Rapid and Stable Re-Entry Within the Pulmonary Vein as a Mechanism Initiating Paroxysmal Atrial Fibrillation
Sunny S. Po, MD, PhD*,*,
Yuhua Li, PhD ,
David Tang, MS,
Hong Liu, PhD,
Ning Geng, MD ,
Warren M. Jackman, MD*,
Benjamin Scherlag, PhD*,
Ralph Lazzara, MD* and
Eugene Patterson, PhD
* Cardiac Arrhythmia Research Institute, Department of Medicine, Oklahoma City, Oklahoma
College of Engineering, School of Electrical and Computer Engineering, University of Oklahoma, Norman, Oklahoma
Cardiology Department, 2nd Affiliated Hospital of China Medical University, Shenyang, China
Department of Veterans Affairs Medical Center, Oklahoma City, Oklahoma
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Figure 1 A superfused left superior pulmonary vein (PV) preparation viewed from the endocardial surface (A) and action potentials recorded using the microelectrode technique (B, endocardial; C, epicardial), and optical mapping (D, endocardial). (A) LA, PS, and DS indicate left atrium, proximal PV with visible myocardial sleeves, and distal PV without visible myocardial sleeves, respectively. Black squares delineate the PV-LA junction. (B to D) All recordings were performed at a pacing cycle length of 1 s. Notice progressive changes of action potential duration and action potential amplitude as the recording electrodes move from LA to DS. Insets illustrate the bipolar electrograms (at different gains) recorded in corresponding regions.
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Figure 2 Wavefront propagation recorded by optical mapping. (A) The S1 (cycle length [CL] = 700 ms) wavefront propagated relatively fast and homogeneously across the preparation. (B) In contrast, the S2 (coupling CL = 225 ms) wavefront propagated slower and took a counterclockwise course as conduction block was encountered. The numeric sequence indicates progressive times of propagation. Arrows indicate the site of stimulation. Frames are 32 ms apart. White dots outline the margin of the preparation. Stars indicate the leading edge of wavefront. Abbreviations as in Figure 1.
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Figure 3 (A) Automaticity was associated with more depolarized membrane potential. Phase 4 depolarization was observed. The slow automatic rhythm (CL = 1,150 ms) failed to conduct into PS and LA. (B) Concentration-response relationship between percent of action potential duration (APD90) abbreviation and acetylcholine (ACH) concentrations. The concentration that produces 50% of the maximal effect (EC50) was 1.35 ± 0.53 x 10–7 mol/l (n = 12). (C) Concentration-response relationship between the incidence of induced sustained PV tachycardia (>2 s) and ACH concentrations. The EC50 was 3.80 ± 0.85 x 10–7 mol/l (n = 15). Other abbreviations as in Figures 1 and 2.
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Figure 4 Pulmonary vein tachycardias in ACH. (A) A representative episode of sustained tachycardia (CL = 75 ms) induced with a premature extrastimulus delivered at DS. (B) Dashed box highlighted in A. A premature beat delivered from PS during PV tachycardia advanced the next beat of tachycardia (interval = 45 ms), demonstrating a positive resetting response. (C) An example of double potentials (arrows) recorded during another episode of PV tachycardia originating in PS. (D) Wavefront propagation of PV tachycardia recorded by optical mapping. The trajectory of wavefront propagation took a repetitive clockwise course, verifying re-entry as the mechanism underlying the PV tachycardia, and also demonstrated that the entire re-entrant circuit was confined to PV. Note that the tachycardia circuit was oval (not circular), and the conduction velocity was not uniform along the circuit. Frames are 32 ms apart. *Indicates the leading edge of wavefront. White dots outline the margin of the preparation. ACH = 10–7 mol/l for all. Abbreviations as in Figures 1 through 3.
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Figure 5 Restitution properties in ACH. (A) An example of APDs and diastolic intervals (DIs) measured using the dynamic restitution protocols (DI = 840 ms, APD90 = 160 ms) at a pacing CL of 1 s. (B) Representative AP restitution curves and Rt (the steepest slope of the restitution curve) from PS before (black circles, Rt = 0.75) and after (open circles, Rt = 0.22) exposure to ACH. Insert shows the linear regression (Rt) of the shortest DIs preceding refractoriness. Dashed line represents unitary slope. (C) Mean values and standard errors of Rt from LA (black), PS (striped), and DS (open) before and after ACH (n = 12). *p < 0.05 for comparisons before and after ACH. (D) Suppression of AP alternans by ACH at a pacing CL of 130 ms (recorded from PS). ACH = 10–7 mol/l for all. Other abbreviations as in Figures 1 through 3.
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Table 1 Basic Electrophysiologic Properties of Pulmonary Veins
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