Analysis of J waves during myocardial ischaemia.
ABSTRACT The aim of this study was to investigate the relationship between J-wave dynamics and arrhythmias during myocardial ischaemia in patients with vasospastic angina (VSA).
Sixty-seven consecutive patients diagnosed with VSA by a provocation test for coronary spasm were grouped according to whether they had a J wave in the baseline electrocardiograms or not (VSA-JW group, n = 14; VSA-non-JW group: n = 53). We retrospectively studied the associations between J-wave and ST-segment dynamics and induced ventricular fibrillations (VFs) during coronary spasm. In the VSA-JW group, 7 of the 14 patients showed changes in J-wave morphology and/or gains in J-wave voltage, followed by VF in 4 patients. Compared with patients without VF, the four patients with VF showed similar maximal voltage in the baseline J waves but a higher voltage during induced coronary spasms (0.57 ± 0.49 vs. 0.30 ± 0.11 mV; P = 0.011). In three patients with VF, J waves progressively increased and were accompanied by the characteristic coved-type or lambda-shaped ST-segment elevations. In the VSA-non-JW group, only four patients showed new appearances of J waves during coronary spasms and another patient without a distinct J wave developed VF. Ventricular fibrillations were induced more frequently in the VSA-JW group than in the VSA-non-JW group [4/14 (29%) vs. 1/53 (2%); P = 0.012].
J-wave augmentations were caused by myocardial ischaemia during coronary spasms. The presence and augmentation of J waves, especially prominent J waves with the characteristic ST-elevation patterns, were associated with VF.
- The American Journal of Cardiology 10/1984; 54(6):672-3. · 3.21 Impact Factor
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ABSTRACT: ST-segment elevation in a structurally normal heart is associated with an electrocardiographic (ECG) J wave, which can be observed in the early repolarization syndrome (ERS), idiopathic ventricular fibrillation (VF), and the Brugada syndrome. Animal studies have demonstrated that the J wave is the consequence of a transmural voltage gradient resulting from an Ito-mediated action potential notch (spike and dome) in epicardium but not endocardium. Ito-mediated spike and dome morphology predisposes loss or depression of the dome in epicardium, leading to ST-segment elevation. Despite the fact that 3 clinical syndromes share many common ECG features, their clinical consequences are remarkably different. The ERS is a benign ECG finding characterized by a distinct J wave and ST segment in left precordial leads V4 through V6. In contrast, idiopathic VF and the Brugada syndrome, characterized by a J wave and ST-segment elevation in the inferior and right precordial leads, respectively, are the leading causes for sudden cardiac death in young Southeast Asian males. The underlying mechanism for such a difference in clinical consequences among these syndromes is due to a difference in Ito density and Ito-mediated epicardial spike and dome. When Ito is prominent, complete loss of the dome may occur due to either a decrease in inward currents or an increase in outward currents, leading to phase 2 reentry capable of initiating VF as in idiopathic VF and the Brugada syndrome. When Ito is relatively small as in the ERS, partial depression of the dome occurs without the development of phase 2 reentry.Journal of Electrocardiology 11/2005; 38(4 Suppl):26-32. · 1.09 Impact Factor
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ABSTRACT: A 52-year-old man with a history of vasospastic angina experienced a severe ischemic episode accompanied by a non-Q wave myocardial infarction. Two episodes of ventricular fibrillation (VF) occurred during the acute phase of the event. Osborn waves were observed on the ECG preceding each episode of VF. In the second episode, the gradual development of Osborn waves until VF occurred was confirmed on ECG. The Osborn waves appeared to be related to the occurrence of VF. This case may provide clinical evidence that a prominent I(to) participates in the development of VF during myocardial ischemia.Journal of Cardiovascular Electrophysiology 06/2002; 13(5):486-9. · 3.48 Impact Factor