Ventricular Arrhythmias in Acute Coronary Artery Ligation in Dogs: Electrophysiological Mechanism and Its Relation to the Severity of Myocardial Ischemia

Analysis of conduction characteristics within the ischemic myocardium and the incidence of ventricular arrhythmias for the first 30 minutes of coronary artery ligation identified two phases of ventricular arrhythmias with different electrophysiological mechanisms. The first phase appearing during 2–10 minutes (immediate ventricular arrhythmias: IVA) was closely related to the degree of epicardial delay and thus considered to be initiated by reentry within the ischemic epicardial zone. In contrast, the second or delayed phase (12—30 minutes, delayed ventricular arrhythmias: DVA) of ventricular arrhythmias appearing independently from epicardial delay was suggested to originate from the subendocardial Purkinje network, since endocardial activation of the ischemic zone consistently preceded the QRS complexes of ventricular arrhythmias. Measurements of myocardial adenosine triphosphate (ATP) contents demonstrated that in animals developing a profound myocardial ischemia by 3 — 5 minutes, epicardial delay was not observed and thereby IVA was not initiated. In contrast, epicardial delay and IVA were associated with a significant, but milder or slower ischemic process. At the time of DVA, myocardial ATP contents were at extremely low levels for both groups with and without DVA, supporting the concept that DVA is not originated from the ischemic myocardial cells, but from Purkinje fibers depressed secondarily by surrounding ischemic myocardial cells.