The treatment of atrial fibrillation. An evaluation of drug therapy, electrical modalities and therapeutic considerations.
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia in clinical practice, and is responsible for considerable morbidity. Basic studies have shown that AF is usually due to the coexistence of multiple functional atrial re-entry circuits, and that the main determinant of its haemodynamic manifestations is the ventricular response rate. The major adverse clinical consequences of AF include palpitations, impaired cardiac function and thromboembolism. One approach to treating AF is to convert the patient's cardiac rhythm to sinus rhythm by direct current electrical cardioversion, which is initially successful in about 90% of cases. However, the AF recurrence rate over the year subsequent to cardioversion is very high, in the order of 75% in patients receiving no drug therapy. Class I and class III antiarrhythmic drugs reduce the rate of recurrence of AF, but at the expense of a variety of potential adverse effects including ventricular proarrhythmia. The latter is a rare effect (occurring in 1 to 2% of patients receiving most drugs), but can be lethal. A second approach to therapy is to leave the patient in AF, but to control the ventricular response rate and to prevent thromboemboli with oral anticoagulants. Disadvantages of this approach include the possibilities of functional limitations imposed by the arrhythmia, adverse effects of drug therapy, and major bleeding related to anticoagulation. New approaches currently under study include surgery to prevent AF from sustaining itself, implantable cardioverter devices to maintain sinus rhythm, and modification of AV nodal function by the induction of controlled radiofrequency injury.
Nattel
S
S
Department of Medicine, Montreal Heart Institute, Quebec, Canada.
Hadjis
T
T
Talajic
M
M
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D000925:Anticoagulants / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000188:drug therapy / Q000503:physiopathology / Q000628:therapy*; D004594:Electrophysiology; D006801:Humans
D000889:Anti-Arrhythmia Agents; D000925:Anticoagulants