Occurrence of “J Waves” in 12‐Lead ECG as a Marker of Acute Ischemia and Their Cellular Basis

Abstract

The "J wave" (also referred to as "the Osborn wave,""the J deflection," or "the camel's hump") is a distinctive deflection occurring at the QRS-ST junction. In 1953, Dr. John Osborn described the "J wave" as an "injury current" resulting in ventricular fibrillation during experimental hypothermia. Although "J Wave" is supposed to be pathognomonic of hypothermia, it is seen in a host of other conditions such as hypercalcemia, brain injury, subarachnoid hemorrhage, cardiopulmonary arrest from over sedation, the Brugada syndrome, vasospastic angina, and idiopathic ventricular fibrillation. However, there is paucity of literature data as regards to ischemic etiology of "J Wave." In this article, we present a case where "J waves" were probably induced by ischemia. We also discuss the mechanism of ischemia-induced "J wave" accentuation and its prognostic implications.

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…”

“…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. In contrast, if activation starts from the epicardium and travels to the endocardium, the J wave disappears from the ECG because it is buried within the QRS complex (Rituparna et al 2007). However, a spike-and-dome morphology of the action potential is clearly present in cells other than epicardial cells (Yan and Antzelevitch 1996).…”

“…On the other hand, the presence of J waves can represent a "current of injury" and seem to be indicative of severe ischaemia (Yan and Antzelevitch 1996). 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).…”

“…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).…”