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Low‐Level But Not High‐Level Baroreceptor Stimulation Inhibits Atrial Fibrillation in a Pig Model of Sleep Apnea
Author(s) -
LINZ DOMINIK,
HOHL MATHIAS,
KHOSHKISH SHAYAN,
MAHFOUD FELIX,
UKENA CHRISTIAN,
NEUBERGER HANSRUPRECHT,
WIRTH KLAUS,
BÖHM MICHAEL
Publication year - 2016
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/jce.13020
Subject(s) - medicine , baroreceptor , anesthesia , atrial fibrillation , cardiology , stimulation , heart rate , obstructive sleep apnea , blood pressure
Baroreflex Stimulation and Atrial Fibrillation Background Obstructive sleep apnea (OSA) increases susceptibility to atrial fibrillation (AF) by a combined sympatho‐vagal hyperactivation. The purpose of this study was to investigate the effect of autonomic nervous system modulation by low‐level baroreceptor stimulation (LL‐BRS) compared to high‐level BRS (HL‐BRS) on atrial arrhythmogenic changes in a pig model of OSA. Methods and Results Sixteen pigs received tracheotomy under general urethane/chloralose anesthesia. Group 1 pigs (n = 8) received LL‐BRS (at 80% of that slowing sinus rate) for 3 hours and group 2 pigs (n = 8) received HL‐BRS (slowing sinus rate). Changes in atrial effective refractory period (AERP) and AF‐inducibility were determined during applied negative thoracic pressure (NTP) for 2 minutes before and at the end of the 3‐hour stimulation protocol. Group 1: LL‐BRS prolonged AERP from 150 ± 5 to 172 ± 19 milliseconds (P < 0.001). After 3 hours of LL‐BRS, NTP‐induced AERP‐shortening was diminished from –51 ± 10 milliseconds (–34%) to –22 ± 4 milliseconds (–13%) (P < 0.01). AF‐inducibility during NTP maneuvers decreased from 90% at baseline to 15% (P < 0.01). Group 2: HL‐BRS shortened AERP from 150 ± 17 to 132 ± 8 milliseconds (P = 0.024). After 3 hours of HL‐BRS, NTP‐induced AERP‐shortening was increased from –55 ± 7 milliseconds (–36%) to –72 ± 11 milliseconds (–54%) (P < 0.05) and AF‐inducibility was not affected. NTP‐induced changes in blood gases and blood pressure were not different between the groups. Conclusion LL‐BRS suppressed NTP‐induced AERP‐shortening and AF‐inducibility. By contrast HL‐BRS further perpetuated NTP‐induced AERP‐shortening and increased AF‐inducibility. These findings support only the use of LL‐BRS as a novel therapeutic modality to treat AF in OSA.