Background In experimental models, ischemic preconditioning of the heart protects against ischemic damage and ventricular arrhythmias during subsequent coronary occlusion. In this study, we investigated whether protection against ischemic suffering and ischemia-induced arrhythmias may occur after spontaneous transmural ischemia in humans. Methods and Results We performed 24-hour Holter monitoring in 10 patients with variant angina who developed complex ventricular arrhythmias (CVAs, more than five premature ventricular beats per minute or repetitive ventricular arrhythmias) during episodes of ST-segment elevation. A total of 150 episodes of ST-segment elevation were detected on Holter monitoring, 21 (14%) of which showed CVAs. Episodes separated from the previous one by a time interval of less than or equal to 30 minutes or by a time interval of >30 minutes did not differ in either magnitude or duration of ST-segment elevation, but CVAs occurred more frequently in the second group (3% versus 29%, P<.0001). The time interval from the preceding ischemic episode was longer for the episodes with compared with those without CVAs (197+/-275 versus 57+/-87 minutes, P<.001), but these two groups of episodes also had similar severities and durations of ST-segment elevation. Finally, when we analyzed 13 clusters of two to six ischemic episodes, CVAs were found much more frequently in the first (92%) than in the last (23%, P=.009) episode of the clusters, while ST-segment elevations were similar (2.1+/-1.6 versus 2.2+/-1.1 mm) and ischemia durations shorter in the first than in the last episode (3.9+/-3.6 versus 6.1+/-1.7 minutes, P=.03). Conclusions Our data indicate that preconditioning by transient ischemia induces a significant protection against ischemia-induced CVAs in patients with variant angina. This beneficial effect was not related to a reduction in either severity or duration of ischemia, suggesting that arrhythmic protection was a direct consequence of preconditioning rather than an epiphenomenon of ischemic protection.
Preconditioning by transient myocardial ischemia confers protection against ischemia-induced ventricular arrhythmias in variant angina
Patti G;
1996-01-01
Abstract
Background In experimental models, ischemic preconditioning of the heart protects against ischemic damage and ventricular arrhythmias during subsequent coronary occlusion. In this study, we investigated whether protection against ischemic suffering and ischemia-induced arrhythmias may occur after spontaneous transmural ischemia in humans. Methods and Results We performed 24-hour Holter monitoring in 10 patients with variant angina who developed complex ventricular arrhythmias (CVAs, more than five premature ventricular beats per minute or repetitive ventricular arrhythmias) during episodes of ST-segment elevation. A total of 150 episodes of ST-segment elevation were detected on Holter monitoring, 21 (14%) of which showed CVAs. Episodes separated from the previous one by a time interval of less than or equal to 30 minutes or by a time interval of >30 minutes did not differ in either magnitude or duration of ST-segment elevation, but CVAs occurred more frequently in the second group (3% versus 29%, P<.0001). The time interval from the preceding ischemic episode was longer for the episodes with compared with those without CVAs (197+/-275 versus 57+/-87 minutes, P<.001), but these two groups of episodes also had similar severities and durations of ST-segment elevation. Finally, when we analyzed 13 clusters of two to six ischemic episodes, CVAs were found much more frequently in the first (92%) than in the last (23%, P=.009) episode of the clusters, while ST-segment elevations were similar (2.1+/-1.6 versus 2.2+/-1.1 mm) and ischemia durations shorter in the first than in the last episode (3.9+/-3.6 versus 6.1+/-1.7 minutes, P=.03). Conclusions Our data indicate that preconditioning by transient ischemia induces a significant protection against ischemia-induced CVAs in patients with variant angina. This beneficial effect was not related to a reduction in either severity or duration of ischemia, suggesting that arrhythmic protection was a direct consequence of preconditioning rather than an epiphenomenon of ischemic protection.Pubblicazioni consigliate
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