Arrhythmogenic Substrate of the Pulmonary Veins Assessed by High-Resolution Optical Mapping

Abstract

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-cm 2 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 (31.3Ϯ4.47 versus 90.2Ϯ20.7 cm/s, Pϭ0.001) and endocardial (45.8Ϯ6.90 versus 67.6Ϯ10.4 cm/s, Pϭ0.012) 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, 155Ϯ30.3 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.

A mathematical model of the unidirectional block caused by the pulmonary veins for anatomically induced atrial reentry

“…But, conduction failure does not occur, possibly due to the absence of anisotropy. Since the propagation follows the direction of anisotropy in the atrium with increased conduction velocity, the decrease of the conduction speed can be more dramatic in the actual atrium as in vivo observed by Arora et al [1]. This phenomenon seems to confirm the dominance of the circumferential anisotropy in the actual PV as reported in ref.…”

“…Numerous experimental and clinical studies have been reported to support this phenomenon [1][2][3][4] and have been used to develop a series of successful surgical procedures by isolating the PVs with ablation lesions in the left atrium (LA) [5][6][7]. Many hypotheses have been proposed as the microscopic or macroscopic cause of the PV reentry but can be classified into four major types [8]: the first hypothesis is on the properties of the PV cells for a pacemaker such as voltage-dependent Ca i release [9], different cell morphology [10] and intracellular calcium transients [10].…”

Remodeling of cardiac passive electrical properties and susceptibility to ventricular and atrial arrhythmias

“…Interestingly, a similar situation of sudden changes in fiber direction was observed in canine and human pulmonary veins. In this area atrial fibrillation is usually initiated, and this structural particularity may contribute to the arrhythmogeneity of this region (Hocini et al, 2002;Arora et al, 2003).…”

Is there a role for remodeled connexins in AF? No simple answers

“…The decreased upstroke velocity and shorter action potential duration of pulmonary vein musculature also favor reentry [16]. Reentry in isolated pulmonary veins has been mapped with optical recordings [17,18].…”