V. Pasceri et al., PRECONDITIONING BY TRANSIENT MYOCARDIAL-ISCHEMIA CONFERS PROTECTION AGAINST ISCHEMIA-INDUCED VENTRICULAR ARRHYTHMIAS IN VARIANT ANGINA, Circulation, 94(8), 1996, pp. 1850-1856
Background In experimental models, ischemic preconditioning of the hea
rt protects against ischemic damage and ventricular arrhythmias during
subsequent coronary occlusion. In this study, we investigated whether
protection against ischemic suffering and ischemia-induced arrhythmia
s may occur after spontaneous transmural ischemia in humans. Methods a
nd Results We performed 24-hour Holter monitoring in 10 patients with
variant angina who developed complex ventricular arrhythmias (CVAs, mo
re than five premature ventricular beats per minute or repetitive vent
ricular arrhythmias) during episodes of ST-segment elevation. A total
of 150 episodes of ST-segment elevation were detected on Holter monito
ring, 21 (14%) of which showed CVAs. Episodes separated from the previ
ous 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 du
ration of ST-segment elevation, but CVAs occurred more frequently in t
he second group (3% versus 29%, P<.0001). The time interval from the p
receding ischemic episode was longer for the episodes with compared wi
th 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, w
hile 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 ind
icate that preconditioning by transient ischemia induces a significant
protection against ischemia-induced CVAs in patients with variant ang
ina. This beneficial effect was not related to a reduction in either s
everity or duration of ischemia, suggesting that arrhythmic protection
was a direct consequence of preconditioning rather than an epiphenome
non of ischemic protection.