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Atrial fibrillation: the remodelling phenomenon

G.L. Botto*, M. Luzi and A. Sagone

Department of Cardiology, St Anna Hospital, Como, Italy

* Giovanni Luca Botto, MD, FESC, Divisione di Cardiologia, Ospedale ‘Sant’ Anna', Via Napoleona 60, 22100, Como, Italy

Abstract

Atrial fibrillation (AF) is a progressive disease and may be self-sustaining. The processes that lead to the worsening of AF over time include electrical, contractile, neurohormonal, macroanatomical and ultrastructural changes, and these may occur over different periods of time. The term ‘electrical remodelling’ indicates long-term changes in atrial electrophysiological parameters that result from prolonged changes in atrial rate. The mechanism of tachycardia-induced remodelling is associated with altered ion channel function, the most important of which is a reduction in L-type calcium current, which is responsible for a reduction in the duration of the action potential, atrial refractory period and refractory period adaptation to rate. Recovery from atrial electrical remodelling occurs within a few days, even in cases of very long-lasting AF, although clinically the atria remain vulnerable for weeks after cardioversion. A so-called ‘second factor’ may play a role in this prolonged vulnerability to recurrent AF. In animals tachycardia-induced electrophysiological modification is reduced by verapamil and angiotensin II receptor antagonists, but the effect of these drugs in preventing atrial electrical remodelling in humans is disputed. Despite these findings, there is growing clinical evidence that verapamil and angiotensin II receptor antagonists could reduce the recurrence of AF after cardioversion. In this report current knowledge of the mechanisms and clinical consequences of AF-induced electrical remodelling is discussed.

Key Words: Antiarrhythmic drugs • Atrial fibrillation • Atrial remodelling • Cardioversion of atrial fibrillation • Electrophysiological remodelling

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