Electroide cather recording during malignant ventricular arrythmia following experimental acute myocardial ischemia. Evidence for re-entry due to conduction delay and block in ischemic myocardium.

In 20 anesthetized opened-chest dogs, plunge wire and electrode catheter recordings of the this bundle electrogram which also showed septal activation, were monitored before and after ligation of the anterior septal artery. The average time to onset of ventricular tachycardia after ligation was 5-1/2 min. The evolution of the arrhythmia was temporally related to progressive fragmentation and delay of the septal potential, resulting in a marked increase in total ventricular activation time (up to 335 msec). In six experiments the fragmented, delayed septal depolarization was inscribed well beyond the T wave of the surface QRS prior to the onset of arrhythmias. Various conduction disorders involving the ischemic septal myocardium were observed which closely correlated to the patterns of conduction disorder in the ischemic proximal His-Purkinje system. First degree block, 2 degree block of the Mobitz II and Wenckebach types, higher degree block and paroxysmal complete block occurred. The onset of the arrhythmia was characteristically associated with a Wenckebach pattern of conduction delay of a part of the septal deflection. Conduction disorders of the ischemic myocardium were tachycardia-dependent. Bradycardia resulted in recovery of form, duration, and timing of the septal potential with the coincident disappearance of ventricular arrhythmias. The study shows that the basic prerequisites for re-entry do exist during the early period following occlusion of a major coronary artery and can explain the malignant phase of ventricular arrhythmias. Similar disorders in man may be detected by intracardiac electrode catheter recordings.