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International Journal of Bioelectromagnetism
Vol. 4, No. 2, p. 3, 2002.

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Atrial fibrillation, the complete arrhythmia:
Back to the future

S. Nattel
Institut de cardiologie de Montréal, Université de Montréal,
5000 Bélanger est, Montréal, Québec, CANADA H1T 1C8

A common term for atrial fibrillation (AF) in French is  “l’arythmie complète”. In French, this term means complete arrhythmia, and is used in the sense of a total absence of predictable ventricular rhythmicity. However, the literal translation, “the complete arrhythmia”, could also be applied to AF, in terms of the breadth and depth of the mechanisms underlying AF. Over the past 10 years, we have learned a great deal about the complexity of the mechanisms underlying AF: the roles of electrical remodeling and structural remodeling; the roles of reentry, ectopic activity and triggered automaticity; the roles of the complex 3-dimensional atrial structure and of the thoracic veins; the roles of membrane ion channels, ion transporters and connexins; the roles of the autonomic nervous system and of neurohumoural factors; the roles of genetic determinants and a variety of environmental factors.

At the same time, we have returned in our thinking to a variety of simple concepts put forward by investigators in the early 20th century. At that time, debates raged about whether AF was due to rapidly-firing ectopic foci, to single very rapid reentry circuits with fibrillatory conduction, or to multiple simultaneous functional reentry circuits. For about 50 years, the multiple-reentry circuit theory held sway. Over the past few years, however, increasing evidence suggests that all of the notions of the early 20th century have validity for certain forms of AF at certain points in the pathophysiology of various patient groups.

The role of ectopic activity has been highlighted by the demonstration of the critical role of the pulmonary veins as a trigger in AF.  The role of single-circuit reentry has been suggested by observations in animal models of AF due to enhanced cholinergic tone, inflammatory pericarditis and congestive heart failure, and has more recently received theoretical support from advanced computer simulation studies. The potential role of multiple-circuit reentry has been clarified by studies of atrial  electrophysiological remodeling caused by atrial tachycardia, which indicate that such remodeling favours multiple-circuit reentry by causing spatially-heterogeneous decreases in refractory period and atrial connexin expression, making multiple-circuit reentry a final common pathway for AF arising by different initial mechanisms.  Tackling this “complete arrhythmia” effectively will require the development of a complete range of solutions that consider all aspects of its complex pathophysiology. Although the challenge is enormous, recent successes and the great pace of ongoing work are extremely promising. Presently-active research aims to clarify the determinants of AF at the genetic, molecular, ionic, functional, structural and cellular signaling levels. Theoretical analyses seek to relate these basic mechanistic observations to arrhythmic consequences in realistic simulations of atrial electrical activity. This detailed and complimentary approach promises to produce an entire new range of insights into the mechanisms underlying the arrhythmia, as well as to result in a range of novel therapeutic options.

 

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