Cellular electrophysiologic characteristics of surviving subendocardial fibers in chronically infarcted right ventricular myocardium susceptible to inducible sustained ventricular tachycardia.
Permanent occlusion of the right coronary artery (RCA) is associated with inducible sustained ventricular tachyarrhythmias (VT) during days 3 to 10 post RCA occlusion period in the conscious dog; VT could no longer be induced beyond this post occlusion period. The aims of the present study were to determine if subendocardial (SE) fibers in the infarcted right ventricle (RVI) during both inducible and noninducible phases of VT remain viable, and if so, to characterize their transmembrane potential properties with the microelectrode and to assess their morphologic features. The RCA was occluded in 13 closed-chest anesthetized dogs with intracoronary balloon inflation. In one group (N = 7), the infarcted tissues were isolated during the VT inducible phase and in another group (N = 6) these tissues were isolated during the VT noninducible phase. Resting membrane potential, action potential amplitude, maximum upstroke velocity, and action potential duration of the surviving SE Purkinje fibers (PF) and ventricular muscle (VM) in the IZ (first layer) were not significantly different in the two groups. Conduction velocity for both basic and premature stimuli from the base to the apex were similar in the two groups. Rapid stimulation at cycle lengths of 300 to 200 msec failed to induce triggering of automatic activity in the two groups. Electron microscopy of SEPF in the IZ showed a drastic reduction in cytosolic lipid droplet accumulation when compared to 24-hour-old infarct. We conclude that: (1) SEPF and VM network in the infarct zone remain electrically viable during the chronic phase of RVI; (2) transmembrane potential properties of this fiber network remain constant and independent of temporal changes of VT inductibility; and (3) ultrastructural improvement of this fiber network suggests an evolution toward normalcy.
D000200:Action Potentials; D000818:Animals; D002304:Cardiac Pacing, Artificial; D002908:Chronic Disease; D003327:Coronary Disease / Q000150:complications; D004198:Disease Susceptibility; D004285:Dogs; D004594:Electrophysiology; D004727:Endothelium / Q000473:pathology / Q000503:physiopathology; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology*; D006352:Heart Ventricles; D008297:Male; D009132:Muscles / Q000473:pathology / Q000503:physiopathology; D009203:Myocardial Infarction / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology / Q000648:ultrastructure; D011690:Purkinje Fibers / Q000503:physiopathology*; D013610:Tachycardia / Q000209:etiology*