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Atrial fibrillation (AF) is the commonest cardiac arrhythmia, and it is responsible for one million hospital admissions per annum in the United States. The prevalence of atrial fibrillation (AF) increases with age. Among 18,403 civil servants in Britain AF was present in 0.2% of subjects aged 40 to 49 years and 1.1% among those aged 60-64 years. Among patients in a geriatric hospital the prevalence of AF in subjects older than 84 years was found to be 14%. Therefore, as the population continues to age physicians will increasingly will face the therapeutic challenge of atrial fibrillation, atrial fibrilation, palpitations, irregular heartbeat.
Atrial Fibrillation and Left Ventricular Function
Although originally thought to be a "benign" arrhythmia in the Framingham Heart Study total mortality among subjects with AF was nearly twice that of subjects with out. Increasingly attention is now being focused on the potentially harmful effects of chronic atrial fibrillation on cardiac function. This phenomenon has been called tachycardia-related cardiomyopathy, and in both patients and animal models the syndrome is characterized by reduced left ventricular ejection fraction, ventricular dilatation and, frequently, reversibility of the syndrome if the tachycardia is abolished. Benefits are clearly seen with restoration of sinus rhythm. Van Gelder et al. reported eight patients with chronic atrial fibrillation who were cardioverted then successfully maintained in sinus rhythm throughout a six month follow-up period. At follow-up there was improvement in atrial contribution to left ventricular filling and in ejection fraction and exercise capacity. In cases where sinus rhythm cannot be restored, there is also evidence that palliation by rate and rhythm control provides benefit. Grogan, et al. reported a dramatic improvement in
Pharmacologic control of heart rate is a well established treatment, and often successful, however there are concerns about the safety of anti-arrhythmic drugs. Commonly used drugs include quinidine (Class 1A) and flecainide (Class 1C). Potential dangers of quinidine were recently highlighted by a meta-analysis of six controlled trials of quinidine versus placebo which has raised new concerns about the safety of quinidine therapy in AF patients. Although the meta-analysis found a fair level of efficacy (50% of. the quinidine group remained in sinus rhythm at one year versus 25% of the placebo group.), it also found a mortality of 2.9% among the quinidine treated patients versus 0.8% for those treated with placebo. In the case of flecainide, which is
Patients with heart failure are those in whom the benefits of rate and rhythm control of atrial fibrillation could be most effective, since in this group some or all of then left ventricular dysfunction might be due to tachycardia-induced cardiomyopathy. The effect of anti-arrhythmic drugs in this group is therefore of great interest. The results of the recently published Stroke Prevention in Atrial Fibrillation Study (SPAF) provide the most compelling direct information regarding potential risks of antiarrhythmic drug therapy. For patients in AF with a history of
Pharmacologic Therapy
The above noted findings created a therapeutic dilemma. The patients who might benefit the most from the maintenance of sinus rhythm (atrial fibrillation and CHF) may also be at the highest risk.
Amiodarone is a unique antiarrhythmic agent originally developed as an antianginal agent. Although classified as a type III agent, amiodarone also has sodium and calcium channel, and beta receptor blocking properties. Studies have shown the maintenance of sinus rhythm in up to 70% of patients, including those who have failed other antiarrhythmic agents. In addition, amiodarone does not have the same proarrhythmic potential as other agents. In fact it may offer protection against sudden death in patients with heart failure. Although clearly the most efficacious antiarrhythmic available for the treatment of both atrial and ventricular arrhythmias, amiodarone therapy is associated with significant toxicities (pulmonary, thyroid, hepatic, neurologic, ophthalmologic). These toxicities appear to be somewhat does related, and the incidence is less on the standard atrial fibrillation dose of 200 mg/day.
Non-Pharmacologic Management of Atrial Fibrillation
Pacing to Prevent Atrial Fibrillation
For some time it has been suggested that atrial pacing may prevent the development of atrial fibrillation. The perception is based on retrospective and prospective studies of patients with sinus node dysfunction in whom dual chamber pacing was compared to ventricular pacing. Ventricular pacing was associated with a significantly higher incidence of atrial fibrillation and CVA. Recently, the use of multi-site atrial pacing has been investigated to prevent atrial fibrillation in patients with a history of PAF. Daubert reported the prevention of atrial fibrillation in 12/12 patients at a mean F/U of 18 months utilizing right atrial appendage and coronary sinus pacing. Saksena reported on the use of high and low (near the ostium of the coronary sinus) right atrial pacing to acutely and chronically prevent atrial fibrillation. In 8/13 patients the induction of atrial fibrillation was prevented in the EP laboratory and in 14 patients dual site pacing reduced the recurrence rate from 2.01 to 0.39 episodes per week. Which patients will benefit from this approach and what the optimal location and method of pacing is has yet to be determined.
Atrial Defibrillation
The use of internal direct current shocks to electrically convert atrial fibrillation has recently been investigated. Bilateral energy delivery has been shown to significantly reduce the energy required to convert atrial fibrillation. This approach has been used to successfully cardiovert patients who had failed chemical or external direct current cardioversion.
