Electrocardiographic manifestations of dual atrioventricular node conduction during sinus rhythm.
OBJECTIVE
The objective of this study was to correlate electrocardiographic (ECG) PR interval changes during normal sinus rhythm with recent observations regarding the anatomy and physiology of the dual, slow and fast atrioventricular (AV) pathways.


BACKGROUND
The least common manifestation of dual AV conduction is an abrupt PR interval change in the setting of sinus rhythm. Whereas isolated cases of this phenomenon have been reported, the relatively large series we have collected makes it possible to correlate the ECG findings with the anatomy, composition and electrophysiology of the dual AV pathways.


METHODS
The ECGs of 21 patients with sinus rhythm and PR interval changes consistent with dual AV node physiology were studied. Observations include duration of the short and long PR intervals, the difference between the two and the events responsible for the PR interval change.


RESULTS
Eighteen of the 21 ECGs exhibited an abrupt and persistent PR interval change. Two of the other three ECGs manifested PR interval alternans, with slow and fast pathway, and a Wenckebach type I AV block; in the third ECG, findings compatible with simultaneous conduction along both pathways in response to a single stimulus were noted. Events responsible for the PR change included atrial premature complexes, atrial tachycardia, interpolated ventricular premature complexes and interpolated junctional premature complexes. In two the PR interval change appeared during a regular sinus rhythm.


CONCLUSIONS
The behavior of the PR interval is consistent with dual AV conduction. The PR interval duration hypothesized to represent slow pathway conduction is in keeping with the calculated anatomic length of the slow pathway. The Wenckebach type I block in the slow and fast pathways, as well as the altered conduction time in the slow pathway parallel with changing sinus rate, is evidence that the pathway is influenced by autonomic (?parasympathetic) innervation, supporting the premise that the pathways contain AV node-like tissue.
Fisch
C
C
Krannert Institute of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis 46202, USA.
Mandrola
J M
JM
Rardon
D P
DP
D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D001283:Atrioventricular Node / Q000503:physiopathology*; D004562:Electrocardiography; D006327:Heart Block / Q000503:physiopathology; D006801:Humans; D013611:Tachycardia, Atrioventricular Nodal Reentry / Q000503:physiopathology; D018879:Ventricular Premature Complexes / Q000503:physiopathology