![]() Study participants in the smoking/vaping cohort were instructed to refrain from using their tobacco product on the day of the study. In the current study we compared the frequency of the maximal Tp‐e at rest and during abrupt standing among the 12‐ECG leads in healthy young adults, then validated our findings in an independent cohort, and finally extended these findings to a cohort of smokers and vapers.Īll study participants were instructed to abstain from caffeine and exercise for at least 12 h prior to their study session. Before embarking on a large, prospective study of the impact of vaping and smoking on the Tp‐e interval, given the lack of consensus on lead selection for Tp‐e measurement, we felt that it was first critical to determine systematically which leads, if any, were most sensitive, thus preferable, to detect the longest Tp‐e interval at rest and during an evocative maneuver. In a retrospective analysis of ECG recordings from only two leads, we recently reported that acutely smoking a tobacco cigarette significantly increased the Tp‐e interval more than vaping an electronic cigarette (Ip et al., 2020). Additionally, just as the QT interval may require interventions to unmask abnormal repolarization (Viskin et al., 2010 Wong et al., 2010), interventions to unmask Tp‐e prolongation have also been recommended (Takenaka et al., 2003 Markiewicz‐Loskot et al., 2020), but again, which leads are most sensitive to detect these changes remains unstudied and uncertain. In fact, we have not found any publications comparing the Tp‐e interval in all 12 leads in healthy adults. Surprisingly, the sources commonly referenced as evidence for specific lead selection have not systematically compared the Tp‐e interval among the 12 ECG leads (Castro Hevia et al., 2006 Haarmark et al., 2010). 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). ![]()
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