Atrial fibrillation: classification, pathophysiology, mechanisms and drug treatment

The prevalence of atrial fibrillation (AF), already the most common sustained cardiac arrhythmia, is constantly rising, even after adjusting for age and presence of structural heart disease. AF increases the risk of stroke sixfold and is associated with a twofold increase in mortality, which remains above 1.5-fold after adjusting for co-morbidity, predominantly caused by cerebrovascular events, progressive ventricular dysfunction, and increased coronary mortality. The adverse haemodynamic effects of AF are well described and relate not only to loss of atrial contraction, but also to the accompanying rapidity and irregularity of ventricular contraction. Although AF may be asymptomatic, up to two thirds of patients report that the arrhythmia is disruptive to their lives. Finally, the treatment of AF and its associated complications creates a significant and increasing economic burden. This article focuses predominantly on the pathophysiology of the arrhythmia and its pharmacological treatment. Anticoagulation for prevention of thromboembolism, a fundamental principle in the management of this arrhythmia, electrical cardioversion, percutaneous ablation techniques, and surgery for AF are not discussed in any detail. AF may be classified based on aetiology, depending on whether it occurs without identifiable aetiology in patients with a structurally normal heart (lone AF), or whether it complicates hypertensive, valvar, or other structural heart disease. A classification system based on the temporal pattern of the arrhythmia has been recently recommended.1 Patients presenting to medical attention may have a first detected episode of AF or, if previous episodes have been documented, recurrent arrhythmia. Episodes themselves may be paroxysmal , if they terminate spontaneously, usually within seven days, or persistent if the arrhythmia continues requiring electrical or pharmacological cardioversion for termination. AF that cannot be successfully terminated by cardioversion, and longstanding (> 1 year) AF, where cardioversion is not indicated or has not been attempted, is termed permanent (fig 1). …

[1]  Wei Huang,et al.  KCNQ1 Gain-of-Function Mutation in Familial Atrial Fibrillation , 2003, Science.

[2]  Ying Wang,et al.  KCNQ1 gain-of-function mutation in familial atrial fibrillation. , 2003, Science.

[3]  C. Lau,et al.  Defibrillation-guided radiofrequency ablation of atrial fibrillation secondary to an atrial focus. , 1999, Journal of the American College of Cardiology.

[4]  N. Kerin,et al.  The efficacy of intravenous amiodarone for the conversion of chronic atrial fibrillation. Amiodarone vs quinidine for conversion of atrial fibrillation. , 1996, Archives of internal medicine.

[5]  R. Falk Time of occurrence, duration, and ventricular rate of paroxysmal atrial fibrillation: the effect of digoxin. , 1990, British heart journal.

[6]  M. Allessie,et al.  Atrial fibrillation begets atrial fibrillation. A study in awake chronically instrumented goats. , 1995, Circulation.

[7]  L. Køber,et al.  Efficacy of Dofetilide in the Treatment of Atrial Fibrillation-Flutter in Patients With Reduced Left Ventricular Function: A Danish Investigations of Arrhythmia and Mortality ON Dofetilide (DIAMOND) Substudy , 2001, Circulation.

[8]  Allessie,et al.  Circus movement in rabbit atrial muscle as a mechanism of tachycardia. III. The "leading circle" concept: a new model of circus movement in cardiac tissue without the involvement of an anatomical obstacle. , 1977, Circulation research.

[9]  Frank J. Hildner,et al.  ArticlesAntithrombotic Therapy in Atrial Fibrillation , 1989 .

[10]  Hendrik Bonnemeier,et al.  Autonomic tone variations before the onset of paroxysmal atrial fibrillation. , 2003, Circulation.

[11]  S Nattel,et al.  Amiodarone to prevent recurrence of atrial fibrillation. Canadian Trial of Atrial Fibrillation Investigators. , 2000, The New England journal of medicine.

[12]  A L Waldo,et al.  A comparison of rate control and rhythm control in patients with atrial fibrillation. , 2002, The New England journal of medicine.

[13]  S. Hohnloser,et al.  Rhythm or rate control in atrial fibrillation—Pharmacological Intervention in Atrial Fibrillation (PIAF): a randomised trial , 2000, The Lancet.

[14]  J Haaksma,et al.  Early recurrences of atrial fibrillation after electrical cardioversion: a result of fibrillation-induced electrical remodeling of the atria? , 1998, Journal of the American College of Cardiology.

[15]  G. Lip,et al.  Antithrombotic therapy for atrial fibrillation , 2002, BMJ : British Medical Journal.

[16]  M. Allessie,et al.  Circus Movement in Rabbit Atrial Muscle as a Mechanism of Tachycardia , 1973, Circulation research.

[17]  Amiodarone to Prevent Recurrence of Atrial Fibrillation , 2000 .

[18]  A. Kadish,et al.  Endocardial mapping of atrial fibrillation in the human right atrium using a non-contact catheter. , 2000, European heart journal.

[19]  V. Fuster,et al.  ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conference , 2001, Circulation.

[20]  李永军,et al.  Atrial Fibrillation , 1999 .

[21]  J Clémenty,et al.  Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. , 1998, The New England journal of medicine.

[22]  Crijns,et al.  Functional capacity before and after cardioversion of atrial fibrillation: a controlled study. , 1994, British heart journal.

[23]  C. Pandozi,et al.  Electrophysiological characteristics of the human atria after cardioversion of persistent atrial fibrillation. , 1998, Circulation.

[24]  H. Wellens,et al.  Are electrophysiological changes induced by longer lasting atrial fibrillation reversible? :observations using the atrial defibrillator. , 1999, Circulation.