Why the study?
Does left ventricular hypertrophy increase the incidence of reperfusion-associated ventricular fibrillation in a canine model of ischemia and reperfusion?
Does left ventricular hypertrophy increase the incidence of reperfusion-associated ventricular fibrillation in a canine model of ischemia and reperfusion?
Answers are grounded in this paper and cite their sources.
Left ventricular hypertrophy significantly increases the risk of reperfusion-induced ventricular fibrillation in a canine model, and this risk is not mitigated by lidocaine.
Important electrophysiological alterations that may predispose hearts to arrhythmias have been described for hypertrophied myocytes, and hypertrophy coupled with ischemia has been associated with an increased incidence of sudden death; however, an influence of hypertrophy on reperfusion arrhythmias has not been previously described. We hypothesized that reperfusion-associated arrhythmias would be potentiated by left ventricular hypertrophy. After induction of renovascular hypertension, 37 awake, unsedated dogs (17 with left ventricular hypertrophy and 20 without hypertrophy) underwent 15 minutes of coronary artery occlusion and reperfusion. All dogs were pretreated with lidocaine bolus injections and with lidocaine by continuous infusion during coronary occlusion and reperfusion. Reperfusion-associated ventricular fibrillation occurred in seven of 17 dogs with left ventricular hypertrophy versus one of 18 dogs without hypertrophy (p less than or equal to 0.05). The presence of hypertension was not significantly associated with an increased incidence of reflow ventricular arrhythmias. Neither QT interval nor area-at-risk was different between the dogs with and without reperfusion ventricular fibrillation; however, increased heart rate just before reperfusion did correlate with an increased incidence of ventricular fibrillation at reperfusion. Thus, 1) left ventricular hypertrophy was associated with a significantly increased incidence of reperfusion-induced ventricular fibrillation after 15 minutes of ischemia, 2) this increased incidence was independent of the presence of hypertension, and 3) lidocaine protected control and hypertrophied hearts against ventricular fibrillation during ischemia but was ineffective in protecting hypertrophied hearts against reperfusion-induced ventricular fibrillation.
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Taylor et al. (1990) studied Left ventricular hypertrophy and reperfusion arrhythmias (n=37). Left ventricular hypertrophy vs. Without left ventricular hypertrophy was evaluated on Reperfusion-associated ventricular fibrillation (p=<=0.05).
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