CELLULAR MECHANISMS FOR CARDIAC-ARRHYTHMIAS
CELLULAR MECHANISMS FOR CARDIAC-ARRHYTHMIAS
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DOI:
10.1161/01.res.49.1.1
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发表时间:
1981-01-01
影响因子:
20.1
通讯作者:
ROSEN, MR
中科院分区:
文献类型:
--
作者:
HOFFMAN, BF;ROSEN, MR
THE general classification of cardiac arrhythmias that we have employed for a number of years (Hoffmann, 1960; Hoffman and Cranefield, 1964; Wit et al., 1974a, 1974b, 1974c) assumed that all disturbances of rhythm resulted from one of two primary abnormalities in electrical activity. The first was an abnormality in impulse initiation and the second an abnormality in impulse propagation. Also, because there was no reason to assume a priori that these two conditions might not coexist, we classified some arrhythmias as resulting from coexisting abnormalities of impulse initiation and conduction. For the arrhythmias due to abnormal impulse initiation we assumed that the rhythms were automatic in the sense that generation of one impulse did not depend in any crucial way on a prior impulse. Arrhythmias due to abnormal automaticity thus might arise from some change in the normal automatic mechanism or from the development of some abnormal automatic mechanism. In general, this simple scheme has been modified in only one important way. Recent studies on abnormal electrical activity of Purkinje fibers and on the electrical activity of fibers in the AV valves (Wit and Cranefield, 1976) and coronary sinus (Wit and Cranefield, 1977) have led to the concept of triggered arrhythmias. A triggered rhythm differs from a truly automatic rhythm in the sense that the abnormal impulse or repetitive activity is initiated by either an automatic or a stimulated action potential. In the absence of such an action potential (the" trigger") activation or repetitive firing does not occur. The concept is quite an Important one and, although the answers to some questions about differences between automatic and triggered rhythms remain moot, two recent detailed considerations of