Linking phenomenon during atrial stimulation with accessory pathways.
Linking is an electrophysiologic phenomenon in which each successive impulse entering a macroreentry circuit propagates preferentially along 1 limb because of the functional impedance to conduction in the contralateral limb produced by the previous impulse. Electrophysiologic studies were performed in 12 patients with a bidirectionally conducting accessory pathway. Linking was analyzed while 1:1 atrioventricular conduction took place through the normal pathway. When atrial pacing (at the same cycle length) could be initiated during sinus rhythm in patients with rapidly conducting accessory pathways, linking was dynamically maintained by repetitive local refractoriness (interference). When it could be initiated during the usual type of orthodromic circus movement tachycardia, linking was sustained by actual impulse collision, the underlying mechanism having also been called entrainment. When it could be initiated during sinus rhythm in a patient with a slowly conducting accessory pathway, linking was maintained by impulse collision, but the underlying mechanism could not be called entrainment because stimulation had not been started during tachycardia. This study showed that 2 terms--linking and entrainment--may be applied to the same mechanism and, conversely, that the same name could not be used in reference to the same mechanism when pacing was initiated under different circumstances. However, using the proposed conceptual formulation for linking, it is apparent that seemingly diverse mechanisms associated with macroreentry circuits involving accessory pathways are, in fact, variations on a common electrophysiologic theme.
D000293:Adolescent; D000328:Adult; D001283:Atrioventricular Node / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D004594:Electrophysiology; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D014927:Wolff-Parkinson-White Syndrome / Q000503:physiopathology* / Q000628:therapy