Atrial fibrillation is usually divided into paroxysmal and chronic. Recently it has been suggested that persistent be included as a third classification. These patients have paroxysmal AF, however their episodes are not self limited and cardioversion is required to restore sinus rhythm. Eventually, attempts at restoring sinus rhythm are abandoned in these patients and they are classified as having chronic atrial fibrillation. Interestingly, it is now thought that atrial fibrillation produces chronic changes in atrial tissue and promotes the production and maintenance of AF. This concept of "afib begetting afib" was recently investigated by Wijffels. Clear electrophysiologic and structural changes occurred in an animal model of atrial fibrillation. Therefore, early cardioversion (minutes to hours) may lessen the tendency to arrhythmia recurrence and the development of chronic atrial fibrillation. This has led to the development of an implantable atrial defibrillator. The advantages of such a device would be: the avoidance of potentially toxic medications, reduction of embolic risk and obviate the need for repeated hospitalizations. In addition, it may decrease the incidence of atrial fibrillation by preventing the structure and electrophysiologic changes in the atrium. Questions yet to be answered concern the safety, clinical utility, tolerability, and cost effectiveness of such a device. Human trials are now underway in Europe and soon to start in the US. Clinical trials of an atrial defibrillator have been ongoing in Europe and recently begun in the United States. Over 100 devices have now been implanted without any proarrhythmia and with fair patient satisfaction.
Catheter Ablation of the AV Junction
Concern about the potential risks of anti-arrhythmic drugs has grown at a time of rapid development of non-pharmacologic treatment for cardiac arrhythmias by catheter based techniques. This began with the relatively crude method of high energy, direct current (DC) ablation of the AV junction (AVJ), which was described in 1982 by both Gallagher et al. and Scheinman et al, but has become much more refined with the advent of radiofrequency ablation. Chronic success rates of 94% and 88% have been in reports, but in current practice now approaches 100%. Patients undergoing catheter ablation of the AVJ subsequently receive a permanent ventricular pacemaker, usually equipped with a sensor that provides a 'physiological' increase in heart rate in response to exercise, to simulate the normal increase in heart rate. Whilst ventricular pacing is not as efficient as normal conduction, this combination of AVJ ablation and pacing appears to be responsible for improving left ventricular function in certain patients. This effect is presumably achieved by slowing and/or regularizing ventricular contraction, but the exact mechanism remains unclear. Several groups have now reported that patients in chronic AF with ventricular dysfunction may experience improvement in ventricular function following AVJ ablation, but
AV Node Modification
Recently, some authors have suggested that a technique of AV node modification might be applied in patients with established atrial fibrillation, slowing ventricular rates by increasing the overall refractoriness of the AV node and thereby improving ventricular function. This technique may have significant advantages over complete AVJ ablation since conduction would be modified rather than abolished, and no pacemaker would be required. However, more data are needed to evaluate acute and chronic success rates, to establish end-points for the technique, to
Curative Procedures for Atrial Fibrillation
The main limitation of both AV node ablation with pacing and AV modification is that sinus rhythm and atrial transport (and therefore the risk of embolization) are not restored. Recently, surgical techniques, involving multiple atriotomies, have been proposed to meet this goals. Current thinking is that atrial fibrillation is due to multiple reentrant wavelets throughout the atria. The "Maze" procedure was devised to create multiple line of conduction block thereby preventing the initiation and maintenance of these reentrant circuits. Preliminary results have been encouraging in selected patients, although the long term stability of sinus rhythm and risk of embolization is not known. In addition there is a significant morbidity and mortality associated with this (and any) type of cardiac surgery. Therefore, a catheter based technique to cure atrial fibrillation would be ideal, and is actively being pursued.
Currently there are a variety of catheter technologies being developed to facilitate the production of continuous linear lesions in the right and left atrium. These include: catheters with multiple, long ablation coils; multi-electrode catheters with flexible spines to improve tissue contact; and a variety of long molded vascular sheaths to assist in the positioning of standard ablation catheters. Schwartz reports the results of a series of 15 patients undergoing a catheter based curative approach to chronic atrial fibrillation. The procedure involves the production of 8 linear lesions (3 right atrial, 4 left atrial, 1 interatrial septum). These patients had chronic atrial fibrillation (4-192 months, mean 48 months) and had failed multiple antiarrhythmic medications (3-9, 5.5 mean). Atrial fibrillation was terminated acutely in 13/15 patients. The procedure time ranged from 7 16 hours. Nine patients required repeat ablation for intra-atrial reentrant tachycardia. Complications included one CVA and one pericardial effusion. At a mean F/U of 14 months one patient died of heart failure (present prior to ablation), 2 patients remained in atrial fibrillation and 2 patients had atrial flutter. These results are encouraging but clearly this is a procedure early in its evolution. Since there have been multiple reports from multiple centers demonstrating variable results. Clearly there are differences in atrial fibrillation from patient to patient, and we must better identify those amenable to curative ablation. One such group appears to patients with a rapid atrial tachycardia originating most often from the region of the ostia of the pulmonary veins. This atrial tachycardia degenerates into atrial fibrillation or is conducted in a