Determination of refractory periods and conduction velocity during atrial fibrillation using atrial capture in dogs: Direct assessment of the wavelength and its modulation by a sodium channel blocker, pilsicainide

Kaori Shinagawa, Hideo Mitamura, Akiko Takeshita, Toshiaki Sato, Hideaki Kanki, Seiji Takatsuki, Satoshi Ogawa

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Abstract

OBJECTIVES: The purposes of this study were to measure the atrial refractory period and the conduction velocity (CV) during atrial fibrillation (AF) and to explore the antiarrhythmic mechanism of a sodium channel blocker, pilsicainide, during AF. BACKGROUND: Sodium channel blockers not only decrease the CV, but also prolong the atrial refractory period, particularly during rapid excitation. Because these effects on the wavelength are counteractive and rate dependent, it is critical to measure these parameters during AF. METHODS: In eight dogs, after AF was induced under vagal stimulation, a single extra-stimulus was repeatedly introduced from the left atrium and its capture was statistically determined for each coupling interval. The local CV was also measured during constant capture of the fibrillating atrium by rapid pacing. The same procedure was repeated after pilsicainide administration. RESULTS: Pilsicainide significantly increased the mode of AF intervals from 81 ± 10 to 107 ± 16 ms (p < 0.01). While the CV was decreased from 0.9 ± 0.1 to 0.7 ± 0.1 m/s (p < 0.02), the effective refractory period during AF was increased from 69 ± 11 ms to 99 + 17 ms (p < 0.01). As a result, the wavelength was significantly increased by pilsicainide from 6.6 ± 0.9 to 7.6 ± 1.2 cm (p < 0.05). CONCLUSIONS: During AF, whereas the sodium channel blocker pilsicainide decreases CV, it lengthens the wavelength by increasing the refractory period, an action that is likely to contribute to the drug's ability to terminate the arrhythmia. The direct measurement of refractoriness and CV during AF may provide new insights into the determinations of the arrhythmia and antiarrhythmic drug action.

Original languageEnglish
Pages (from-to)246-253
Number of pages8
JournalJournal of the American College of Cardiology
Volume35
Issue number1
DOIs
Publication statusPublished - 2000 Jan

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Sodium Channel Blockers
Atrial Fibrillation
Dogs
Cardiac Arrhythmias
pilsicainide
Anti-Arrhythmia Agents
Heart Atria

ASJC Scopus subject areas

  • Nursing(all)

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Determination of refractory periods and conduction velocity during atrial fibrillation using atrial capture in dogs : Direct assessment of the wavelength and its modulation by a sodium channel blocker, pilsicainide. / Shinagawa, Kaori; Mitamura, Hideo; Takeshita, Akiko; Sato, Toshiaki; Kanki, Hideaki; Takatsuki, Seiji; Ogawa, Satoshi.

In: Journal of the American College of Cardiology, Vol. 35, No. 1, 01.2000, p. 246-253.

