ECG Repolarization Waves: Their Genesis and Clinical Implications

Abstract

The electrocardiographic (ECG) manifestation of ventricular repolarization includes J (Osborn), T, and U waves. On the basis of biophysical principles of ECG recording, any wave on the body surface ECG represents a coincident voltage gradient generated by cellular electrical activity within the heart. The J wave is a deflection with a dome that appears on the ECG after the QRS complex. A transmural voltage gradient during initial ventricular repolarization, which results from the presence of a prominent action potential notch mediated by the transient outward potassium current (I to ) in epicardium but not endocardium, is responsible for the registration of the J wave on the ECG. Clinical entities that are associated with J waves (the J-wave syndrome) include the early repolarization syndrome, the Brugada syndrome and idiopathic ventricular fibrillation related to a prominent J wave in the inferior leads. The T wave marks the final phase of ventricular repolarization and is a symbol of transmural dispersion of repolarization (TDR) in the ventricles. An excessively prolonged QT interval with enhanced TDR predisposes people to develop torsade de pointes. The malignant "Ron-T" phenomenon, i.e., an extrasystole that originates on the preceding T wave, is due to transmural propagation of phase 2 reentry or phase 2 early afterdepolarization. A pathological "U" wave as seen with hypokalemia is the consequence of electrical interaction among ventricular myocardial layers at action potential phase 3 of which repolarization slows. A physiological U wave is thought to be due to delayed repolarization of the Purkinje system. A.N.E. 2005;10(2):211-223electrocardiography; J wave; T wave; U wave

The Canine J wave

“…It may indicate the presence of a transient electrical heterogeneity (difference in action potentials) between ventricular endocardium and epicardium during early repolarisation (Hlaing et al 2005;Rituparna et al 2007;Shinde et al 2007). The mechanism can be explained by…”

“…It may indicate the presence of a transient electrical heterogeneity (difference in action potentials) between ventricular endocardium and epicardium during early repolarisation (Hlaing et al 2005;Rituparna et al 2007;Shinde et al 2007). The mechanism can be explained by doi: 10.17221/8109-VETMED a prominent transient outward current (I to ) in the ventricular epicardium that produces a transmural voltage gradient during the early ventricular repolarisation which can be accountable for the presence of the J wave (Yan and Antzelevitch 1996;Hlaing et al 2005;Rituparna et al 2007;Shinde et al 2007). Moreover, it is possible to distinguish a J wave coincident with the epicardial action potential notch in the ECG when the electrical activation originates in the endocardium and spreads to the epicardium.…”

“…The presence of a prominent I to in the epicardium has been shown to sensitise tissue to the effects of high calcium whereas hypothermia accentuates the voltage gradient across ventricular myocardium (Rituparna et al 2007). Intracranial pathology can induce differences in electrophysiological responsiveness of the epicardium and endocardium to acetylcholine and isoproterenol (Hlaing et al 2005). J waves in coronary artery disease are likely to be transient and may indicate a current of injury in imminent myocardial infarctions (useful in localising the infarct-related arterial territory) or in myocardial revascularisation (Rituparna et al 2007).…”

“…Several other conditions have been described to occur together with the presence of J waves, such as hypothermia, hypercalcaemia, brain injury, subarachnoid haemorrhage, Chagas disease, sepsis, vasospastic angina, Brugada syndrome, acute myocardial ischaemia, Prinzmetal angina, hypertrophy of the left ventricle, cocaine or haloperidol overdosing and idiopathic ventricular fibrillation associated with J waves in inferior leads (Rituparna et al 2007). Typically, the J waves should have an amplitude and duration of at least 1 mm and 10 milliseconds, respectively, in at least two consecutive beats (Hlaing et al 2005). In humans they occur frequently in leads II, III, and aVF and the precordial leads: V 5 -V 6 (Shinde et al 2007;Borggrefe and Schimpf 2010).…”

Salt Loading on QT Dispersion and the Protective Role of Potassium Supplement in Normotensive Adults

“…It has also been widely applied in researches, as well as evaluations of drug efficacy, on heart diseases including hypertension, coronary heart disease, arrhythmia, etc. T peak -T end interval (Tp-Te) is an interval from the peak to the end of T wave, which closely represents transmural dispersion of repolarization [5,6]. It is also an important predictor of ventricular arrhythmia events [7].…”