Electrophysiologic mechanisms underlying XXXX due to reperfusion of @entity63 myocardium.

@entity1165 @entity4486 @entity63 @entity591 @entity2224 @entity468 @entity943
The mechanisms responsible for malignant @entity943 associated with reperfusion of @entity63 myocardium were delineated with a computerized, three-dimensional mapping system, with simultaneous eight-level transmural recordings from 232 bipolar sites. In six @entity4486 -anesthetized @entity468 , regional @entity63 was induced for 10 min by occlusion of the left anterior descending coronary artery, followed by reperfusion. At 10 min after @entity63 , just before reperfusion, total ventricular activation time during sinus rhythm was significantly delayed (63 +/- 8 vs 25 +/- 2 msec before @entity63 , p less than .001). @entity1165 ( @entity1165 ) occurred within 15 sec after reperfusion and in three animals culminated in @entity2224 . In 75% of cases of nonsustained @entity1165 , initiation occurred in the subendocardium, at the border of the reperfused zone via a mechanism not involving reentry, as determined by the fact that continuous activation was not apparent and the time from the end of the sinus beat to the beginning of @entity1165 (142 +/- 14 msec) was not associated with any intervening depolarizations. In the remaining 25% of cases of nonsustained @entity1165 , initiation of the @entity1165 resulted from intramural reentry in the subendocardium adjacent to the site of delayed midmyocardial activation from the preceding sinus beat (total activation time = 151 +/- 9 msec, p less than .001 vs just before reperfusion). This reentrant mechanism was similar to that responsible for the majority of cases of @entity1165 during @entity63 without reperfusion. Maintenance of @entity1165 during reperfusion occurred by nonreentrant mechanisms as well as by intramural reentry, with most cases of @entity1165 involving both mechanisms. @entity1165 leading to @entity2224 was initiated in the subendocardium at the border of the reperfused zone by a nonreentrant mechanism and was maintained by both nonreentrant and reentrant mechanisms, at times in combination in the same beat. The coupling interval of the first ectopic beat of @entity1165 leading to @entity2224 was not significantly different from that of nonsustained @entity1165 (199 +/- 16 vs 189 +/- 9 msec, p = NS). However, during the transition from @entity1165 to @entity2224 , nonreentrant mechanisms arising both in the subendocardium and subepicardium led to very rapid acceleration of the @entity591 to the coupling interval of 92 +/- 2 msec, resulting in enhanced functional block and further conduction delay, with the total activation time of the transition beats exceeding the coupling interval of the @entity591 .(ABSTRACT TRUNCATED AT 400 WORDS)
