Treatment of atrial fibrillation

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 c ARRHYTHMIA MECHANISMSMapping 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 AF 2 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 previously appreciated.This has opened up the therapeutic option of catheter ablation of focal AF. 3 In some patients the autonomic nervous system is involved in the genesis of paroxysmal AF.Enhanced sympathetic or parasympathetic tone may both shorten refractoriness and increase dispersion of refractoriness, and sympathetic drive is associated with atrial ectopy.Sympathetic adrenergic AF is relatively rare.It relates to stress and exercise and is frequently associated with coronary artery disease.w9 Parasympathetic vagal AF occurs more frequently in otherwise normal patients.It predominantly starts during the night or after heavy meals.w10 The atrial substrate for AF frequently develops as a result of hypertension, coronary artery disease, or valvar disease, especially if these are complicated by heart failure.The patho-anatomic substrate mostly consists of fibrosis.In turn, fibrosis is associated with arrhythmogenic changes such as slowing and dispersion of conduction and an increase in heterogeneity of refractoriness.w11 These notions comply with the fact that AF tends to start in the fifth to sixth decade in life, in particular the persistent form of AF.The continued presence of the patho-anatomic substrate explains why both paroxysmal and persistent AF recurs sooner or later in almost all patients.w12 w13 In this respect, treatment of underlying heart disease is of major importance for long term prevention of AF. ARRHYTHMIA MANAGEMENT: GENERAL CONSIDERATIONSAntiarrhythmic treatment of AF can be divided in three strategies: termination of the arrhythmia in paroxysmal and persistent AF, maintenance of sinus rhythm in paroxysmal and persistent AF, and finally control of ventricular rate during paroxysmal, persistent, and permanent AF (table 1).Removal of precipitating factors such as pericarditis, pulmonary embolism, thyrotoxicosis or excessive alcohol intake may result in disappearance of the arrhythmia.For this reason, a thorough diagnostic evaluation and optimal treatment of underlying heart disease should always precede considering a patient for cardioversion or maintenance treatment.Antiarrhythmic drugs are given to suppress recurrences, but breakthrough arrhythmias may occur.Patients should be informed that a breakthrough arrhythmia does not necessarily mean drug failure.Antiarrhythmic drugs may cause ventricular proarrhythmia, conduction disturbances, and heart failure.Therefore, these patients should be informed about the symptoms associated with these AAD side effects.