Short-term repeatability of electrocardiographic Tpeak–Tend and QT intervals

Gellert, Kapuaola S.; Rautaharju, Pentti M.; Snyder, Michelle; Whitsel, Eric A.; Matsushita, Kunihiro; Heiss, Gerardo; Soliman, Elsayed Z.

doi:10.1016/j.jelectrocard.2014.03.002

Cited by 11 publications

(10 citation statements)

References 24 publications

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“…Although the ECG measures used in this analysis are not routinely reported on a standard 12-lead tracing, these measures are easily obtained with excellent repeatability for clinical and research purposes. 20 Several baseline characteristics were ascertained by self-reported history and potentially subjected our analyses to misclassification bias. Similarly, it is possible that some cases of SCD were missed despite rigorous attempts to identify all events.…”

Section: Discussionmentioning

confidence: 99%

Association Between QT-Interval Components and Sudden Cardiac Death

O’Neal

Singleton

Roberts

et al. 2017

Circ: Arrhythmia and Electrophysiology

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Background Several reports have demonstrated that prolongation of the QT interval is associated with sudden cardiac death (SCD). However, it is unknown whether any of the components within the QT interval are responsible for its association with SCD. Methods and Results We examined the association of the individual QT interval components (R-wave onset to R-peak, R-peak to R-wave end, ST-segment, T-wave onset to T-peak, and T-peak to T-wave end) with SCD in 12,241 participants (54 ± 5.7 years; 26% black; 55% women) from the Atherosclerosis Risk In Communities (ARIC) study. The QT interval and its components were measured at baseline (1987-1989) from 12-lead electrocardiograms. SCD cases were adjudicated by a group of physicians through December 31, 2012. Over a median follow-up of 23.6 years, a total of 346 cases of SCD were identified. While prolongation of the QT interval was associated with a 49% increased risk of SCD (HR=1.49, 95%CI=1.01, 2.18), only the T-wave onset to T-peak component (per 1-SD increase: HR=1.19, 95%CI=1.06, 1.34) was associated with SCD, and not any of the other components in separate models. When all of the QT interval components were included in the same model, T-wave onset to T-peak remained the strongest predictor of SCD (per 1-SD increase: HR=1.21, 95%CI=1.06, 1.37). Conclusion The risk of SCD with the QT interval is driven by prolongation of the T-wave onset to T-peak component. This suggests that shifting the focus from the overall QT interval to its individual components will refine SCD prediction in the community.

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Section: Discussionmentioning

confidence: 99%

Association Between QT-Interval Components and Sudden Cardiac Death

O’Neal

Singleton

Roberts

et al. 2017

Circ: Arrhythmia and Electrophysiology

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“…In this study, we examined the reproducibility of QTc at rest and after exercise. Some researchers have studied the reproducibility of QTc, but the subjects often consist only of healthy controls or adults. In addition, those studies utilized Holter ECG, or QTc measurement was done automatically or via a unique way, or they analyzed only QTc at rest.…”

Section: Discussionmentioning

confidence: 99%

“…Corrected QT interval (QTc) at rest and after exercise is important for diagnosis of long QT syndrome (LQTS), and for estimation of the risk of torsade de pointes (TdP) . The intra‐subject reproducibility of QTc, especially QTc after exercise, however, has not been thoroughly examined …”

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confidence: 99%

Reproducibility of corrected QT interval in pediatric genotyped long QT syndrome

Ogawa

Tanaka

Kido

2016

Pediatrics International

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Reproducibility of corrected QT interval (QTc), especially QTc after exercise, has not been thoroughly investigated. We reviewed charts of pediatric patients who underwent treadmill-exercise stress testing without medication multiple times within 1 year. In patients with long-QT syndrome (LQTS; n = 22), the discrepancy in QTc between two treadmill exercise stress tests using Fridericia's formula was 14 ± 12 ms at rest, 13 ± 12 ms 4 min after exercise, with a maximum of 14 ± 12 ms after exercise. There was no statistically significant difference in QTc between the two tests. Intraclass correlation coefficients (ICC) were 0.84, 0.85, and 0.85, respectively. In controls (n = 13), the discrepancy in QTc was 18 ± 12 ms at rest, 14 ± 7 ms 4 min after exercise, with a maximum of 14 ± 9 ms after exercise. There was no significant difference in QTc between the two tests. ICC were 0.78, 0.80, and 0.80, respectively. QTc calculated using Bazett's formula also showed high reproducibility. Reproducibility of QTc in children is high at rest and after exercise.

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“…To derive the individual QT interval component lengths, the median value in all 12 leads for each of the following was computed: intrinsicoid R wave (onset of R wave to R-wave peak), R-peak to R-end (R-wave peak to R-wave end), JT segment (J-point to T-wave onset), T-onset to T-peak (Twave onset to T-wave peak), and T-peak to T-end (T-wave peak to T-wave end) (O'Neal et al, 2017;Roberts et al, 2017). Due to the automated processing of the digitally acquired data, there are 0 variability and high repeatability (Gellert et al, 2014;Soliman, Prineas, Case, Zhang, & Goff, 2009).…”

Section: Me Thodsmentioning

confidence: 99%

Associations between QT interval subcomponents, HIV serostatus, and inflammation

Bhondoekhan

Haberlen

et al. 2019

Noninvasive Electrocardiol

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Background The 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. Methods Twelve‐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. Results After 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. Conclusions HIV 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.

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Short-term repeatability of electrocardiographic Tpeak–Tend and QT intervals

Cited by 11 publications

References 24 publications

Association Between QT-Interval Components and Sudden Cardiac Death

Association Between QT-Interval Components and Sudden Cardiac Death

Reproducibility of corrected QT interval in pediatric genotyped long QT syndrome

Associations between QT interval subcomponents, HIV serostatus, and inflammation

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