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It has been known for some time that in atria from patients with
paroxysmal atrial fibrillation refractory periods were shorter than normal, and did not show normal
rate-adaptation. In addition, there is an increased dispersion in refactory periods.
More recently, it became apparent that some of these changes were the result, rather than the cause,
of atrial fibrillation. Both in experimental animals and in humans, prolonged periods of atrial fibrillation,
or rapid pacing, lead to a long term shortening of the refractory period and loss of rate adaptation. These
changes persist for a long time after restoration of sinus rhythm, which is one of the reasons why after
cardioversion of long standing atrial fibrillation, recurrence of this arrhythmia is common. This proces,
whereby “atrial fibrillation begets atrial fibrillation”, is known as electrical remodeling, and is primarily
due to a downregulation of the L-type Calcium channels.
Since the refractory period reaches a steady state after a few days of atrial fibrillation, whereas it takes an
additional two to three weeks before atrial fibrillation becomes chronic, other factors besides electrical
remodeling must play a role in the development of permanent atrial fibrillation. One of these is the
development of hibernation, during which atrial cells lose their contractile elements and are filled with
glycogen. Loss of contractile function will lead to dilatation of the atria, and this may be another factor
favoring maintenance of fibrillation. Finally, over a period of several months, fibrosis completes the structural
abnormalities, and this has consequences for conduction, where the impuls travels in a “zig-zag” course,
contributing to slow conduction and reentry.
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