REENTRY AND ATRIAL-FIBRILLATION

被引:0
作者
ALLESSIE, MA
RENSMA, PL
BRUGADA, J
SMEETS, JLRM
PENN, O
KIRCHHOF, CJHJ
机构
[1] STATE UNIV LIMBURG,MAASTRICHT HOSP,DEPT CARDIOL,6200 MD MAASTRICHT,NETHERLANDS
[2] STATE UNIV LIMBURG,MAASTRICHT HOSP,DEPT CARDIOSURG,6200 MD MAASTRICHT,NETHERLANDS
来源
PROCEEDINGS OF THE KONINKLIJKE NEDERLANDSE AKADEMIE VAN WETENSCHAPPEN-BIOLOGICAL CHEMICAL GEOLOGICAL PHYSICAL AND MEDICAL SCIENCES | 1990年 / 93卷 / 04期
关键词
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暂无
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
In patients undergoing cardiac surgery for paroxysmal tachycardia related to the WPW syndrome, atrial fibrillation was induced by programmed electrical stimulation. The electrical activation of the free wall of the right and left atrium was mapped with an epicardial multiple recording electrode (diameter 5 cm) containing 256 individual leads. Multiple reentering wavelets both in the right and left atrium were found to be responsible for the arrhythmia. In 19 chronically instrumented conscious dogs atrial fibrillation was induced by single early premature beats. The vulnerability to atrial fibrillation was correlated with measurements of the refractory period, conduction velocity and wavelength of the early impulse. A variety of drugs were administered intravenously (acetylcholine, propafenone, lidocaine, ouabain, quinidine, d-sotalol). It turned out that the wavelength (product of refractory period and conduction velocity) was the major determinant for the inducibility of atrial fibrillation. Drugs that shorten the wavelength (acetylcholine) facilitate atrial fibrillation, whereas the antifibrillatory action of drugs like quinidine and d-sotalol was based on a clear prolongation of the atrial wavelength.
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页码:351 / 364
页数:14
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