Author + information
- Received December 27, 2000
- Revision received May 25, 2001
- Accepted August 10, 2001
- Published online November 15, 2001.
- Tsu-Juey Wu, MD*,*,† (, )
- Young-Hoon Kim, MD, FACC†,
- Masaaki Yashima, MD†,
- Charles A Athill, MD†,
- Chih-Tai Ting, MD, PhD*,
- Hrayr S Karagueuzian, PhD, FACC† and
- Peng-Sheng Chen, MD, FACC†
- ↵*Reprint requests and correspondence: Dr. Tsu-Juey Wu, Division of Cardiology, Department of Medicine, Taichung Veterans General Hospital, 160, Section 3, Chung-Kang Road, Taichung, Taiwan
We sought to evaluate the effects of progressive shortening of the action potential duration (APD) on atrial wave front stability.
The mechanisms of conversion from atrial flutter to atrial fibrillation (AF) are unclear.
Isolated canine right atria were perfused with 1 to 5 μmol/l of acetylcholine (ACh). We mapped the endocardium by using 477 bipolar electrodes and simultaneously recorded transmembrane potentials from the epicardium. The APD90was measured during regular pacing (S1) with cycle lengths of 300 ms. Atrial arrhythmia was induced by a premature stimulus (S2).
At baseline, only short runs of repetitive beats (<10 cycles) were induced. After shortening the APD90from 124 ± 15 ms to 72 ± 9 ms (p < 0.01) with 1 to 2.5 μmol/l of ACh, S2pacing induced single, stable and stationary re-entrant wave fronts (307 ± 277 cycles). They either anchored to pectinate muscles (5 tissues) or used pectinate muscles as part of the re-entry (4 tissues). When ACh was raised to 2.5 to 5 μmol/l, the APD90was further shortened to 40 ± 12 ms (p < 0.01); S2pacing induced in vitro AF by two different mechanisms. In most episodes (n = 13), AF was characterized by rapid, nonstationary re-entry and multiple wave breaks. In three episodes with APD90<30 ms, AF was characterized by rapid, multiple, asynchronous, but stationary wave fronts.
Progressive APD shortening modulates atrial wave front stability and converts atrial flutter to AF by two mechanisms: 1) detachment of stationary re-entry from the pectinate muscle and the generation of multiple wave breaks; and 2) formation of multiple, isolated, stationary wave fronts with different activation cycle lengths.
☆ This study was performed in part during the tenure of a National Institutes of Health (NIH, Bethesda, Maryland) Fellowship Grant to Dr. Athill, a Fellowship Grant from the Department of Medicine of Korea University to Dr. Kim, a Cedars-Sinai ECHO Foundation Award to Dr. Karagueuzian and a Pauline and Harold Price Endowment to Dr. Chen, and it was supported in part by NIH SCOR Grant in Sudden Death no. P50-HL52319, NIH Grant R01-HL66389 (National Heart, Lung and Blood Institute), University of California Tobacco-Related Disease Research Program 9RT-0041, American Heart Association (National Center) Grants-in-Aid 9750623N and 9950464N, the Ralph M. Parsons Foundation (Los Angeles, California) and the Yen Tjing Ling Medical Foundation (CI-89-7-3, Taipei, Taiwan).
- Received December 27, 2000.
- Revision received May 25, 2001.
- Accepted August 10, 2001.
- American College of Cardiology