Ventricular Fibrillation and Shortening, Alternans and Afterdepolarizations of Epicardial Monophasic Action Potentials During Coronary Occlusion and Reperfusion

Abstract

entricular fibrillation (VF) occurs frequently in a setting of acute coronary occlusion and reperfusion, and constitutes a major cause of sudden cardiac death. The mechanisms of the induction of VF by coronary occlusion have been investigated in animal models by recording unipolar electrograms, 1 bipolar electrograms, 2 composite electrograms, 3 and by a mapping technique. 4 According to Kaplinsky et al, there are 2 peaks in the occurrence of ventricular arrhythmias early after acute coronary occlusion: the first peak occurs within 10 min (immediate ventricular arrhythmias) and the second peak occurs between 15 and 20 min (delayed ventricular arrhythmias). 3 The former is attributed to reentry based on a marked conduction delay in the subepicardial layer of the ischemic myocardium. However, ventricular arrhythmias can occur immediately after acute coronary occlusion even without a marked increase in activation time. 4 In such cases, reentry based on repolarization abnormalities, such as shortening or increased dispersion of repolarization, or other mechanisms, including triggered activity and abnormal automaticity, may be involved in the arrhythJapanese Circulation Journal Vol.63, March 1999 mogenesis. However, these possibilities remain to be confirmed, because repolarization abnormalities in ischemic myocardium cannot be examined by the techniques used in the previous studies. [1][2][3][4] Therefore, in the present study we examined the temporal relationship between the ischemia-and reperfusioninduced changes in monophasic action potential (MAP) configurations recorded from the epicardial ischemic zone and the occurrence of VF. We also examined the effects of the repetition of ischemia on MAP changes and the incidence of VF. MethodsThis study was performed in 32 mongrel dogs weighing 12-25 kg. The dogs were anesthetized with pentobarbital (30 mg/kg, iv), and additional doses were given when necessary to maintain anesthesia. The animals were intubated and ventilated with room air by a constant volumecycled respirator (Bird Corporation Mark7). The heart was exposed through a left thoracotomy and pericardotomy. The epicardial surface temperature was kept at 37-38°C with an overhead heat lamp. A cannula in the femoral vein was used to infuse normal saline at a rate of 100-200 ml/h to replace spontaneous fluid loss. A fluid-filled cannula was placed in the right femoral artery and connected to a transducer (Nihon Kohden model TP-400T) to monitor arterial blood pressure.The left anterior descending coronary artery (LAD) was The relationship between the occurrence of ventricular fibrillation (VF) and repolarization abnormalities of the ischemic and reperfused myocardium is poorly understood. The present study examined the temporal relationship between ischemia-and reperfusion-induced changes in monophasic action potential (MAP) configurations and the occurrence of VF, and assessed the effects of repetition of ischemia. The left anterior descending coronary artery of 32 anesthetized dogs was occluded twice for 5 mi...

Sodium-Hydrogen Exchange Inhibition During Ventricular Fibrillation

“…In this setting, prominent repolarization abnormalities occur that are characterized by shortening of the APD and change to a more triangular shape, decreased amplitude, APD alternans, and afterdepolarizations. 5,13 APD shortening is partly explained by opening of sarcolemmal K ϩ ATP channels. 14 However, recent evidence also implicates NHE-1 activation.…”