Early afterdepolarizations induced in vivo by reperfusion of ischemic myocardium. A possible mechanism for reperfusion arrhythmias.
- 1 June 1990
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation
- Vol. 81 (6) , 1911-1920
- https://doi.org/10.1161/01.cir.81.6.1911
Abstract
Recent studies in vitro have shown that afterdepolarizations may develop during reperfusion after hypoxia, thus suggesting that these afterdepolarizations may contribute to the genesis of reperfusion arrhythmias. We recorded monophasic action potentials (MAPs) during myocardial ischemia and reperfusion to investigate whether afterdepolarizations develop in vivo when reperfusion arrhythmias occur. In 15 anesthetized cats, 24 trials of 10 minutes of occlusion of the left anterior descending coronary artery were followed by reperfusion. In 13 of 24 (54%) trials, afterdepolarizations developed at the moment of reperfusion, with a mean amplitude of 2.4 +/- 1.1 mV (13 +/- 8% of MAP amplitude). When cycle length was either increased by vagal stimulation or decreased by atrial pacing, early afterdepolarization (EAD) amplitude was modified, according to what has been described for EAD in vitro, with a positive linear correlation between cycle length and EAD amplitude (r = 0.91, p less than 0.0001). The occurrence of EAD was not related to rapid changes in left ventricular pressure. In the eight of 13 (62%) cases in which EAD development was associated with reperfusion arrhythmias, the coupling interval of the EAD and of premature ventricular contractions showed a significant correlation (r = 0.86, p less than 0.0001). However, in five of 13 (38%) cases, occurrence of reperfusion arrhythmias was not accompanied by the presence of EAD on the MAP recording. In two animals, a 2:1 block of EAD conduction was observed, and this was reflected on the intracavitary electrocardiogram as T wave alternans. Thus, EADs occur frequently after reperfusion in vivo, with a time course that parallels the onset of reperfusion arrhythmias. This finding further supports the role of triggered activity in the genesis of reperfusion arrhythmias in vivo.This publication has 23 references indexed in Scilit:
- Repolarization interactions between cardiac segments of varying action potential durationAmerican Heart Journal, 1989
- Torsade de Pointes and Other Pause‐Induced Ventricular Tachycardias: The Short‐Long‐Short Sequence and Early AfterdepolarizationsPacing and Clinical Electrophysiology, 1988
- Lack of correlation between occlusion and reperfusion arrhythmias in the catAmerican Heart Journal, 1985
- Idiopathic long QT syndrome: Progress and questionsAmerican Heart Journal, 1985
- Afterdepolarizations as a mechanism for the long QT syndrome: Electrophysiologic studies of a caseJournal of the American College of Cardiology, 1984
- Ventricular fibrillation caused by myocardial reperfusion in Prinzmetal's anginaAmerican Heart Journal, 1983
- Reperfusion arrhythmia: A marker of restoration of antegrade flow during intracoronary thrombolysis for acute myocardial infarctionAmerican Heart Journal, 1983
- Differing mechanisms for ventricular vulnerability during coronary artery occlusion and releaseAmerican Heart Journal, 1976
- Vulnerability to ventricular fibrillation during acute coronary arterial occlusion and releaseThe American Journal of Cardiology, 1975
- Ventricular fibrillation during and after coronary artery occlusionThe American Journal of Cardiology, 1960