Sudden Wenckebach Periods and Their Relationship to Neurocardiogenic Syncope

• Published in: Pacing and clinical electrophysiology Vol. 21; no. 8; pp. 1580 - 1588
• Main Authors: CASTELLANOS, AGUSTIN, MOLEIRO, FEDERICO, ACOSTA, HELBERT, FERREIRA, ALEXANDRE, COX, MARILYN M., INTERIAN JR, ALBERTO, MYERBURG, ROBERT J.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.08.1998
• Subjects: Acute Disease; Adult; apparent type II AV block; Electrocardiography, Ambulatory; Female; Follow-Up Studies; Heart Block - etiology; Heart Block - physiopathology; Heart Rate; Humans; Male; Middle Aged; neurocardiogenic syncope; paroxysmal AV block; Prospective Studies; Syncope, Vasovagal - complications; Syncope, Vasovagal - physiopathology; type I AV block; vagal bloc
• ISSN: 0147-8389; 1540-8159
• DOI: 10.1111/j.1540-8159.1998.tb00246.x

Throughout a 9‐month period during which 1, 125 Hoiter tapes were reviewed prospectively we identified 13 non medicated 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 (± 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 11 included 2 patients with syncope. There were 26 episodes of sudden WP in Group 1. 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 A V 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 Hoiter findings in Group II appeared to refiect unusual (but natural, i.e., nonprovoked) electrocardiographic manifestations of certain patients with neurocardiogenic syncope.