Ventricular repolarization components on the electrocardiogram

Abstract

Ventricular repolarization components on the surface electrocardiogram (ECG) include J (Osborn) waves, ST-segments, and T- and U-waves, which dynamically change in morphology under various pathophysiologic conditions and play an important role in the development of ventricular arrhythmias. Our primary objective in this review is to identify the ionic and cellular basis for ventricular repolarization components on the body surface ECG under normal and pathologic conditions, including a discussion of their clinical significance. A specific attempt to combine typical clinical ECG tracings with transmembrane electrical recordings is made to illustrate their logical linkage. A transmural voltage gradient during initial ventricular repolarization, which results from the presence of a prominent transient outward K(+) current (I(to))-mediated action potential (AP) notch in the epicardium, but not endocardium, manifests as a J-wave on the ECG. The J-wave is associated with the early repolarization syndrome and Brugada syndrome. ST-segment elevation, as seen in Brugada syndrome and acute myocardial ischemia, cannot be fully explained by using the classic concept of an "injury current" that flows from injured to uninjured myocardium. Rather, ST-segment elevation may be largely secondary to a loss of the AP dome in the epicardium, but not endocardium. The T-wave is a symbol of transmural dispersion of repolarization. The R-on-T phenomenon (an extrasystole originating on the T-wave of a preceding ventricular beat) is probably due to transmural propagation of phase 2 re-entry or phase 2 early after depolarization that could potentially initiate polymorphic ventricular tachycardia or fibrillation.

Predictors of Ventricular Fibrillation at Reperfusion in Patients With Acute ST-Elevation Myocardial Infarction Treated by Primary Percutaneous Coronary Intervention

“…This is in line with previously published data concerning VF in STEMI, but not directly related to reperfusion (11-13). The higher incidence of VF in inferior STEMI, especially with right ventricular involvement can be explained by much more prominent I to in epicardium of the right ventricle than the left one (14). We also observed a tendency to the prevalence of RCA as IRA that previously had been reported to be predictive for VF (1).…”

Orally administered moxifloxacin prolongs QTc in healthy Chinese volunteers: a randomized, single-blind, crossover study

“…Drugs that block the rapidly activated delayed rectifier potassium current (I Kr ) and induce a delay in cardiac repolarization may create an electrophysiological environment that favors the development of cardiac arrhythmias, including Torsades de pointes (TdP) [1] . The recent high-profile non-approvals and withdrawals of newly approved drugs due to adverse cardiac effects, primarily QT prolongation and TdP [2] , have triggered public concerns, increased regulatory scrutiny and resulted in new guidelines for the pharmaceutical development of new drugs [3] .…”

Mechanisms linking short- and long-term electrical remodeling in the heart .....is it a stretch?

“…28 Electrical activity in the ventricles results in two major deflections on the surface ECG: the QRS complex which reflects ventricular activation; and the T wave which reflects ventricular repolarization (Fig. 1A).…”

“…As mentioned above, this feature is referred to as "transmural dispersion of repolarization" and plays a key role in arrhythmogenesis. 28 Although the transmural gradient is demonstrated clearly in experimental models, it remains unclear whether these gradients are attenuated in vivo by cell-cell coupling via gap junctions. 22 In addition, the possible contributions of other heterogeneities in myocardial electrical and/or structural properties to the pattern of action potential propagation remains poorly understood.…”