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Background: The T wave of the electrocardiogram (ECG) reflects ventricular repolarization. Repolarization heterogeneity is associated with reentrant arrhythmias. Several T‐wave markers (including QT interval) have been associated with ventricular arrhythmias, but studies linking such markers to underlying local repolarization time (RT) inhomogeneities are lacking. We aimed to investigate the relation of several T‐wave markers to controlled drug‐induced regional RT gradients in intact pig hearts. Methods: Repolarization time gradients were created by regional infusion of dofetilide and pinacidil in four atrially paced porcine Langendorff‐perfused hearts placed inside a torso tank. From the 12‐lead ECG on the torso tank, the mean, maximum, and dispersion (max–min) of QTtime, JTtime, Tpeak–end, Twidth, TQratio, dV/dtmax, Tarea, Tamp, and T‐upslope duration were determined, as well as upslope end difference between leads V1 and V6. Results: Temporal T‐wave parameters Tpeak–end, Twidth, and TQratio show a significant and high correlation with RT gradient, best reflected by mean value. Tarea (mean, max and dispersion) and dV/dtmax dispersion show only a moderate significant correlation. T‐upslope duration shows a significant correlation in particular for mean values. Mean, maximum, or dispersion of QTtime and V1–V6 upslope end difference were not significantly correlated with RT gradient. Conclusion: Composite 12‐lead ECG T‐wave parameters Tpeak–end, Twidth, TQratio, upslope duration, and Tarea show a good correlation with underlying RT heterogeneity, whereas standard clinical metrics such as QTtime do not reflect local RT heterogeneity. The composite T‐wave metrics may thus provide better insights in arrhythmia susceptibility than traditional QTtime metrics. [ABSTRACT FROM AUTHOR]

Background: Coronavirus disease‐2019 (COVID‐19) has been associated with an increased risk of acute cardiac events. However, the effect of COVID‐19 on repolarization heterogeneity is not yet established. In this study, we evaluated electrocardiogram (ECG) markers of repolarization heterogeneity in patients hospitalized with COVID‐19. In addition, we performed a systematic review and meta‐analysis of the published studies. Methods: QT dispersion (QTd), the interval between T wave peak to T wave end (TpTe), TpTe/QT (with and without correction), QRS width, and the index of cardio‐electrophysiological balance (iCEB) were calculated in 101 hospitalized COVID‐19 patients and it was compared with 101 non‐COVID‐19 matched controls. A systematic review was performed in four databases and meta‐analysis was conducted using Stata software. Results: Tp‐Te, TpTe/QT, QRS width, and iCEB were significantly increased in COVID‐19 patients compared with controls (TpTe = 82.89 vs. 75.33 ms (ms), p‐value =.005; TpTe/QT = 0.217 vs. 0.203 ms, p‐value =.026). After a meta‐analysis of 679 COVID‐19 cases and 526 controls from 9 studies, TpTe interval, TpTe/QT, and TpTe/QTc ratios were significantly increased in COVID‐19 patients. Meta‐regression analysis moderated by age, gender, diabetes mellitus, hypertension, and smoking reduced the heterogeneity. QTd showed no significant correlation with COVID‐19. Conclusion: COVID‐19 adversely influences the ECG markers of transmural heterogeneity of repolarization. Studies evaluating the predictive value of these ECG markers are warranted to determine their clinical utility. [ABSTRACT FROM AUTHOR]

T-wave changes are thought to be associated with the repolarization phase of myocardial action potential. Although it has been known that persistent T-wave change is associated with the heart disease or the prognosis, the sensitivity and the specificity are not necessarily satisfactory for clinical therapeutic strategy. Recent basic studies have shown that, in some kinds of pathological states, transient repolarization changes of myocardial action potential were associated with life-threatening arrhythmia. Also clinical studies are being conducted to elucidate the clinical implication of transient T-wave changes on electrocardiography (ECG) in such an arrhythmia. Transient repolarization or T-wave change is thought to occur because of environmental or neurohumoral factors, circadian variation, stretching of myocardium or other triggers in daily life, resulting in fatal arrhythmia. Such fatal arrhythmias are thought to occur under restricted conditions even in the patients with serious heart disease. It is important to clarify and utilize the transient T-wave change directly associated with the fatal arrhythmia on a clinical basis. In this article, we first assess the mechanisms of transient repolarization or T-wave changes on ECG concerning fatal arrhythmia, and afterwards refer to possible attempts at clinical evaluation and application. [Copyright &y& Elsevier]

