Tomos E Walters1, Geoffrey Lee1, Steven Spence1, Marco Larobina1, Victoria Atkinson1, Phillip Antippa1, John Goldblatt1, Michael O'Keefe1, Prashanthan Sanders1, Peter M Kistler1, Jonathan M Kalman2. 1. From the Department of Cardiology (T.E.W., G.L., S.S., J.M.K.) and Department of Cardiothoracic Surgery (M.L., V.A., P.A., J.G., M.O.K.), Royal Melbourne Hospital, Melbourne, Australia; Department of Medicine, University of Melbourne, Melbourne, Australia (T.E.W., G.L., P.M.K., J.M.K.); Centre for Heart Rhythm Disorder, University of Adelaide and Department of Cardiology, Royal Adelaide Hospital, Adelaide, Australia (P.S.); and Department of Cardiology, Alfred Hospital and Baker IDI, Melbourne, Australia (P.M.K.). 2. From the Department of Cardiology (T.E.W., G.L., S.S., J.M.K.) and Department of Cardiothoracic Surgery (M.L., V.A., P.A., J.G., M.O.K.), Royal Melbourne Hospital, Melbourne, Australia; Department of Medicine, University of Melbourne, Melbourne, Australia (T.E.W., G.L., P.M.K., J.M.K.); Centre for Heart Rhythm Disorder, University of Adelaide and Department of Cardiology, Royal Adelaide Hospital, Adelaide, Australia (P.S.); and Department of Cardiology, Alfred Hospital and Baker IDI, Melbourne, Australia (P.M.K.). jon.kalman@mh.org.au.
Abstract
BACKGROUND: The pulmonary vein-left atrial (PV-LA) junction is key in pathogenesis of AF, and acute stretch is an important stimulus to AF. We aimed to characterize the response of the junction to acute stretch, hypothesizing that stretch would result in electrophysiological changes predisposing to re-entry. METHODS AND RESULTS: Fifteen participants undergoing cardiac surgery underwent evaluation of the right superior PV-LA junction using an epicardial mapping plaque. In 10, this was performed before and after atrial stretch imposed by rapid volume expansion, and in 5, it was performed with an intervening observation period. Activation was characterized by conduction slowing and electrogram fractionation transversely across the PV-LA junction, with lines of block also demonstrated perpendicular to the junction. Conduction was decremental (plaque activation time 135.8 ± 46.8 ms with programmed extra stimuli at 10 ms above effective refractory period versus 66.1 ± 22.9 ms with pacing at 400 ms; P<0.001) and percentage fractionation was greater with programmed extra stimuli at 10 ms above (33.5%± 15.3% versus 20.7%± 14.0%, P=0.001). Right atrial pressure increased by 2.5 ± 1.8 mm Hg (P=0.002) with volume expansion. Stretch resulted in conduction slowing across the PV-LA junction (increase in activation time 10.9 ± 14.6 ms in acute stretch group versus -0.1 ± 4.5 ms in control group; P=0.002). Conduction slowing was more marked with programmed extra stimuli at 10 ms above effective refractory period than with stable pacing (13.4 ± 16.5 ms versus 1.7 ± 5.4 ms; P=0.003). Stretch resulted in a significant increase in fractionated electrograms (7.9%± 7.0% versus -0.4 ± 3.3; P=0.004). CONCLUSIONS: Acute stretch results in conduction slowing across the PV-LA junction, with a greater degree of signal complexity. This substrate may be important in AF initiation and maintenance by promoting re-entry.
BACKGROUND: The pulmonary vein-left atrial (PV-LA) junction is key in pathogenesis of AF, and acute stretch is an important stimulus to AF. We aimed to characterize the response of the junction to acute stretch, hypothesizing that stretch would result in electrophysiological changes predisposing to re-entry. METHODS AND RESULTS: Fifteen participants undergoing cardiac surgery underwent evaluation of the right superior PV-LA junction using an epicardial mapping plaque. In 10, this was performed before and after atrial stretch imposed by rapid volume expansion, and in 5, it was performed with an intervening observation period. Activation was characterized by conduction slowing and electrogram fractionation transversely across the PV-LA junction, with lines of block also demonstrated perpendicular to the junction. Conduction was decremental (plaque activation time 135.8 ± 46.8 ms with programmed extra stimuli at 10 ms above effective refractory period versus 66.1 ± 22.9 ms with pacing at 400 ms; P<0.001) and percentage fractionation was greater with programmed extra stimuli at 10 ms above (33.5%± 15.3% versus 20.7%± 14.0%, P=0.001). Right atrial pressure increased by 2.5 ± 1.8 mm Hg (P=0.002) with volume expansion. Stretch resulted in conduction slowing across the PV-LA junction (increase in activation time 10.9 ± 14.6 ms in acute stretch group versus -0.1 ± 4.5 ms in control group; P=0.002). Conduction slowing was more marked with programmed extra stimuli at 10 ms above effective refractory period than with stable pacing (13.4 ± 16.5 ms versus 1.7 ± 5.4 ms; P=0.003). Stretch resulted in a significant increase in fractionated electrograms (7.9%± 7.0% versus -0.4 ± 3.3; P=0.004). CONCLUSIONS: Acute stretch results in conduction slowing across the PV-LA junction, with a greater degree of signal complexity. This substrate may be important in AF initiation and maintenance by promoting re-entry.
Authors: Yuriy V Egorov; Di Lang; Leonid Tyan; Daniel Turner; Evi Lim; Zachary D Piro; Jonathan J Hernandez; Rylie Lodin; Rose Wang; Eric G Schmuck; Amish N Raval; Carter J Ralphe; Timothy J Kamp; Leonid V Rosenshtraukh; Alexey V Glukhov Journal: J Am Heart Assoc Date: 2019-10-10 Impact factor: 5.501
Authors: Andrew P Holmes; Ting Y Yu; Samantha Tull; Fahima Syeda; Stefan M Kuhlmann; Sian-Marie O'Brien; Pushpa Patel; Keith L Brain; Davor Pavlovic; Nigel A Brown; Larissa Fabritz; Paulus Kirchhof Journal: PLoS One Date: 2016-05-05 Impact factor: 3.240