Research output: Contribution to journalArticle

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abstract = "OBJECTIVES: The purposes of this study were to measure the atrial refractory period and the conduction velocity (CV) during atrial fibrillation (AF) and to explore the antiarrhythmic mechanism of a sodium channel blocker, pilsicainide, during AF. BACKGROUND: Sodium channel blockers not only decrease the CV, but also prolong the atrial refractory period, particularly during rapid excitation. Because these effects on the wavelength are counteractive and rate dependent, it is critical to measure these parameters during AF. METHODS: In eight dogs, after AF was induced under vagal stimulation, a single extra-stimulus was repeatedly introduced from the left atrium and its capture was statistically determined for each coupling interval. The local CV was also measured during constant capture of the fibrillating atrium by rapid pacing. The same procedure was repeated after pilsicainide administration. RESULTS: Pilsicainide significantly increased the mode of AF intervals from 81 ± 10 to 107 ± 16 ms (p < 0.01). While the CV was decreased from 0.9 ± 0.1 to 0.7 ± 0.1 m/s (p < 0.02), the effective refractory period during AF was increased from 69 ± 11 ms to 99 + 17 ms (p < 0.01). As a result, the wavelength was significantly increased by pilsicainide from 6.6 ± 0.9 to 7.6 ± 1.2 cm (p < 0.05). CONCLUSIONS: During AF, whereas the sodium channel blocker pilsicainide decreases CV, it lengthens the wavelength by increasing the refractory period, an action that is likely to contribute to the drug's ability to terminate the arrhythmia. The direct measurement of refractoriness and CV during AF may provide new insights into the determinations of the arrhythmia and antiarrhythmic drug action.",
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N2 - OBJECTIVES: The purposes of this study were to measure the atrial refractory period and the conduction velocity (CV) during atrial fibrillation (AF) and to explore the antiarrhythmic mechanism of a sodium channel blocker, pilsicainide, during AF. BACKGROUND: Sodium channel blockers not only decrease the CV, but also prolong the atrial refractory period, particularly during rapid excitation. Because these effects on the wavelength are counteractive and rate dependent, it is critical to measure these parameters during AF. METHODS: In eight dogs, after AF was induced under vagal stimulation, a single extra-stimulus was repeatedly introduced from the left atrium and its capture was statistically determined for each coupling interval. The local CV was also measured during constant capture of the fibrillating atrium by rapid pacing. The same procedure was repeated after pilsicainide administration. RESULTS: Pilsicainide significantly increased the mode of AF intervals from 81 ± 10 to 107 ± 16 ms (p < 0.01). While the CV was decreased from 0.9 ± 0.1 to 0.7 ± 0.1 m/s (p < 0.02), the effective refractory period during AF was increased from 69 ± 11 ms to 99 + 17 ms (p < 0.01). As a result, the wavelength was significantly increased by pilsicainide from 6.6 ± 0.9 to 7.6 ± 1.2 cm (p < 0.05). CONCLUSIONS: During AF, whereas the sodium channel blocker pilsicainide decreases CV, it lengthens the wavelength by increasing the refractory period, an action that is likely to contribute to the drug's ability to terminate the arrhythmia. The direct measurement of refractoriness and CV during AF may provide new insights into the determinations of the arrhythmia and antiarrhythmic drug action.

AB - OBJECTIVES: The purposes of this study were to measure the atrial refractory period and the conduction velocity (CV) during atrial fibrillation (AF) and to explore the antiarrhythmic mechanism of a sodium channel blocker, pilsicainide, during AF. BACKGROUND: Sodium channel blockers not only decrease the CV, but also prolong the atrial refractory period, particularly during rapid excitation. Because these effects on the wavelength are counteractive and rate dependent, it is critical to measure these parameters during AF. METHODS: In eight dogs, after AF was induced under vagal stimulation, a single extra-stimulus was repeatedly introduced from the left atrium and its capture was statistically determined for each coupling interval. The local CV was also measured during constant capture of the fibrillating atrium by rapid pacing. The same procedure was repeated after pilsicainide administration. RESULTS: Pilsicainide significantly increased the mode of AF intervals from 81 ± 10 to 107 ± 16 ms (p < 0.01). While the CV was decreased from 0.9 ± 0.1 to 0.7 ± 0.1 m/s (p < 0.02), the effective refractory period during AF was increased from 69 ± 11 ms to 99 + 17 ms (p < 0.01). As a result, the wavelength was significantly increased by pilsicainide from 6.6 ± 0.9 to 7.6 ± 1.2 cm (p < 0.05). CONCLUSIONS: During AF, whereas the sodium channel blocker pilsicainide decreases CV, it lengthens the wavelength by increasing the refractory period, an action that is likely to contribute to the drug's ability to terminate the arrhythmia. The direct measurement of refractoriness and CV during AF may provide new insights into the determinations of the arrhythmia and antiarrhythmic drug action.

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