Proximal His-Purkinje conduction defects due to peripheral myocardial ischemia and infarction.

Abstract

Clinical reports have described 2:1 A-V block distal to the recorded His bundle potential which was induced by sudden, rapid atrial pacing. This functional effect was thought to be a normal variant of refractoriness in the His-Purkinje system. Using standard ECG leads and His bundle recordings, 10 control and 3 sham operated dogs were studied. No incidence of 2:1 A-V block distal to the His bundle potential in response to abrupt rapid atrial pacing (from 50-90 beats/min to 250-330 beats/min) was observed. Also in response to closely coupled atrial premature beats (H-H equal to 250-300 msec) aberrant QRS complexes were seen but H-V delays were restricted to a range from 35 to 50msec. Another group of 13 anesthetized dogs was studied using similar methods and pacing procedures 3 to 10 days after left anterior descending artery ligation. In 4 dogs, high grade stenosis (equal to or greater than 70%) was induced and these dogs studied 4 to 22 days later. In the 13, postmortem examination revealed the area of gross infarction was localized to the apical and midseptal portions of anterior wall of left ventricle not involving the His bundle or proximal bundle branches. Eight of the 13 (62%) showed 2:1 A-V block distal to the recorded His bundle potential in response to abrupt rapid atrial pacing. In addition, presented are evidences of intra-His bundle block (marked widening of H potentials) and marked prolongation of H-V intervals (35-80 msec) in response to atrial premature beats with H-H intervals similar to those of the control group. Furthermore, in association with the prolonged H-V intervals of aberrant beats, ventricular echo beats localized within the His-Purkinje system were noted. In the 4dogs with high grade stenosis, 3 showed functional 2:1 A-V block distal to the His bundle potential. We suggest that substances released from peripheral ischemic or necrotic tissue can alter the refractoriness of conduction in non-infarcted areas, e.g., non-ischemic His-Purkinje system. Such conduction defects can lead to functional 2:1 A-V block distal to the His bundle recording and/or reentrant arrhythmias localized within the His-Purkinje system.