Ventricular Fibrillation Induced Prior to Cardioplegic Arrest in Hypertrophied Pig Hearts

Abstract We hypothesized that by inducing ventricular fibrillation (VF) prior to cardioplegic arrest in nonvented hypertrophied hearts of pigs, the metabolic characteristics of the epicardial and endocardial regions would be compromised compared with animals in which cardioplegic solution was infused while the hearts were in normal sinus rhythm (NSR). These abnormalities would be reflected not only in greater deterioration of myocardial metabolism after reperfusion in the VF group, but they would also be more pronounced in the subendocardial layers of hypertrophied left ventricles. Results obtained in hypothermic hearts (28°C) maintained at 8° to 12°C during cardioplegic arrest demonstrated no major consistent differences in the stores of glycogen, creatine phosphate, adenine nucleotides, and lactate in both groups of hearts, for either layer of the left ventricular myocardium. The only significant difference was slightly lower creatine kinase content in the VF hearts than in the NSR group. It is concluded that induction of VF in hypothermic (28°C), nonvented, hypertrophied hearts prior to infusion of cardioplegic solution does not affect myocardial energy stores compared with hearts in NSR, provided that the period of VF prior to clamping is short (3 minutes) and that the myocardial temperature is lowered to 28°C prior to VF and is maintained at 8° to 12°C during cardioplegic arrest.