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Ventricular repolarization components on the electrocardiogram

Cellular basis and clinical significance

^* Main Line Health Heart Center, Wynnewood, Pennsylvania, USA

View larger version (50K): [in a new window]   Figure 1 Cellular basis for the J-wave. (A) A prominent J-wave in lead II was recorded from a healthy, young Asian male. (B) Simultaneous recording of transmembrane action potentials (APs) from epicardial (Epi) and endocardial (Endo) regions and a transmural electrocardiogram (ECG) in an arterially perfused canine ventricular wedge preparation. An Ito-mediated AP notch in the epicardium, but not endocardium, was associated with a J-wave. A premature stimulus (S1 – S2 = 300 ms) caused a parallel decrease in the amplitude of the epicardial AP notch and J-wave. Modified from Yan and Antzelevitch (4), with permission.

View larger version (38K): [in a new window]   Figure 2 Possible mechanisms responsible for ST-segment elevation. (A) The concept of "injury current." The "injury zone" in the epicardium, with a reduction in resting membrane potential, produces an injury current during the resting phase that should result in TQ depression instead of ST-segment elevation. (B) The concept of "loss of action potential (AP) dome or plateau amplitude." A difference in the AP plateau amplitude generates a transmural voltage gradient that could manifest as ST-segment displacement.

View larger version (62K): [in a new window]   Figure 3 The mechanism responsible for J-wave–related arrhythmogenesis. (A) Polymorphic ventricular tachycardia (VT) in a patient with prominent J-waves. Reprinted from Aizawa et al. (5), with permission. (B) Polymorphic VT initiated by phase 2 re-entry in a canine right ventricular wedge in the presence of 2.5 µmol/l pinacidil. The action potentials (APs) were simultaneously recorded from two epicardial sites (Epi 1 and Epi 2) and one endocardial (Endo) site. A loss of the AP dome in Epi 1, but not in Epi 2, led to phase 2 re-entry capable of initiating polymorphic VT.

View larger version (50K): [in a new window]   Figure 4 Cellular basis for the T-wave. (A) The electrocardiogram (ECG) tracings were recorded in patients with various serum potassium concentrations. A pathologic U-wave was seen under hypokalemia, whereas a tall and upright T-wave was associated with hyperkalemia. (B) Simultaneous recording of action potentials (APs) from epicardial (Epi) and M cells or endocardial cells (Endo), together with a transmural ECG under various extracellular potassium concentrations. Extracellular potassium primarily influenced the AP phase 3 slope (repolarization rate); hyperkalemia accelerated phase 3 repolarization, whereas hypokalemia reduced it. The alteration of AP phase 3 slopes and their interplay among different myocardial layers determined the T-wave morphologies under various extracellular potassium concentrations. A pathologic U-wave was present with hypokalemia. Reprinted from Yan et al. (32), with permission.

View larger version (66K): [in a new window]   Figure 5 The mechanism responsible for the initiation of torsade de pointes (TdP). (A) An R-on-T extrasystole initiated an episode of torsade de pointes in a patient with a prolonged QT interval who was receiving sotalol. (B) Transmembrane action potentials (APs) from the epicardium (Epi) and endocardium (Endo) were simultaneously recorded together with a transmural electrocardiogram (ECG) in an arterially perfused rabbit left ventricle. dl-sotalol, an IKr blocker, markedly prolonged the QT interval and induced phase 2 early afterdepolarization (EAD) in the endocardium. The phase 2 EADs, in turn, produced R-on-T extrasystoles capable of initiating torsade de pointes. Reprinted from Yan et al. (35), with permission.