EXPERIMENTAL STUDIES
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, MDa,
Hideo Mitamura, MDa,
Akiko Takeshita, MDa,
Toshiaki Sato, MDa,
Hideaki Kanki, MDa,
Seiji Takatsuki, MDa and
Satoshi Ogawa, MDa
a Cardiopulmonary Division, Department of Medicine, Keio University School of Medicine, Tokyo, Japan
Manuscript received January 15, 1999;
revised manuscript received August 11, 1999,
accepted September 10, 1999.
Reprint requests and correspondence: Dr. Hideo Mitamura, Cardiopulmonary Division, Department of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan mitamura{at}med.keio.ac.jp
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 drugs 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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Abbreviations and Acronyms
| | AF | = atrial fibrillation | | Avg FF | = average of 100 atrial activation (FF) intervals | | CI | = coupling interval | | CV | = conduction velocity | | ERPAF | = effective refractory period during atrial fibrillation | | FRPAF | = functional refractory period during atrial fibrillation | | Mode FF | = mode of 100 FF intervals |
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