Introduction: QT dispersion (QTd, range of QT intervals in 12 KCG leads) is thought to reflect spatial heterogeneity of ventricular refractoriness. However, QTd may be largely due to projections of the repolarization dipole rather than ‘nondipolar’ signals. Methods and Results: Seventy-eight normal subjects (47 ± 16 years, 23 women), 68 hypertrophic cardiomyopathy patients (HCM; 38 ± 15 years. 21 women), 72 dilated cardiomyopathy patients (DCM; 48 ± 15 years, 29 women), and 81 survivors of acute myocardial infarction (AMI; 63 ± 12 years, 20 women) had digital 12-lead resting supine ECGs recorded (10 ECGs recorded in each subject and results averaged). In each ECG lead, QT interval was measured under operator review by QT Guard (GE Marquette) to obtain QTd. QTd was expressed as the range, standard deviation, and highest-to-lowest quartile difference of QT interval in all measurable leads. Singular value decomposition transferred ECGs into a minimum dimensional time orthogonal space. The first three components represented the ECG dipole; other components represented nondipolar signals. The power of the T wave nondipolar within the total components was computed to measure spatial repolarization heterogeneity (relative T wave residuum, TWR). QTd was 33.6 ± 18.3, 47.0 ± 19.3, 34.8 ± 21.2. and 57.5 ± 25.3 msec in normals, HCM, DCM, and AMI, respectively (normals vs DCM: NS, other P < 0.009). TWR was 0.029% ± 0.031%, 0.067% ± 0.067%, 0.112% ± 0.154%, and 0.186% ± 0.308% in normals, HCM, DCM, and AMI (HCM vs DCM: NS, other P < 0.006), The correlations between QTd and TWR were r = -0.0446, 0.2805, -0.1531, and 0.0771 (P = 0.03 for HCM, other NS) in normals, HCM, DCM, and AMI, respectively. Conclusion: Spatial heterogeneity of ventricular repolarization exists and is measurable in 12-lead resting ECGs. It differs between different clinical groups, but the so-called QT dispersion is unrelated to it. [ABSTRACT FROM AUTHOR]

Background Early life trauma has been associated with increased cardiovascular risk, but the arrhythmic implications are unclear. We hypothesized that in patients with coronary artery disease, early life trauma predicts increased arrhythmic risk during mental stress, measured by elevated microvolt T-wave alternans (TWA), a measure of repolarization heterogeneity and sudden cardiac death risk. Methods and Results In a cohort with stable coronary artery disease (NCT04123197), we examined early life trauma with the Early Trauma Inventory Self Report-Short Form. Participants underwent a laboratory-based mental stress speech task with Holter monitoring, as well as a structured psychiatric interview. We measured TWA during rest, mental stress, and recovery with ambulatory electrocardiographic monitoring. We adjusted for sociodemographic factors, cardiac history, psychiatric comorbidity, and hemodynamic stress reactivity with multivariable linear regression models. We examined 320 participants with noise- and arrhythmia-free ECGs. The mean (SD) age was 63.8 (8.7) years, 27% were women, and 27% reported significant childhood trauma (Early Trauma Inventory Self Report-Short Form ≥10). High childhood trauma was associated with a multivariable-adjusted 17% increase in TWA ( P =0.04) during stress, and each unit increase in the Early Trauma Inventory Self Report-Short Form total score was associated with a 1.7% higher stress TWA ( P =0.02). The largest effect sizes were found with the emotional trauma subtype. Conclusions In a cohort with stable coronary artery disease, early life trauma, and in particular emotional trauma, is associated with increased TWA, a marker of increased arrhythmic risk, during mental stress. This association suggests that early trauma exposures may affect long-term sudden cardiac death risk during emotional triggers, although more studies are warranted.