Article Text

Treatment of atrial fibrillation
  1. Y Blaauw1,
  2. I C Van Gelder2,
  3. H J G M Crijns1
  1. 1Cardiovascular Research Institute Maastricht (CARIM), Maastricht, The Netherlands
  2. 2Thoraxcenter, Department of Cardiology, University Hospital Groningen, Groningen, The Netherlands
  1. Correspondence to:
    H J G M Crijns, MD, Department of Cardiology, Academic Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, The Netherlands;

Statistics from

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 …

View Full Text

Supplementary materials

    Y Blaauw, I C van Gelder, H J G M Crijns

    Web-only References
    [View PDF]

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Linked Articles

  • Miscellanea
    BMJ Publishing Group Ltd and British Cardiovascular Society
  • Miscellanea
    BMJ Publishing Group Ltd and British Cardiovascular Society
  • Miscellanea
    BMJ Publishing Group Ltd and British Cardiovascular Society
  • Miscellanea
    BMJ Publishing Group Ltd and British Cardiovascular Society