@entity3416 termination of XXXX stress as a trigger of coronary vasospasm in variant angina.

@entity3347 @entity1 @entity3416 @entity63 @entity4341 @entity951 @entity453 @entity3693
@entity4341 testing represents an alternative to exercise stress testing for documentation of @entity63 related to @entity453 ( @entity453 ). In such a case, @entity63 is attributed to maldistribution of coronary flow during @entity4341 -induced vasodilation. The present study evaluated the potential role of @entity4341 testing in producing @entity63 through a vasospastic mechanism, following rapid @entity3347 induced by @entity3416 . The possibility was tested in 36 in-hospital @entity1 with variant @entity951 who underwent @entity4341 infusion (up to 0.84 mg/kg over 10 minutes) with continuous 12-lead electrocardiographic and 2-dimensional echo monitoring. Medications were withdrawn from all @entity1 . The test was pharmacologically stopped with the @entity4341 antidote ( @entity3416 , 80 to 240 mg intravenously over 1 to 3 minutes) in all @entity1 . Two to 6 minutes after starting @entity3416 infusion, 10 @entity1 (28%) developed (greater than 0.10 mV) ST-segment elevation (2.9 +/- 0.8 mm from baseline), always accompanied by obvious asynergy detected by echocardiography, in the same electrocardiographic leads showing spontaneous or @entity3693 -induced ST-segment elevation. Nitrates promptly resolved @entity63 in all @entity1 . At coronary angiography, 5 of these 10 @entity1 showed significant @entity453 (greater than 70% lumen diameter reduction of at least 1 major coronary artery), whereas 5 had nonsignificant @entity453 . The rate pressure product at the onset of ST-segment elevation (after @entity4341 plus @entity3416 ) was considerably less than that recorded at peak exercise stress test in these @entity1 (9,600 +/- 2,200 vs 18,400 +/- 4,900, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
