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Analysis of 21 episodes of vagal-induced atrioventricular block showed that the uncorrected QT intervals at the end of the corresponding RR pauses were not prolonged, in reference to the pre-block QT intervals, with pauses shorter than 1,280 ms. Subsequently, they gradually lengthened as the RR pauses progressively increased to 13,710 ms. This dynamic behavior of the QT interval in subjects without structural heart disease could have resulted from a complex interaction between the cumulative effects of previous cycle lengths (memory effect?) and the autonomic nervous system.

A subgroup of patients with neurocardiogenic syncope and negative electrophysiologic studies and adenosine tests (in 5 of 6 cases), who developed symptomatic paroxysmal atrioventricular block in the natural, ambulatory state, had positive tilt tests without advanced block. Lack of concordance between electrocardiographic changes may have reflected differential effects of the autonomic nervous system in the sinus and atrioventricular nodes, occurring in diverse circumstances and less likely because of the protocol used for tilt testing.

The modes of regression of very high degrees of atrioventricular nodal block (> or = 8:1) were studied in patients with atrial flutter and a specific variant of the tachycardia-bradycardia syndrome. The occurrence of reverse alternating Wenckebach periods, previously reported only in 2:1 atrioventricular block, emphasizes the complexities of multilevel block.

Throughout a 9-month period during which 1,125 Holter tapes were reviewed prospectively we identified 13 nonmedicated patients with an arrhythmia, which for the purposes of this presentation was categorized, because of their mode of initiation, as sudden Wenckebach periods (WP). The episodes emerged abruptly from a normal (< or = 200 ms) PR interval with sudden prolongation of PR and PP intervals (and reversed PR-RP relationship) that took place over 1-8 cycles. The postpaced PR interval was shorter than that of the last conducted beat. The episodes were separated into two groups. Group I included 11 patients with symptoms other than syncope and Group II included 2 patients with syncope. There were 26 episodes of sudden WP in Group I. Twenty-five terminated in a single (and one in double) blocked P waves. Most episodes occurred between 10 PM and 7 AM. Symptoms did not correlate with the episodes. Mean 24-hour rates were < 90. In Group II there were 22 episodes, all occurring between 6 AM and 10 PM. The mean sinus cycle lengths before the phenomenon started to occur in Group I (861 +/- 185 ms) as well as the cycle lengths at the onset of block (1,096 +/- 215 ms) were statistically longer than those in Group II (591 +/- 40 ms and 747 +/- 63 ms, respectively, P < 0.0001). Although the mode of onset in the episodes in Group II was similar to Group I, 16 episodes terminated in 2-6 blocked P waves. Thus, the entire number of episodes could be categorized as an unusual type (because of the PR prolongation) of paroxysmal, or advanced second degree AV block. Because these patients had negative electrophysiological studies, positive tilt tests, and absent syncope after oral propranolol therapy, they were considered as having neurocardiogenic syncope. In addition, the faster than normal (> 100) mean 24-hour rates) suggested that they also had so-called inappropriate sinus tachycardia. In summary, Group I consisted of patients with a normal, benign, vagal-induced second-degree AV block, whereas the Holter findings in Group II appeared to reflect unusual (but natural, i.e., nonprovoked) electrocardiographic manifestations of certain patients with neurocardiogenic syncope.

A 53-year-old patient had a complex ventricular arrhythmia, which most likely was an intermittent pure (nonmodulated) parasystole, due to protection limited to the first part of the cycle coexisting with exit block. However, other interpretations of the observations were possible. Foremost among these was modulated parasystole with partial protection or with an attenuated or nondetectable early delaying phase, with exit block. Interestingly, the parasystole appeared to have fulfilled the dynamic rules regarding the number of sinus beats interposed between manifest parasystolic beats, as has been reported for pure or weakly modulated parasystole. This case corroborates unusual manifestations of an arrhythmia, which because of its newly found complexities and various possible interpretations seems to be discussed with decreasing frequency in most textbooks on general cardiology.

In summary, the irregular dynamics of progression of 4:1 AV block in atrial flutter, presumably different from those observed in similar degrees of rate-dependent block, most likely reflected the complex electrophysiologic mechanisms operating during the highest degrees of AV nodal block. Occurrence of previously undescribed arrhythmias, namely Wenckebach periods during 4:1 and 6:1 block, tends to support the multilevel block hypothesis.

Clinical, surface ECG, and intracardiac findings were analyzed in 20 patients with spontaneous conduction disturbances in whom vagally mediated AV block could be induced by carotid sinus pressure during electrophysiologic evaluation. The latter demonstrated that the surface ECG pattern attributed to bradycardia-dependent (phase 4), and paroxysmal block within the His bundle and bundle branches could reflect vagally mediated, bradycardia-associated (rather than bradycardia-dependent), and paroxysmal AV nodal (AH) block. The decision regarding the use of pacemakers was not based on QRS duration or on patterns (or site) of block but on the underlying clinical settings and the correlation of symptoms with maximal ventricular (R-R) pauses. However, more studies are required to extend our findings, especially to other subgroups of patients (or normal individuals) in whom vagally mediated block occurs.

Short runs of symptomatic atrioventricular (A-V) block occurred after spontaneous cessation of reciprocating A-V junctional tachycardia in a patient with right bundle branch block, normal H-V interval and sinus nodal dysfunction. These episodes were characterized by long (more than 1 sec) P-P intervals during which the A deflections were not followed by His bundle electrograms. Three possible explanations are: (1) a posttachycardia-induced period of abnormally prolonged A-V nodal refractoriness; (2) pseudo-A-V block produced by concealed A-V junctional tachycardia, or (3) bradycardia-dependent (phase 4) A-V block at the "upper" His bundle, above the site from which the H deflection was recorded.