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J Am Coll Cardiol, 2002; 39:1329-1336
© 2002 by the American College of Cardiology Foundation
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Action potential duration restitution kinetics in human atrial fibrillation

Byung-Soo Kim, MD*, Young-Hoon Kim, MD, FACC*,*, Gyo-Seung Hwang, MD*, Hui-Nam Pak, MD*, Sang Chil Lee, MD*, Wan Joo Shim, MD*, Dong Joo Oh, MD* and Young Moo Ro, MD, FACC*

* Division of Cardiology, Department of Medicine, Korea University, Seoul, South Korea



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Figure 1 (A) Examples of monophasic action potentials recorded at the high lateral wall of the right atrium by S1S2 in patients with chronic atrial fibrillation. A single extrastimulus (S2) was given at progressively shorter S1S2 intervals. As diastolic interval decreased from 138 to 0 ms, the action potential duration (APD) at 90% repolarization decreased from 240 to 158 ms, and then reached the effective refractory period with a coupling interval of 200 ms. (B) The right atrium was paced at progressively shorter S1S1 intervals until APD alternans and then 2:1 atrial capture failure occurred. Pacing with cycle lengths of 220 and 190 ms resulted in APD and diastolic interval alternans.

 


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Figure 2 Monophasic action potentials recorded at the high lateral wall of the atrium by S1S2 in each group (patients with chronic atrial fibrillation [CAF] in the left panel; patients with paroxysmal atrial fibrillation [PAF] in the middle panel; and control subjects in the right panel). In the patients with CAF and PAF, as the diastolic interval progressively decreased to 0 ms, the changes in action potential duration at 90% repolarization ({Delta}APD90) were 110 and 100 ms, respectively. In the control subjects, the change in APD90 was 55 ms as the diastolic interval decreased from 147 to 0 ms.

 


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Figure 3 The action potential duration restitution (APDR) curves by S1S2 in each group (patients with chronic atrial fibrillation [CAF] in the left panel; patients with paroxysmal atrial fibrillation [PAF] in the middle panel; and control subjects in the right panel). In patients with CAF, action potential duration at 90% repolarization (APD90) shortening became 30 ms as the diastolic interval (DI) decreased to <30 ms ({Delta}APD90) and the maximal slope (Slopemax) was 1.6. In patients with PAF, the change in APD90 was 31 ms, and the maximal slope was 1.4. In contrast, the decrease in APD90 with increasing prematurity was small in the control group, which resulted in a flat APDR curve (Slopemax = 0.8).

 


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Figure 4 Representative examples of action potential duration restitution (APDR) by S1S2 (left panels) and rapid pacing (right panels). The slope of APDR by rapid pacing was slightly steeper than that of restitution by S1S2 in each patient. APD90 = action potential duration at 90% repolarization; CAF = chronic atrial fibrillation; DI = diastolic interval; PAF = paroxysmal atrial fibrillation; Slopemax = maximal slope.

 


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Figure 5 (A, top row) The action potential duration restitution (APDR) curves. (B, bottom row) Corresponding nonlinear slopes plotted as a function of DI obtained at four sites of the right atrium (high lateral [HL], high septal [HS], mid posterior [MP] and mid lateral [ML]). Shortening of action potential duration at 90% repolarization (APD90) with decreasing diastolic interval (DI) in patients with chronic atrial fibrillation (CAF) (left panels) was greater at the HL and ML sites than at the MP and HS sites, resulting in a change in the maximal slope (Slopemax) of 2.1. In patients with paroxysmal atrial fibrillation (PAF) (middle panels), {Delta}Slopemax was 1.7. Regional differences of the APDR curve were not evident in the control subjects (right panels), and resulted in a {Delta}Slopemax of 0.8.

 




 
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