Aberrant Beats of Wolff-Parkinson-White Configuration in Arteriosclerotic Heart Disease

Abstract

Evidence has been presented by Prinzmetal et al. (1952) and Borduas et al. (1955) that electrocardiographic beats characterized by short P-R and long QRS intervals may occur in the absence of an accessory pathway by-passing the A-V node. In animal experiments, Prinzmetal observed beats of WPW type after repeated electrical stimulation of the A-V node, and noted in these same animals the spontaneous occurrence of various supraventricular tachycardias. Several arteriosclerotic patients studied by Prinzmetal demonstrated similar electrocardiographic phenomena, and at necropsy were found to have fibrotic disease of the A-V node and no accessory conduction system. These clinical and experimental observations indicate that WPW beats may occur on an acquired basis, secondary to nodal disease.In other experiments, Prinzmetal induced beats of WPW type in dogs after repeated ventricular stimulation with the A-V node intact. These observations harmonize with those of Kossman et al. (1950) who recorded such beats during cardiac catheterization when the catheter was in direct contact with the endocardial surface. Similar complexes have been observed by Prinzmetal during the course of acute myocardial infarction, frequently in association with ventricular premature beats and ventricular arrhythmias.On the basis of his extensive studies, including high-speed cinematographic techniques, Prinzmetal has deduced that accelerated conduction through part of the A-V node is responsible for aberrant complexes. He believes this to be true both in instances of nodal disease (" nodal " accelerated conduction) and ventricular irritability (" ventricular " accelerated conduction). In this latter type, the accelerated conduction through the A-V node may be on a reflex basis.Five instances of WPW aberration have been seen during the past two years in patients with arteriosclerotic heart disease. Of these, four are considered to be of acquired type, and only one an example of classical, congenital, Wolff-Parkinson-White syndrome (1954). CASE REPORTS Case 1. A 54-year-old man, who had had effort angina for one year, was admitted because of severe chest pain, of 48 hours' duration. The clinical course and serial electrocardiograms were characteristic of posterior wall infarction. On three separate occasions, the oral administration ot procaine amide or quinidine abolished the premature ventricular beats, the beats of WPW type, and the short runs of ventricular tachycardia.This case represents the " ventricular " type of acquired WPW aberration. In the experience of Prinzmetal (1952) " ventricular " WPW is usually associated with anterior infarction, and " nodal " WPW with posterior infarcts. Perhaps with increasing experience additional examples 301 on 12 May 2018 by guest. Protected by copyright.

The Wolff-Parkinson-White Syndrome and Second Degree Heart Block

“…In 1 ! )")(> Hoffman and associates (24) reported the case of a 62-year-old man who was admitted because of fatigue, dyspnea and inter mittent claudication. The electrocardiogram while being taken displayed spon taneous change from normal sinus rhythm to 2 :1 A-V block.…”