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Stimulation of the Intrinsic Cardiac Autonomic Nervous System Results in a Gradient of Fibrillatory Cycle Length Shortening Across the Atria During Atrial Fibrillation in Humans
Author(s) -
LIM PHANG BOON,
MALCOLMELAWES LOUISA C.,
STUBER THOMAS,
KOJODJOJO PIPIN,
WRIGHT IAN J.,
FRANCIS DARREL P.,
WYN DAVIES D.,
PETERS NICHOLAS S.,
KANAGARATNAM PRAPA
Publication year - 2011
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.2011.02097.x
Subject(s) - medicine , atrial fibrillation , coronary sinus , cardiology , atropine , autonomic nervous system , atrium (architecture) , vagal tone , stimulation , anesthesia , refractory period , heart rate , blood pressure
Autonomic Stimulation Promotes AFCL Gradients in AF. Introduction: The intrinsic cardiac autonomic nervous system (ANS) is implicated in atrial fibrillation (AF) but little is known about its role in maintenance of the electrophysiological substrate during AF in humans. We hypothesized that ANS activation by high‐frequency stimulation (HFS) of ganglionated plexi (GP) increases dispersion of atrial AF cycle lengths (AFCLs) via a parasympathetic effect.Methods and Results:During AF in 25 patients, HFS was delivered to presumed GP sites to provoke a bradycardic vagal response and AFCL was continuously monitored from catheters placed in the pulmonary vein (PV), coronary sinus (CS), and high right atrium (HRA). A total of 163 vagal responses were identified from 271 HFS episodes. With a vagal response, the greatest reduction in AFCL was seen in the PV adjacent to the site of HFS (16% reduction, 166 ± 28 to 139 ± 26 ms, P < 0.0001) followed by the PV‐atrial junction (9% reduction, 173 ± 21 to 158 ± 20 ms, P < 0.0001), followed by the rest of the atrium (3–7% reduction recorded in HRA and CS). Without a vagal response, AFCL changes were not observed. In 10 patients, atropine was administered in between HFS episodes. Before atropine administration, HFS led to a vagal response and a reduction in PV AFCL (164 ± 28 to 147 ± 26 ms, P < 0.0001). Following atropine, HFS at the same GP sites no longer provoked a vagal response, and the PV AFCL remained unchanged (164 ± 30 to 166 ± 33 ms, P = 0.34).Conclusions:Activation of the parasympathetic component of the cardiac ANS may cause heterogenous changes in atrial AFCL that might promote PV drivers. (J Cardiovasc Electrophysiol, Vol. pp. 1‐8)