Differences in the upslope of the precordial body surface ECG T wave reflect right to left dispersion of repolarization in the intact human heart

N. Srinivasan,M. Orini,R. Providência,R. Simon,M. Lowe,O. Segal,A. Chow,R. Schilling,R. Hunter,P. Taggart,P. Lambiase

Published 2019 in Heart Rhythm

ABSTRACT

Background The relationship between the surface electrocardiogram (ECG) T wave to intracardiac repolarization is poorly understood. Objective The purpose of this study was to examine the association between intracardiac ventricular repolarization and the T wave on the body surface ECG (SECGTW). Methods Ten patients with a normal heart (age 35 ± 15 years; 6 men) were studied. Decapolar electrophysiological catheters were placed in the right ventricle (RV) and lateral left ventricle (LV) to record in an apicobasal orientation and in the lateral LV branch of the coronary sinus (CS) for transmural recording. Each catheter (CS, LV, RV) was sequentially paced using an S1–S2 restitution protocol. Intracardiac repolarization time and apicobasal, RV–LV, and transmural repolarization dispersion were correlated with the SECGTW, and a total of 23,946 T waves analyzed. Results RV endocardial repolarization occurred on the upslope of lead V1, V2, and V3 SECGTW, with sensitivity of 0.89, 0.91, and 0.84 and specificity of 0.67, 0.68, and 0.65, respectively. LV basal endocardial, epicardial, and mid-endocardial repolarization occurred on the upslope of leads V6 and I, with sensitivity of 0.79 and 0.8 and specificity of 0.66 and 0.67, respectively. Differences between the end of the upslope in V1, V2, and V3 vs V6 strongly correlated with right to left dispersion of repolarization (intraclass correlation coefficient 0.81, 0.83, and 0.85, respectively; P <.001). Poor association between the T wave and apicobasal and transmural dispersion of repolarization was seen. Conclusion The precordial SECGTW reflects regional repolarization differences between right and left heart. These findings have important implications for accurately identifying biomarkers of arrhythmogenic risk in disease.

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