Key result
Late reperfusion at 180 minutes cuts arrhythmic death from 42% to ~8% despite unchanged infarct size.
Why the study?
Reperfusion of the infarct-related artery might increase electrical stability independently of ischemic myocardium salvage, prompting an effort to delineate salvage-dependent from salvage-independent reperfusion effects on arrhythmias and arrhythmic death in acute MI.
Does coronary reperfusion at 45, 90, or 180 minutes reduce spontaneously occurring arrhythmias and arrhythmic death in conscious rats with acute myocardial infarction compared to permanent coronary artery occlusion?
Does coronary reperfusion at 45, 90, or 180 minutes reduce spontaneously occurring arrhythmias and arrhythmic death in conscious rats with acute myocardial infarction compared to permanent coronary artery occlusion?
Both early and late coronary reperfusion reduce ventricular arrhythmias and arrhythmia-related mortality in rats with acute MI, demonstrating that reperfusion increases electrical stability independently of myocardial salvage.
Answers are grounded in this paper and cite their sources.
Reperfusion may suppress arrhythmias beyond salvage in experimental MI; leaves open translation to human reperfusion strategies.
OBJECTIVES: This study sought to delineate salvage-dependent from salvage-independent coronary reperfusion in acute myocardial infarction and the effects on spontaneously occurring arrhythmias and arrhythmic death in rats. BACKGROUND: Reperfusion of the infarct-related artery might increase electrical stability independently of salvage of ischemic myocardium. METHODS: In 98 conscious rats the electrocardiogram was monitored by telemetry for 48 h after MI, and all episodes of ventricular tachycardia (VT) and ventricular fibrillation (VF) were analyzed. Reperfusion at 45 min (RP45) (n = 15), 90 min (RP90) (n = 18) and 180 min (RP180) (n = 30) min was compared with permanent coronary artery occlusion (CAO) (n = 35) with respect to the post-reperfusion periods. RESULTS: RP45, RP90 and RP180 reduced the incidence of VT by 93%, 98% and 88% and VF by 89%, 97% and 92%, respectively (all p < 0.01 vs. CAO). The all-cause mortality rate was reduced from 47% (CAO) to 8% (RP45, p < 0.05) and 0% (RP90, p < 0.01); after RP180 it was 17% (CAO 42%, p = 0.08). All reperfusion regimens reduced arrhythmic deaths: 47% to 8% (RP45, p < 0.05), 47% to 0% (RP90, p < 0.01) and 42% to 8% (RP180, p < 0.05). Infarct size was identical to that during CAO (49 +/- 10% [mean +/- SD]) and RP180 (49 +/- 10%), whereas preferentially epicardial salvage occurred at RP45 (36 +/- 8%, p < 0.001) and RP90 (38 < 10%, p < 0.001). CONCLUSIONS: Early and late reperfusion reduce the incidence and duration of VT and VF in conscious rats with acute MI. Thereby, arrhythmia-related mortality is improved through the prevention of fatal VF episodes. Thus, reperfusion increases the electrical stability of the heart independently of myocyte salvage, as proposed by the open artery hypothesis.
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Opitz et al. (1998) studied Acute myocardial infarction (coronary artery occlusion in rats) (n=98). Coronary reperfusion at 45, 90, or 180 minutes vs. Permanent coronary artery occlusion (n=35) was evaluated on Arrhythmic death and spontaneous ventricular tachycardia (VT) and ventricular fibrillation (VF) (p=<0.05). Late reperfusion at 180 minutes reduced VT by 88%, VF by 92% (p<0.01), and arrhythmic death from 42% to 8% (p<0.05) despite identical infarct size (49%).
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