Effect of beta-blocker atenolol on spatial dispersion of ventricular repolarization of sheep following acute myocardial ischemia.
Abstract
AIM: To investigate the effect of beta-blockers on spatial dispersion of
ventricular repolarization following acute myocardial ischemia.
METHODS: Twenty sheep were randomized into control (normal saline,iv) and
atenolol (1.5 mg/kg,iv) group. Acute myocardial ischemia was induced by occlusion
of the obtuse marginal coronary artery. Unipolar ECG was simultaneously acquired
from 64 epicardial sites in both ischemic and non-ischemic regions.
Activation-recovery intervals (ARI), an index of ventricular repolarization, was
determined from the epicardial ECG. The difference between the longest and
shortest ARI was defined as ARI dispersion.
RESULTS: Ischemic zone in atenolol group was less than that of control group (13
%+/-2 % vs 19 %+/-3 %, P=0.04). In the control group, pooled ARI dispersion was
increased by (18+/-21), (27+/-21), and (16+/-10) ms at 30, 60, and 90 min of
coronary artery occlusion respectively (P <0.01), whereas in the atenolol group,
ARI dispersion was only increased by (6+/-4), (6+/-7), and (2+/-7) ms
respectively (P >0.05).
CONCLUSION: These findings indicate that atenolol suppresses ischemia-induced
increase in spatial dispersion of ventricular repolarization, which may explain
the antiarrhythmic effect of beta-blockers.
Keywords:
ventricular repolarization following acute myocardial ischemia.
METHODS: Twenty sheep were randomized into control (normal saline,iv) and
atenolol (1.5 mg/kg,iv) group. Acute myocardial ischemia was induced by occlusion
of the obtuse marginal coronary artery. Unipolar ECG was simultaneously acquired
from 64 epicardial sites in both ischemic and non-ischemic regions.
Activation-recovery intervals (ARI), an index of ventricular repolarization, was
determined from the epicardial ECG. The difference between the longest and
shortest ARI was defined as ARI dispersion.
RESULTS: Ischemic zone in atenolol group was less than that of control group (13
%+/-2 % vs 19 %+/-3 %, P=0.04). In the control group, pooled ARI dispersion was
increased by (18+/-21), (27+/-21), and (16+/-10) ms at 30, 60, and 90 min of
coronary artery occlusion respectively (P <0.01), whereas in the atenolol group,
ARI dispersion was only increased by (6+/-4), (6+/-7), and (2+/-7) ms
respectively (P >0.05).
CONCLUSION: These findings indicate that atenolol suppresses ischemia-induced
increase in spatial dispersion of ventricular repolarization, which may explain
the antiarrhythmic effect of beta-blockers.