Giant J Waves in Hypothermia
A 65-year-old man was admitted after being resuscitated from out-of-hospital cardiac arrest. He had had high blood pressure for many years but no evidence of previous myocardial infarction. A 12-lead ECG on admission (Figure⇓, left panel) showed sinus tachycardia and signs of left ventricular hypertrophy with a strain pattern. Seventy-two hours later, he developed hypothermia (31°C) consequent to anoxic-ischemic encephalopathy. The ECG at this time (central panel) showed sinus bradycardia, flattened P waves, QT prolongation with flattening of the ST segment–T wave, and a prominent J wave distinguishable in all leads (asterisk). The patient was rewarmed, and 96 hours after admission (right panel), his body temperature rose to 34°C. At that moment, the ECG showed progressive normalization of sinus rate, QT normalization, and a decrease in amplitude of the prominence of the J waves (○). J-wave amplitude and duration appeared to be inversely related to temperature. The paper speed was 25 mm/s, at 1 mV/mm.
J waves (Osborn waves) can be seen as a normal variant (early repolarization syndrome), in Chagas’ disease, in the Brugada syndrome, in hypercalcemia, and in hypothermic states. The cellular basis for the J wave was recently clarified.1 The prominent J wave induced by hypothermia is the result of a marked accentuation of the spike-and-dome morphology, with loss of the action potential dome of epicardial and M cells (mediated by a transient outward current, Ito), but not in the endocardium. This heterogeneous distribution of the action potential morphology gives rise to a transmural voltage gradient during ventricular activation that is responsible for the inscription of the J wave. Under hypothermic conditions, the prominent J wave is associated with an increase in the amplitude and width of the action potential notch in the epicardium but not in the endocardium.
The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke’s Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.
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