Does myocardial infarction alter the monophasic action potential duration and effective refractory period across different layers of the ventricular myocardium in vivo?
Myocardial infarction induces significant and differential changes in the action potential duration and effective refractory period across ventricular layers, particularly in mid-myocardial cells, which may provide a substrate for post-MI arrhythmias.
BACKGROUND: The relationship between monophasic action potential duration (MAPD) and effective refractory period (ERP) is poorly understood after myocardial infarction (MI) in vivo. METHODS AND RESULTS: Forty rabbits were randomized into either a sham operation (SO) group (n=10) or MI group (n=30), both of which underwent thoracotomy, but the left anterior descending coronary artery was occluded in the MI group only. The MAPD and ERP of the endocardial, midmyocardial and epicardial cells of the infarction zone were observed at baseline, 2 days after thoracotomy and then 5 min, 15 min, 30 min, 2 days, 14 days and 60 days after coronary occlusion (CO). At baseline, ERP correlated strongly with MAPD90. During the 5-30 min after CO, both MAPD90 and ERP of the 3 layers of the myocardium shortened markedly (eg, MAPD90 Mid) was approximately 50% of the baseline value at 5 min after CO). MAPD90 and ERP recovered gradually over the 2-60 days after MI. ERPMid exceeded MAPD90 Mid and the post repolarization refractoriness phenomenon appeared during the 5-30 min after CO. CONCLUSIONS: The different changing trends of the MAPD and ERP of the mid-myocardial cells may underlie the arrhythmias that occur after MI.
Huang et al. (Thu,) studied this question.