Progressive action potential duration shortening and the conversion from atrial flutter to atrial fibrillation in the isolated canine right atrium

Tsu Juey Wu, Young Hoon Kim, Masaaki Yashima, Charles A. Athill, Chih Tai Ting, Hrayr S. Karagueuzian, Peng Sheng Chen

Research output: Contribution to journalArticle

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Abstract

OBJECTIVES: We sought to evaluate the effects of progressive shortening of the action potential duration (APD) on atrial wave front stability. BACKGROUND: The mechanisms of conversion from atrial flutter to atrial fibrillation (AF) are unclear. METHODS: Isolated canine right atria were perfused with 1 to 5 μmol/1 of acetylcholine (ACh). We mapped the endocardium by using 477 bipolar electrodes and simultaneously recorded transmembrane potentials from the epicardium. The APD90 was measured during regular pacing (S1) with cycle lengths of 300 ms. Atrial arrhythmia was induced by a premature stimulus (S2). RESULTS: At baseline, only short runs of repetitive beats (<10 cycles) were induced. After shortening the APD90 from 124 ± 15 ms to 72 ± 9 ms (p < 0.01) with 1 to 2.5 μmol/1 of ACh, S2 pacing 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/1, the APD90 was further shortened to 40 ± 12 ms (p < 0.01); S2 pacing 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. CONCLUSIONS: 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.

Original languageEnglish
Pages (from-to)1757-1765
Number of pages9
JournalJournal of the American College of Cardiology
Volume38
Issue number6
DOIs
Publication statusPublished - 2001 Nov 15
Externally publishedYes

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Atrial Flutter
Heart Atria
Atrial Fibrillation
Action Potentials
Canidae
Acetylcholine
Muscles
Endocardium
Pericardium
Membrane Potentials
Cardiac Arrhythmias
Electrodes

ASJC Scopus subject areas

  • Nursing(all)

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Progressive action potential duration shortening and the conversion from atrial flutter to atrial fibrillation in the isolated canine right atrium. / Wu, Tsu Juey; Kim, Young Hoon; Yashima, Masaaki; Athill, Charles A.; Ting, Chih Tai; Karagueuzian, Hrayr S.; Chen, Peng Sheng.

In: Journal of the American College of Cardiology, Vol. 38, No. 6, 15.11.2001, p. 1757-1765.

Research output: Contribution to journalArticle

Wu, Tsu Juey ; Kim, Young Hoon ; Yashima, Masaaki ; Athill, Charles A. ; Ting, Chih Tai ; Karagueuzian, Hrayr S. ; Chen, Peng Sheng. / Progressive action potential duration shortening and the conversion from atrial flutter to atrial fibrillation in the isolated canine right atrium. In: Journal of the American College of Cardiology. 2001 ; Vol. 38, No. 6. pp. 1757-1765.
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abstract = "OBJECTIVES: We sought to evaluate the effects of progressive shortening of the action potential duration (APD) on atrial wave front stability. BACKGROUND: The mechanisms of conversion from atrial flutter to atrial fibrillation (AF) are unclear. METHODS: Isolated canine right atria were perfused with 1 to 5 μmol/1 of acetylcholine (ACh). We mapped the endocardium by using 477 bipolar electrodes and simultaneously recorded transmembrane potentials from the epicardium. The APD90 was measured during regular pacing (S1) with cycle lengths of 300 ms. Atrial arrhythmia was induced by a premature stimulus (S2). RESULTS: At baseline, only short runs of repetitive beats (<10 cycles) were induced. After shortening the APD90 from 124 ± 15 ms to 72 ± 9 ms (p < 0.01) with 1 to 2.5 μmol/1 of ACh, S2 pacing 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/1, the APD90 was further shortened to 40 ± 12 ms (p < 0.01); S2 pacing 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. CONCLUSIONS: 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.",
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T1 - Progressive action potential duration shortening and the conversion from atrial flutter to atrial fibrillation in the isolated canine right atrium

AU - Wu, Tsu Juey

AU - Kim, Young Hoon

AU - Yashima, Masaaki

AU - Athill, Charles A.

AU - Ting, Chih Tai

AU - Karagueuzian, Hrayr S.

AU - Chen, Peng Sheng

PY - 2001/11/15

Y1 - 2001/11/15

N2 - OBJECTIVES: We sought to evaluate the effects of progressive shortening of the action potential duration (APD) on atrial wave front stability. BACKGROUND: The mechanisms of conversion from atrial flutter to atrial fibrillation (AF) are unclear. METHODS: Isolated canine right atria were perfused with 1 to 5 μmol/1 of acetylcholine (ACh). We mapped the endocardium by using 477 bipolar electrodes and simultaneously recorded transmembrane potentials from the epicardium. The APD90 was measured during regular pacing (S1) with cycle lengths of 300 ms. Atrial arrhythmia was induced by a premature stimulus (S2). RESULTS: At baseline, only short runs of repetitive beats (<10 cycles) were induced. After shortening the APD90 from 124 ± 15 ms to 72 ± 9 ms (p < 0.01) with 1 to 2.5 μmol/1 of ACh, S2 pacing 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/1, the APD90 was further shortened to 40 ± 12 ms (p < 0.01); S2 pacing 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. CONCLUSIONS: 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.

AB - OBJECTIVES: We sought to evaluate the effects of progressive shortening of the action potential duration (APD) on atrial wave front stability. BACKGROUND: The mechanisms of conversion from atrial flutter to atrial fibrillation (AF) are unclear. METHODS: Isolated canine right atria were perfused with 1 to 5 μmol/1 of acetylcholine (ACh). We mapped the endocardium by using 477 bipolar electrodes and simultaneously recorded transmembrane potentials from the epicardium. The APD90 was measured during regular pacing (S1) with cycle lengths of 300 ms. Atrial arrhythmia was induced by a premature stimulus (S2). RESULTS: At baseline, only short runs of repetitive beats (<10 cycles) were induced. After shortening the APD90 from 124 ± 15 ms to 72 ± 9 ms (p < 0.01) with 1 to 2.5 μmol/1 of ACh, S2 pacing 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/1, the APD90 was further shortened to 40 ± 12 ms (p < 0.01); S2 pacing 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. CONCLUSIONS: 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.

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