Ischemic Preconditioning and Left Ventricular Dysfunction: A Novel Mechanism & Model for Pulseless Electrical Activity

Abstract

AbstractBackgroundPulseless electrical activity (PEA) is a very common rhythm in cardiac arrest and survival is ≈ 5%. Population data suggest coronary ischemia significantly contributes to PEA, but the mechanism is unknown.ObjectivesWe hypothesize ischemic preconditioning (IPC) in the setting of left ventricular (LV) dysfunction can convert ischemia-induced ventricular fibrillation (VF) into ischemia-induced PEA.MethodsUsing percutaneous coronary interventions in anesthetized swine, we studied the effect of IPC prior to ischemia on arrhythmic burden in normal animals and in animals with LV dysfunction. IPC protocol: four cycles of three minutes of coronary occlusion followed by seven minutes of reperfusion. Chronic LV dysfunction protocol: two serial infarcts in two coronary territories, separated by one week of recovery.ResultsIn normal animals, IPC prior to ischemia significantly reduced VF incidence (2/8 IPC vs. 7/8 control). In IPC animals with VF, the time to VF was significantly delayed (37.2 ± 7.3 min vs. 20.7 ± 4.9 min, p<0.005). In chronic LV dysfunction animals (EF 15% ± 5%), ischemia caused PEA in all animals (18/18). In non-preconditioned animals, VF followed PEA in all cases (12/12). In preconditioned animals, PEA sustained without VF in 2/6 animals. In 4/6 animals, PEA was prolonged and time to VF was significantly delayed compared to non-preconditioned animals (33.7 ± 7.8 min vs. 12.2 ± 5.0 min, p<0.0001).ConclusionIPC delays/prevents VF. IPC with LV dysfunction prior to ischemia produces prolonged PEA. IPC with LV dysfunction prior to ischemia is likely an important mechanism for human PEA arrest. This is the first animal model of ischemic pulseless electrical activity.