTc intervals in any of 12 leads. RESULTS: The baseline characteristics were not different between the two groups. We demonstrated the significantly longer mean QTc interval (420 ± 21 vs. 409 ± 21 ms, P < 0.001), and greater QT dispersion in HIV-infected group compared to the control group (85 ± 29 vs. 55 ± 23 ms, P < 0.001). Among the HIV-infectedpatients, those who had lower CD4 lymphocyte count (<350 cells/mm(3)) tended to have greater QT dispersion (92 ± 28 vs. 81 ± 29 ms, P = 0.098). There were no associations between QT parameters and either HRV or cART regimens. CONCLUSIONS:HIV-infectedpatients receiving cART were associated with prolonged QTc interval and increased QT dispersion, independent of autonomic dysfunction and antiretroviral drugs, which may have led to the potentially higher risk of ventricular arrhythmia and cardiac mortality.
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