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(Circulation. 2003;107:1816.)
© 2003 American Heart Association, Inc.
Basic Science Reports |
From the Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis.
Correspondence to Jeffrey E. Olgin, MD, Krannert Institute of Cardiology, Noyes Pavilion/Room E410, 1800 N Capitol Ave, Indianapolis, IN 46202. E-mail jolgin{at}iupui.edu
Background It has recently been recognized that atrial fibrillation can originate from focal sources in the pulmonary veins (PVs). However, the mechanisms of focal atrial fibrillation have not been well characterized. We assessed the electrophysiological characteristics of the PVs using high-resolution optical mapping.
Methods and Results Coronary-perfused, isolated whole-atrial preparations from 33 normal dogs were studied. Programmed electrical stimulation was performed, and a 4-cm2 area of the PV underwent optical mapping of transmembrane voltage to obtain 256 simultaneous action potentials. Marked conduction slowing was seen at the proximal PV, compared with the rest of the vein, on both the epicardial (31.3±4.47 versus 90.2±20.7 cm/s, P=0.001) and endocardial (45.8±6.90 versus 67.6±10.4 cm/s, P=0.012) aspects. Pronounced repolarization heterogeneity was also noted, with action potential duration at 80% repolarization being longest at the PV endocardium. Nonsustained reentrant beats were induced with single extrastimuli, and the complete reentrant loop was visualized (cycle length, 155±30.3 ms); reentrant activity could be sustained with isoproterenol. Sustained focal discharge (cycle length, 330 to 1100 ms) was seen from the endocardial surface in the presence of isoproterenol; each focus was localized near the venous ostium.
Conclusions The normal PV seems to have the necessary substrate to support reentry as well as focal activity. Although reentry occurred more distally in the vein, focal activity seemed to occur more proximally.
Key Words: atrium fibrillation electrophysiology mapping
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