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This study seeks to elucidate whether there was a common mode of initiation of paroxysmal atrial fibrillation (PAF) episodes that might suggest new therapies.A library of 177 digitized and analyzed 24-hour Holter recordings from PAF pharmacotherapy trials was studied. All noise-free PAF episodesor =0.5 minutes were identified. PAF episodes and the preceding 2 minutes of sinus rhythm were printed as tachograms and visually inspected. Heart rate and ectopic beat behavior were used to characterize modes of PAF onset by comparing half-minute segments of the final 2 minutes of sinus rhythm.Thirty-four recordings (from 19 patients, aged 61.7 +/- 11.5 years) provided 231 PAF episodes suitable for analysis. No patients had a consistent mode of PAF onset. This was confirmed by systematic analysis of the five patients with the most episodes. Overall, a highly significant increase in ectopic beats, from 1.34 to 6.52 min(-1) (p0.001) was found, but heart rate did not significantly change (mean heart rate at onset = 64 beats/min). PAF was initiated by a solitary ectopic beat in more than half of the cases. No consistent evidence for short-long-short sequences, seen in ventricular arrhythmias, was found.The mode of onset of atrial fibrillation is inconsistent, both across a population with PAF and within individuals. This has implications for understanding the mechanisms of atrial fibrillation onset in human beings and for the treatment of the disorder.

We performed three consecutive 24-hour ECG recordings in 57 ambulatory patients approximately 8 to 11 days post-myocardial infarction. There was considerable additional detection of each type of complex ventricular ectopic beat (VEB) with recordings beyond 24 hours. Multiform, R-on-T, pairs, and bigeminy were often first detected from 24 to 48 hours and 5 of 12 patients with ventricular tachycardia had this rhythm detected only after 48 hours of monitoring. Complex forms were detected with short recording durations primarily in patients who had complex forms present during a large number of hours during the 72-hour recording session. The occurrence of each type of complex ectopic beat was strongly related to PVC frequency and some type of complex form was seen in virtually all 24-hour recordings with greater than a total of 100 VEBs. Sixty-five percent of 24-hour recordings with infrequent VEBs (2 to 10 per 24 hours) also had complex forms present. The day-to-day reproducibility of VEB frequency and complexity was reasonable, but was largely accounted for by the fact that most recordings were free of frequent ectopic beats and a given type of complex PVC. These data suggest that for longer ECG recording periods, the frequency of occurrence of complex forms rather than simply their presence or absence may be important for identifying high risk subgroups.

A 72-year-old man demonstrated persistent intermittent ventricular parasystole for 6 days during an acute inferior wall myocardial infarction. Entrance block failure occurred at a critical interval of 1.24 sec. after parasystolic beats with resetting of the parasystolic cycle length. The first ectopic beat in each parasystolic series showed coupling to its second preceding conducted beat, and successive cycle lengths in each series usually showed gradual shortening. Concealed extrasystolic bigeminy was also demonstrated between parasystolic series with the number of intervening conducted beats conforming to the formula 2n + 2. After interpolated parasystolic beats, this formula became 2n + 3.

By a delayed diastolic murmur is meant a murmur that cannot come at its usual time in diastole because of the occurrence of ventricular ectopic beats. Therefore, the murmur is delayed until the diastolic phase of the extrasystole. This delayed murmur is usually not recognized because it comes so long after the normal beat, and the sounds are associated with the ectopic beat itself. Phonocardiograms were made to illustrate this point in both mitral stenosis and aortic regurgitation. The possibility that such delayed diastolic murmurs may also be associated with lesions of the right side of the heart is suggested.

1.1. Comparison of contours of the following height-equalized pulses from the brachial artery has been made: (1) an intra-arterial pressure pulse versus an external pressure plethysmogram; (2) a pressure plethysmogram versus an impedance plethysmogram. Fifteen healthy young men and 8 men with cardiovascular disease were studied in this manner. 2.2. Intra-arterial pressure pulses versus pressure plethysmograms: At cuff pressures of 20 mm. Hg or less the contours by the two methods were identical in about two thirds of the cases; in the others the pressure plethysmograms were relatively larger throughout most of each cycle, event though their peak height was adjusted to equal that of the intra-arterial pressure pulse. With higher cuff pressures this relation became constant, i.e., all pressure plethysmograms had areas larger than those of the corresponding height-equalized pressure pulses. When pulses with unequal volume output were compared, as in the case of arrhythmias, the ratio of the pulse sizes with the two methods varied considerably. In every case the pressure plethysmogram preceded the corresponding intra-arterial pulse; this interval was variable and depended directly on the level of intra-arterial pressure at the moment of the ectopic beat. 3.3. Pressure plethysmograms versus impedance plethysmograms: Pulses obtained with either one of these methods were quite alike, and there was no trend in the minor differences in contour which were occasionally observed, even when the applied cuff pressure was varied between considerable levels. 4.4. These data indicate that pressure plethysmograms and arterial impedance plethysmograms, obtained with the techniques described herein, are arterial volume pulses, and differ from pressure pulses recorded from within the same vessel. They may provide further information on the properties of the artery under study, in addition to the information obtained by methods of intra-arterial pressure recording.

Three cases of parasystole with simple interference of two rhythms showing unusual features are described. In the first case the ectopic center was situated in the auriculoventricular bundle above the bifurcation. Combination beats were absent. Both rhythms were occasionally united when the protection of the ectopic center towards normal sinus stimuli disappeared. This phenomenon is explained by a supernormal phase of excitability of the ectopic center. The two other observations concern “intermittent parasystole” in which an ectopic center periodically appears and disappears. The first ectopic beat of each series is coupled to the preceding sinus beat and apparently elicited by the latter. Case 2 shows a parallel variation of the sinus rate and the rate of the ectopic center. Case 3 shows an interesting intraventricular disturbance of conduction following interpolated beats. It is emphasized that the term “protective block” is not applicable because we are not dealing with a zone of unidirectional block. The protection of the ectopic center against conducted stimuli is fully explained by its diminished excitability. Periodic changes of this excitability may cause the appearance and disappearance of parasystole. All three observations show temporary disappearance of the protection of a parasystolic center. This leads to hitherto unknown disturbances of rhythm and permits a better understanding of the mechanism of parasystole.