Repolarization and Activation Restitution Near Human Pulmonary Veins and Atrial Fibrillation InitiationA Mechanism for the Initiation of Atrial Fibrillation by Premature Beats
Sanjiv M. Narayan, MD, FACC*,*,
Dhruv Kazi, MD*,
David E. Krummen, MD* and
Wouter-Jan Rappel, PhD
* University of California and Veterans Affairs Medical Center, San Diego, California
Department of Physics and Center for Theoretical Biology, University of California, San Diego, California
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Figure 1 LA MAP Recording Site in a 74-Year-Old Man With Persistent AF and LA Diameter 48 mm
(A) Fluoroscopy (left anterior oblique 30°) showing the monophasic action potential (MAP) catheter within a transseptal sheath near the left superior pulmonary vein (LSPV), and the coronary sinus (CS) catheter. (B) Digital reconstruction of left atrial (LA) confirming the MAP catheter in the LSPV antrum (NavX, St. Jude Medical, Sylmar, California). (C) Segmented 64-slice computed tomogram imported into NavX for positional reference. AF = atrial fibrillation.
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Figure 2 LA Action Potentials During Constant Pacing (S1) and PACs (S2)
Patients with (A) paroxysmal and (B) persistent AF. For each premature atrial complex (PAC), stimulus artifact (Stim) and phases 1, 2, and 3 of the AP are labeled. Activation time (AT) spans the time from the stimulus artifact to the computed dV/dt maximum of phase 0 (not labeled), and is 25 ms for A and 50 ms in B. Bipolar atrial electrograms are labeled A in the CS. (C) APD90 measurement, calculated as 90% repolarization from phase II voltage to the baseline. DI = diastolic interval; other abbreviations as in Figure 1.
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Figure 3 Steep LA APD Restitution in Paroxysmal AF
This PAC is delivered just outside the effective refractory period (500/320 ms) and results in DI 6 ms and APD restitution slope = 1.8 (same patient as Fig. 2A). The thickened line represents the DI range for which the slope was calculated. APD = action potential duration; other abbreviations as in Figure 2.
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Figure 4 PAC Induces Paroxysmal AF in a Patient With Steep APD Restitution
(A) Very early PAC (DI –4 ms) followed by a pause, then AF. (B) Steep restitution may explain PAC-induced AF (red). S1, S2, F1, and F2 show marked APD oscillations because of steep APD restitution (slope = 1.2; slope >3 by monoexponential fit), then AF onset. The AF cycles continue to track restitution, although wavelets meander (altered activation sequence after F4). Abbreviations as in Figures 1 to 3.
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Figure 5 LA APD Restitution Is Less Steep in Persistent AF
(A) This PAC is early (coupling interval 180 ms), yet significant activation time (AT) delay (93 ms) enables capture (see blocked stimulus artifact at ERP, 170 ms). This prolongs DI and flattens APD restitution. (B) This early PAC also encounters AT delay (106 ms). The APD restitution has a maximum slope 0.85 (i.e., also not steep; same patient as in Fig. 2B). In both patients, FRP (minimum interval from prior beat to PAC) is longer than ERP (minimum distance between stimuli). See Table 2. ERP = effective refractory period; FRP = functional refractory period; other abbreviations as in Figures 1 to 3.
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Figure 6 Right Atrial APD Restitution Has Slope >1 Without AT Prolongation
(A) Paroxysmal AF PACs, and APD restitution for a 74-year-old man with LA diameter 45 mm and AF for 3 years. (B) Persistent AF in the same patient as in Figure 5B. Compared with left atrial data in this patient, ERP (280 ms vs. 200 ms) and APD90 (346 ms vs. 275 ms) were longer, and AT delay (57 ms vs. 106 ms) and minimum DI (13 ms vs. 23 ms) were shorter. See Table 2. Abbreviations as in Figures 1 to 3.
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Figure 7 LA Activation Prolongs for a Wider Range of Beats in Persistent Than Paroxysmal AF
(A) Paroxysmal AF, AT prolongs only at very early DI (<20 ms; i.e., preserved conduction restitution), seen in actual and normalized plots. (B) Persistent AF, AT prolongs at longer DI (<108 ms; i.e., broad conduction restitution) in both plots. See Table 3. Abbreviations as in Figures 1 to 3.
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