The History of Atrial Fibrillation: The Last 100 Years

Eric N. Prystowsky, M.D.


J Cardiovasc Electrophysiol. 2008;19(6):575-582. 

In This Article

Atrial Fibrillation Begets Atrial Fibrillation

Clinicians frequently observed two groups of patients, those in whom paroxysmal atrial fibrillation over time became persistent and often impossible to cardiovert to sinus rhythm, and other patients in whom it appeared that paroxysmal atrial fibrillation would not change form. How then does paroxysmal atrial fibrillation over time become persistent atrial fibrillation? Much research into this question has been done recently, but an earlier observation by Davies and Pomerance[23] gave a strong clue to the possible mechanism. These investigators studied the hearts at autopsy in 100 patients who had atrial fibrillation. When the atrial fibrillation duration was greater than 1 month they noted common findings of sinus node muscle loss, internodal track muscle loss, and dilatation of the atrium. They made a very important observation that the fibrotic changes in the atrial tissue might possibly be the result of the arrhythmia instead of the arrhythmia being the result of the pathology. Thus, they introduced the concept that atrial fibrillation itself might engender pathologic changes in the atrium.

This concept of atrial fibrillation begetting atrial fibrillation was studied by Allessie and colleagues[24] in an elegant experimental model. In goat hearts, the authors attached pacing electrodes to the atria and in the chronic situation subjected the atria to rapid bursts of pacing that would cause atrial fibrillation. Sinus rhythm would then be restored and shortly thereafter pacing would again induce atrial fibrillation. As this iterative process continued, the duration of atrial fibrillation was found to become progressively longer until it would persist for greater than 24 hours. Thus, the atria went from a paroxysmal state to one of a persistent state over a relatively short period of time in this particular experimental model. Scores of studies from many excellent scientists have helped us understand the mechanism of these phenomena.[25,26] Not only do anatomic changes take place, but electrophysiologic ones also occur. At an ionic level, the rapid atrial rate appears to increase cellular calcium loading that would lead to a threat of cell viability. Several changes take place, some rather quickly and others over days, to allow the cell to minimize the calcium loading. There appears to be an activation of the calcium current, and there are also changes in the genetic engineering regarding calcium homoestasis. All of this will lead to a shorter action potential duration that shortens the atrial refractory period and, unfortunately, will make it easier for atrial fibrillation to persist. Thus, the adaptive mechanism to prevent cell death in this model enables persistence of atrial fibrillation. There are also anatomic changes that take place and these depend somewhat on the model, for example, a heart failure model versus a pure atrial pacing model.[26]


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