Electrotonic interactions across an inexcitable region as a cause of ectopic activity in acute regional myocardial ischemia. A study in intact porcine and canine hearts and computer models.
We recorded 60 DC simultaneous electrograms from isolated porcine and canine hearts in the first minutes after coronary occlusion. Ventricular premature beats (VPB) originated from the normal side of the ischemic border, which was frequently separated from the central ischemic area showing delayed activity by a small zone of inexcitable tissue. We attempted in a computer model to generate VPB's at one side of an area showing conduction block. In computer simulations,,, the presence of elements capable of automatic activity greatly facilitated the induction of VPB's. By coupling automatic elements to nonautomatic elements, overt pacemaking activity could be suppressed. Subthreshold depolarizations transmitted through a zone of conduction block could, when properly timed, trigger the latent automatic elements into overt automatic activity, resulting in single or repetitive VPB's. The ventricular premature beats in the intact hearts with acute regional ischemia may be caused by "triggered automaticity" in which the trigger is provided by the "injury current" flowing from ischemic cells showing delayed repolarization via a segment of inexcitable ischemic cells in the border zone to normally perfused cells with suppressed automaticity.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D003201:Computers; D003327:Coronary Disease / Q000503:physiopathology*; D004285:Dogs; D004562:Electrocardiography; D006327:Heart Block / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology; D008955:Models, Cardiovascular; D013552:Swine; D013610:Tachycardia / Q000503:physiopathology