Atrial fibrillation

Atrial fibrillation

Atrial fibrillation (AF) is the commonest arrhythmia in man, with an estimated prevalence of 1% under 60 years and increases rapidly with age to more than 10% in those over 80 years (Figure 10). AF is the commonest arrhythmic cause for hospitalisations, and is associated with increased morbidity (adverse events) and mortality (risk of death). Two decades ago the only treatment options for AF were largely limited to achieving heart rate control. However, extensive research in recent years has provided greater understanding of the pathophysiology and mechanisms that lead to AF. A number of recent clinical trials have provided evidence of improved outcomes using these newer therapeutic strategies for AF management. Patients should now be given the option of these new treatments in a balanced and rational approach to risks and benefits.

Patients with AF typically present with symptoms, which include palpitations, chest pain and breathlessness, that compromise their quality of life and functional capacity. However, some patients may have asymptomatic AF discovered as an incidental finding. In highly symptomatic individuals, conventional rate control strategies may be an unacceptable option, particularly in young patients facing the prospect of several decades of AF combined with the potential side effects of long-term drug therapy. Therefore, for many patients the more attractive alternative is to try to restore and maintain normal cardiac (sinus) rhythm.

Restoration of sinus rhythm from AF can be achieved by electrically jolting the heart back to normal rhythm (DC cardioversion) or by rhythm controlling (anti-arrhythmic) drugs. Despite an acute success rate of over 80% for electrical DC cardioversion, there is a high relapse rate back to AF of more than 70% within 1 year, which may be reduced to 50% by serially trying different antiarrhythmic drugs (Figure 11).

Atrio-ventricular node ablation with pacemaker implantation

Patient symptoms are often related to a rapid irregular ventricular rate. One treatment option involves destroying the normal atrioventicular (AV) nodal connection using thermal heat delivered through a small catheter tip (radiofrequency ablation), which has to be combined with implantation of a ventricular pacemaker. This “ablate and pace” strategy is an effective treatment particularly in older more frail patients, but the process of AV disconnection is irreversible, and commits patients to lifelong dependence on pacing. In particular it should be avoided in young patients who will require multiple revisions of their pacing system during their lifetime. Perhaps what is more disappointing with this approach is that AF continues, thromboembolic stroke risks remain unaltered, and the need for long-term anticoagulation persists. In addition, the incidence of heart failure and mortality in patients with structural heart disease treated with AV node ablation and pacemaker implantation has been shown to be as high as 40%, probably because right ventricular pacing induces incoordination (dyssynchrony), shown to adversely affect cardiac performance.

Despite the prevalence of this condition, it was not until 1998 that the primary cause of AF, due to paroxysmal (intermittent) rapid firing focal triggers located in the left atrium was discovered. These areas usually located around the pulmonary veins that deliver oxygen rich blood back to the heart from the lungs, for some reason has retained autonomous and inappropriate rapid firing electrical activity, capable of sending the whole chamber into complete chaos, resulting in clinical symptoms. Clinical trials of ablation treatment techniques began soon after this discovery. These techniques aim to either eliminate rapid AF triggers or to electrically isolate them to disconnect them from the atrium (Figure 12). Although a number of small trials have shown the efficacy of this approach, it was only recently that large scale studies have directly comparing pulmonary vein isolation against rate control was published. In one non randomised Italian study, almost 1200 patients were enrolled over a 3-year follow-up period. For the first time this preliminary study has shown highly significant acute and medium term improvements (>50% risk reduction) in both cardiovascular and total mortality, and morbidity from heart failure and strokes in the ablation compared with rate control groups. Patient quality of life and functional capacity were also found to be significantly better in the ablation group. A higher success rate of AF prevention was achieved in patients with paroxysmal (85%) compared to persistent (62%) AF ablation. These results are in line with a number of other studies with similar reported success rates of preventing AF recurrence.

Despite the promising results from this study, there are small but significant risks associated with AF ablation. These include the risk from transeptal puncture and anticoagulation (blood thinners required during the procedure), procedure related stroke, pericardial effusion (seepage of blood into the sack that surround the heart that may lead to cardiac compression and compromise) and pulmonary vein stenosis (narrowing of the veins draining from the lungs <2%), culminating in an average overall risk of approximately 5% of which up to 1% may be serious. Clearly, this aggressive strategy is not suitable for all patients, but should be considered in highly symptomatic individuals intolerant or refractory to antiarrhythmic drugs.

In the short space of 8 years, from identifying the triggers of AF, therapeutic strategies to potentially cure this arrhythmia have been developed. It is anticipated that as our understanding of the pathophysiology evolves, techniques and results will also continue to improve. It therefore appears that far from being simplified, the management of AF is likely to become more complex, as evidence from large clinical trials continue to suggests better long term outcome from more aggressive therapeutic strategies.

It is clear that warfarin is far superior compared to aspirin for thromboembolic risk reduction. Therefore, as a minimum, we should be advising formal anticoagulation for patients at thromboembolic risk from AF, unless there are clear contraindications. Those below the age of 60-65 years with structurally normal heart can be treated with aspirin alone.

It is inappropriate to treat all patients using a single approach, and treatment plans should be tailored for each patient according to suitability and careful risk-benefit assessment, aimed at reducing long-term morbidity and mortality, with acceptable clinical risks in mind. It is strongly advised that symptomatic patients, particularly those unresponsive to or have side effects from drugs should be referred to a Cardiac Rhythm Specialist for assessment. Expansion of interventional AF treatment, accumulating as the volume of evidence of long term outcome with time, improving results and lower complication rates is likely to increase the numbers of patients treated by these techniques. Clinicians should be aware of the range of treatment options available, to offer patients the highest quality of care.