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Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. It may cause symptoms such as palpitations, dyspnoea, fatigue, dizziness or chest discomfort. Mortality risk has been reported to be twice as high when patients are in AF compared to sinus rhythm. As the incidence increases with age and the total number of elderly patients expands, the future clinical burden will be significant.w1
Mapping studies in fibrillating atria have confirmed the hypothesis of Moe and colleagues that AF is based on multiple wavelets of re-entry.w2 w3 The stability of AF is mainly dependent on the number of wavelets that can circulate in the atria. In this respect, this explains why atrial dilatation is a risk factor for AF since the enlarged atria may accommodate more wavelets.w4 Since the wavelength is determined by the product of refractory period and conduction velocity, a short refractory period or slow conduction facilitate the stability of AF. Interestingly, atrial refractory periods in patients with AF are shorter than in patients with sinus rhythm.w5
It has only recently been shown that AF itself causes shortening of the atrial refractory period. In an animal model Wijffels and colleagues demonstrated that repetitive induction of AF by atrial burst pacing led to the development of sustained AF in normal hearts. The hallmark of “AF begets AF” was a shortening of the atrial refractory period (electrical remodelling).1 Further studies have shown that, in addition to electrical remodelling, structural and contractile remodelling also occurs.w6 w7 These experimental observations explain why antiarrhythmic drugs (AADs) fail to terminate persistent AF2 and why paroxysmal AF tends to become persistent or permanent.w8
For the induction and maintenance of AF, ectopic beats or rapid focal activity arising from the pulmonary veins play a much greater role than …
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