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Electrocardiograms were taken from a 44-year-old man with irregular ventricular parasystole in whom pure parasystolic cycles without any intervening nonectopic QRS complexes were found. When a sinus impulse fell late in the parasystolic cycle, it hastened occurrence of the next parasystolic discharge. This suggested that type I second degree entrance block occurred in the re-entrant pathway containing the parasystolic focus. When a sinus impulse fell early in the parasystolic cycle, it delayed occurrence of the next parasystolic discharge. This suggested that electrotonic modulation occurred in the parasystolic focus. As a result, the difference in length between the short form and the long form of the parasystolic cycle became markedly great. When the length of two adjacent sinus cycles ranged between the short and the long parasystolic cycle, manifest parasystolic QRS complexes disappeared for a long time. In true ventricular parasystole with pure ectopic cycles, such long disappearance has never been reported before.

This article explains the mechanism of "irregular" parasystole. Two theories have been suggested: "electrotonic modulation" and "type I second degree entrance block." This study attempts to clarify the mechanism of irregular parasystole in cases of true ventricular parasystole associated with ventricular parasystolic couplets. Cases associated with ventricular parasystolic couplets were selected from 37 clinical cases of true ventricular parasystole in which one or more pure parasystolic cycles with no intervening nonectopic QRS complexes were found. Of the 37 cases of true ventricular parasystole, ventricular parasystolic couplets were found in 4 cases. In none of the other 33 cases, ventricular parasystolic couplets were found. In all the cases coexisting with ventricular parasystolic couplets, the latter ectopic QRS complex of the couplet failed to reset the parasystolic rhythm. The above findings suggest that the latter ectopic QRS complex of the parasystolic couplet originated not in the parasystolic pacemaker but in the pathway between the ventricle and the parasystolic pacemaker. It seems that when a sinus impulse fell late in the parasystolic cycle, it passed through the site of second degree entrance block and that the parasystolic couplets originated from the reentrant pathway between the ventricle and the pacemaker. This strengthens our previous suggestion that the mechanism of irregular parasystole is governed by "type I second degree entrance block" and not by "electrotonic modulation."

Electrocardiograms were taken from a 67-year-old woman with high-degree atrioventricular block in which ventricular escape beats of right bundle branch block pattern occurred, accompanying occasional ventricular capture beats. Only when a sinus P wave occurred 0.60 s after the preceding escape beat, it was followed by a capture beat of left bundle branch block pattern with the RP interval of 0.60 s and the PR interval of 0.19 s. Similar left bundle branch block with left axis deviation pattern had been shown in the electrocardiogram taken 2 years before. Such RP and PR intervals in capture beats were invariable. These suggest that capture beats occurred as a result of supernormal conduction in the right bundle branch, which denies the possibility of ventricular extrasystoles. Such capture beats with the above RP and PR intervals were observed repeatedly.

A 79-year-old woman with atrial fibrillation was reported in whom apparent bradycardia-dependent right bundle branch block was suggested. When a conducted supraventricular impulse occurred within a critical period after the preceding conducted impulse, the impulse was blocked in the right bundle branch except when it fell in the supernormal period of the right bundle branch. When the conducted impulse occurred between the critical period and another longer period, it was conducted without bundle branch block. When the impulse occurred beyond that longer period, it was usually blocked in the bundle branch again. However, when the impulse occurred beyond a still longer period, it was conducted without bundle branch block again. These findings suggest that when impulses fell in the right bundle branch shortly after the preceding conducted impulses, they were blocked in both bundle branches; however, it seemed that concealed electrotonic conduction of the blocked impulses affected conduction of the subsequent impulses.

A clinical evaluation of the surface-averaged ECG (SAE) to record His-Purkinje activity (HPA) was made on 70 patients who underwent His bundle electrograms (HBE). The recorded signals first judged as HPA in 43 patients by the noninvasive method alone were later verified in 37 patients by HBE; the accuracy of the HPA recordings (predictive value) was 86.0%. The HPA-V interval measured noninvasively had a high correlation with the HV interval by HBE (r = 0.89, p less than 0.01). The verified detection rate in all 70 patients was 52.9%: HPA was detected in 12 of 18 patients (66.7%) with sclerotic and hypertensive heart disease (Group I), five of 19 patients (26.3%) with rheumatic heart disease (Group II), 11 of 17 patients (64.7%) with congenital heart disease (Group III), and nine of 16 patients (56.2%) with miscellaneous conditions (Group IV). The detection rate was markedly lower in Group II than in other groups (Group II vs Group I or III, p less than 0.025). The PR segment was significantly longer in the patients in whom HPA was detected than in those in whom it was not detected (71.5 +/- 22.3 msec vs 43.9 +/- 19.5 msec, p less than 0.001). His-Purkinje activity (HPA) was detected in 32 of 52 recordings (61.5%) with sinus rhythm and seven of 20 recordings (35.0%) with atrial fibrillation, including two recordings in each of two cardioverted patients (p less than 0.05). We conclude that the surface-averaged ECG (SAE) has clinically acceptable sensitivity and accuracy except in patients with rheumatic heart disease, short PR segments or atrial fibrillations.