Conduction disturbances of the bundle branches produced by lesions in the nonbranching portion of His bundle.

The present experiments were conducted on isolated dog hearts to demonstrate that conduction disturbances can be induced in the bundle branches by transection of about 50 per cent of the cross-sectional area of the His bundle on the right or left side. The His bundle, the posterior and anterior divisions of left bundle, and the right bundle were exposed by careful dissection, and microelectrode techniques were used to record action potentials from the three bundle branches. Pacing stimuli were applied to the nonbranching portion of His bundle proximal and then distal to the site of transection to study the effect of such lesions on impulse conduction to the bundle branches. It was demonstrated that conduction to the bundle branches was not affected by such lesions in the His bundle at pacing rates slower than 100 per minute; however, conduction disturbances were rate-dependent and manifested at faster pacing rates. In nine out of all 16 experiments, partial or complete block occurred in all three bundle branches regardless of the side of the lesion. In the remaining seven experiments, they were observed in the bundle branch on the same side as the lesion. It was assumed that conduction disturbances of the bilateral bundle branches resulted from decremental conduction in the uncut portion of His at the level of lesion, and those of the ipsilateral branch from the functional failure of transverse crossover connections between the longitudinal His bundle fibers. The results indicate that localized lesions in the nonbranching portion of His bundle can indeed produce the pattern of bundle branch block under certain conditions.

Anomalous communication of the left coronary artery with a peripheral branch of the right pulmonary artery.

A 64-year old man had a history of two myocardial infarctions recurrent episodes of paroxysmal ventricular tachycardia and hemoptysis. Cineangiocardiographic studies showed an anomalous vessel connecting the left coronary artery with a peripheral branch of the right pulmonary artery. Although several coronary obstructive lesions and abnormalities in the distribution of the circumflex branches were found, the anomaly apparently produced a real "pulmonary steal" and, thereby a worsening of the coronary insufficiency. We believe that this is the first reported case in the literature with such a coronary-pulmonary fistula. The angiographic findings are presented in detail, and the possible factors in the development of myocardial ischemia are discussed.

Facilitation of A-V nodal reciprocation by procainamide.

Procainamide is known to depress conduction through the A-V node, and this property may facilitate the development of ventricular reciprocal beats or echoes. The occurrence of ventricular reciprocal beats was studied in 20 open-chest dogs before and after the administration of procainamide. While the ventricle was paced by basic stimuli, early ventricular premature beats were introduced at various coupling intervals to induce ventricular echoes. When ventricular echoes could be induced in a given heart, there was a continuous range of coupling intervals (or echo zone) within which ventricular echoes occurred. In the control state, no echo occurred in eight dogs and the echoes developed in 12 dogs with the mean echo zone of 38.3 msec. The effect of procainamide was studied at its therapeutic blood levels about 25 minutes after an intravenous injection of the drug in a dose of 10 mg. per kilogram. Of the first group of eight dogs, in which no echo occurred in the control state, four dogs developed ventricular echoes after the administration of procainamide with the mean echo zone of 29.3 msec. for the group. Of the second group of 12 dogs, in which ventricular echoes were induced in the control state, the administration of procainamide increased the echo zone in 10 dogs with the mean echo zone of 67.8 msec. for the group. Ventricular reciprocal beats were often sustained to produce short runs of supraventricular tachycardia in five dogs after the administration of procainamide. The results demonstrated a potentially deleterious effect of procainamide in facilitating the inducation of A-V nodal reciprocation by closely coupled ventricular premature beats.

Effect of ventricular aberrancy on fibrillation threshold.

VFT's were determined in 12 open-chest dogs at epicardial sites in the right and left ventricles (RV and LV) following normally or aberrantly conducted beats. The normal beats were produced by right atrial pacing, and the aberrant beats by surgical RBBB or ventricular pacing at an RV or LV site. The mean VFT following normal beats was 21.2 plus or minus 1.8 ma. in RV and 23.0 plus or minus 2.7 ma. in LV. The mean VFT following aberrant beats of RBBB was 21.3 plus or minus 2.6 ma. in RV and 25.0 plus or minus 2.8 ma. in LV. The difference between the mean VFT of normal beats and that of aberrant beats was not statistically significant. The mean values of VFT's determined in RV or LV following aberrant beats produced by pacing of the contralateral ventricle were not significantly different from those of the normal beats. The mean VFT was 22.9 plus or minus 3.1 ma. in RV and 20.1 plus or minus 2.1 ma. in LV. These results indicate that the aberrancy of ventricular beats per se is not associated with decreased VFT or increased ventricular vulnerability to fibrillation. The most predictable observation was that the mean VFT's were significantly lower in both ventricles when they were determined at the site of application of pacing stimuli. The mean values were 12.4 plus or minus 1.2 ma. in RV and 13.6 plus or minus 1.6 ma. in LV. This decrease in VFT may be due to slow conduction and increased asynchrony of recovery of excitability at or near the site of application of pacing stimuli.