SUDDEN WENCKEBACH PERIODS AND THEIR RELATIONSHIP TO NEUROCARDIOGENIC SYNCOPE

Citation
A. Castellanos et al., SUDDEN WENCKEBACH PERIODS AND THEIR RELATIONSHIP TO NEUROCARDIOGENIC SYNCOPE, PACE, 21(8), 1998, pp. 1580-1588
Citations number
50
Categorie Soggetti
Cardiac & Cardiovascular System","Engineering, Biomedical
Journal title
PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY
ISSN journal
01478389 → ACNP
Volume
21
Issue
8
Year of publication
1998
Pages
1580 - 1588
Database
ISI
SICI code
0147-8389(1998)21:8<1580:SWPATR>2.0.ZU;2-1
Abstract
Throughout a g-month period during which 1,125 Holter tapes were revie wed prospectively we identified 13 nonmedicated patients with an arrhy thmia, which for the purposes of this:presentation was categorized, be cause of their mode of initiation, as sudden Wenckebach periods (WP). The episodes emerged abruptly from a normal (less than or equal to 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 post paced PR interval was shorter than that of the last conducted beat. Th e episodes were separated into two groups. Group I included 11 patient s with symptoms other than syncope and Group II included 2 patients wi th syncope, There were 26 episodes of sudden WP in Group I. Twenty-fiv e terminated in a single (and one in double) blocked P waves. Most epi sodes 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 (592 +/- 40 ms an d 747 +/- 63 ms, respectively, P < 0.0001). Although the mode of onset in the episodes in Group II was similar to Group 1, 26 episodes termi nated in 2-6 blocked P waves. Thus, the entire number of episodes coul d be categorized as an unusual type (because of the PR prolongation) o f paroxysmal, or advanced second degree AV block. Because these patien ts had negative electrophysiological studies, positive tilt tests, and absent syncope after oral propranolol therapy, they were considered a s having neurocardiogenic syncope. In addition, the faster than normal (> 100) mean 24-hour rates) suggested that they also had so-called in appropriate sinus tachycardia. In summary, Group I consisted of patien ts with a normal, benign, vagal-induced second-degree AV block, wherea s the Holter findings in Group II appeared to reflect unusual (but nat ural, i.e., nonprovoked) electrocardiographic manifestations of certai n patients with neurocardiogenic syncope.