However, it remains uncertain that leads are most sensitive to detect Tp-e prolongation at rest. Very fundamentally, judgments of relative risk for lethal ventricular arrhythmia risk may be based on Tp-e measurements from only a subset of ECG leads. Further underlying the controversy is the lack of uniformity in the measurement of the Tp-e (Malik et al., 2019). That prolongation in the Tp-e represents transmural, global (apical-basal), or even right–left ventricular heterogeneity of repolarization has each been argued and supported by data (Antzelevitch, 2001 Patel et al., 2009 Janse et al., 2012 Srinivasan et al., 2019). Controversy surrounds the very basic electrophysiological question of what the Tp-e actually represents. As an alternative, the interval from the peak of the T wave to the end of the T wave, the Tpeak-Tend (Tp-e) interval, which does not include ventricular depolarization, has been proposed as a better predictor of ventricular arrhythmias and sudden arrhythmic death than the QT interval or the QT interval corrected for heart rate (Bazett's, QTc) (Antzelevitch et al., 2017 Tse et al., 2017).Īlthough Tp-e prolongation has been reported in a wide range of cohorts with increased sudden arrhythmic death risk (Tse et al., 2017 Takenaka et al., 2003 Shimizu et al., 2002 Castro Hevia et al., 2006 Maury et al., 2015 Panikkath et al., 2011 Lubinski et al., 1998 Bachmann et al., 2016), this interval is not universally accepted as a marker of pro-arrhythmia (Malik et al., 2019 Malik et al., 2018). Further, the QT interval may lack sufficient sensitivity and precision, since even minor increases in the QT interval, which do not exceed the normal range, may portend an increased risk for sudden death in specific populations (Deyell et al., 2015 Ahnve, 1985). However, since the QT interval includes both ventricular depolarization and repolarization, subtle but clinically meaningful changes in repolarization may be obscured (Antzelevitch, 2007 Dobson et al., 2013). Traditionally, abnormal ventricular repolarization estimated by prolongation of the QT interval is considered a marker for increased risk of lethal ventricular arrhythmias. The electrocardiogram (ECG) is a powerful noninvasive tool to detect abnormalities in cardiac electrical activity that might be predictive of increased risk for sudden arrhythmic death (Rautaharju et al., 2009). Sudden cardiac death is a leading cause of death in the United States, and thus clinical risk markers and indices to identify increased sudden death risk have been sought (Deyell et al., 2015). If only a subset of ECG leads will be recorded or analyzed for the Tp-e interval, selection of the precordial leads is preferred since these leads are most likely to capture the maximal Tp-e value. These findings were confirmed in the validation cohort, and extended to the smoking/vaping cohort. Upon abrupt standing, grouping leads V2-V6 together, resulted in detection of the maximum Tp-e 85.0% of participants (CI 69.4, 99.9% versus all other leads p < .001). At rest, grouping leads V2–V4 resulted in detection of the maximum Tp-e in 85.7% of participants (CI 70.7, 99.9%) versus all other leads ( p < .001). In the rest and abrupt standing positions, the Tp-e was not uniform among the 12 leads the maximal Tp-e was most frequently captured in the precordial leads. Tp-e was compared to determine which lead(s) most frequently captured the maximal Tp-e interval. In 88 healthy adults (ages 21–38 years), including derivation ( n = 21), validation ( n = 20), and smoker/vaper ( n = 47) cohorts, the Tp-e was measured using commercial computer software (LabChart Pro 8 with ECG module, ADInstruments) in all 12 leads at rest and following a provocative maneuver, abrupt standing. The purpose of the current study was to determine the optimal leads, if any, to capture the maximal Tp-e interval in healthy young adults. If there is variation, it remains uncertain, which lead(s) are preferred for recording in order to capture the maximal Tp-e value. The Tpeak-end(Tp-e) has not been compared in all 12 ECG leads in healthy adults to determine if the Tp-e varies across leads.
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