Current strategies in the management of atrial fibrillation
Atrial fibrillation (AF) is one of the oldest and commonest arrhythmias known to man1. Incidence increases with age and is associated with significant morbidity and mortality2. Previous treatment options were limited to simple rate control.
But with renewed interest in this arrhythmia among electrophysiologists in recent years our understanding of the mechanisms and pathophysiology have evolved, leading to novel therapeutic strategies. What is now needed is a new approach to patient selection and referral for treatment.
The options available and rationale are far more extensive and complex than would first appear and it is our intention here to summarise current concepts, therapies and controversies in the management of AF.
Consequences of AF
With the development of AF there is a 10-25 per cent reduction in cardiac output due to loss of normal atrioventricular synchrony and rapid irregular ventricular rate3.
This may be less important in patients with normal ventricular function, but with significant impairment of left ventricular systolic or diastolic function, AF may precipitate or worsen heart
failure and AF has been shown to be an independent risk factor for adverse outcome and mortality after myocardial infarction4.
Patients may complain of a number of symptoms during AF, which include breathlessness, palpitations, dizziness and chest pain. Perhaps the most serious and feared consequence of AF is thromboembolism, the risk of which increases
six-fold in patients with AF.
Thromboembolic events rise exponentially after the age of 65, even in those with structurally normal hearts (lone AF) and increase 18-fold in the presence of valvular heart disease. Anticoagulation with warfarin significantly reduces the risk of thromboembolic events in clinical trials and is superior to aspirin in efficacy5.
Individuals with lone AF over the age of 65 should be anticoagulated with warfarin, unless there are clear contraindications. Those with lone AF under this age may be managed safely with aspirin alone. Patients with AF who have concomitant hypertension, ventricular dysfunction, valvular or any other structural heart disease, or those with a previous history of thromboembolism, should also be considered for anticoagulation with warfarin regardless of age.
AF is not a single entity but a common pathway of a number of pathophysiological processes. Ischaemic heart disease, hypertension, diabetes, LV dysfunction and valvular heart disease all predispose to development of AF.
Recent data suggests it probably begins in a paroxysmal form and that the occurrence predisposes to more frequent and sustained AF episodes, until the arrhythmia becomes persistent or permanent. 'AF begets AF' is a phrase often used to describe this phenomenon. There is
now growing evidence that a rapidly discharging focal trigger captures and disorganises the atrium and initiates
most forms of AF.
It is now established that, in the vast majority of cases, this focal activity originates from muscular sleeves in the proximal pulmonary veins that drain into the left atrium and these form a potential target for AF therapy.
It is important to prevent AF from becoming persistent, when adverse electrical remodelling would perpetuate AF despite the eradication of initiating triggers.
A number of therapeutic options are available. Sinus rhythm can be restored either chemically by the use of anti-arrhythmics, or electrically by DC cardioversion with high success rates of 70-80 per cent.
However, despite acute restoration of normal sinus rhythm, there is a high rate of AF recurrence even with concomitant anti-arrhythmics use. Electrical cardioversion is also inappropriate for those patients with true paroxysmal AF where the arrhythmia only lasts for short periods.
Restoration and maintenance of sinus rhythm can be achieved with ablation of triggers that initiate AF. Pulmonary vein isolation procedures are now well established for treatment of paroxysmal AF with success rates between 60 and 80 per cent, but it may take more than one procedure for this to be achieved. It is an aggressive approach to rhythm management with small but significant risks.
The left atrium is a relatively inaccessible chamber because of its location, requiring a transeptal puncture from right to left atrium. Anticoagulation is required throughout the procedure to prevent thromboembolic risk and there is an up to 5 per cent risk of pulmonary vein stenosis from an ablation procedure. The procedure takes two to four hours to perform and therefore is generally reserved for drug-refractory patients with severe symptoms.
Although digoxin is often used in isolation to control the ventricular rate during atrial fibrillation, it is now well established that the addition of a
?-blocker or calcium antagonist results in much better rate control, especially during exercise.
For patients with symptomatic AF that is poorly tolerated and controlled by medical therapy, or with periods of slow and rapid ventricular rates, atrioventricular node ablation with the insertion of a pacemaker can be undertaken, especially if an aggressive pulmonary vein ablation strategy is inappropriate.
You should bear in mind it is an irreversible process and the patient will be pacing-dependent lifelong.
What is perhaps more concerning is the 1-2 per cent annual mortality risk with this approach and patients still require long-term anticoagulation, as they remain in AF but become unaware of it due to atrioventricular disconnection.
Rate versus rhythm control
Until recently there was much debate around rate versus rhythm control. Evidence-based clinical findings from the AFFIRM6 and RACE7 studies confirmed there was no difference in clinical endpoints of mortality and morbidity in patients treated using a conservative approach of rate control compared with aggressive rhythm control.
Provided patients are protected from thromboembolic risks, rate control does not confer a worse outcome than strategies designed to maintain sinus rhythm.
It should be emphasised that the results of these studies apply predominantly to elderly patients with risk factors for thromboembolism who tolerate the arrhythmia symptomatically.
A number of different strategies to prevent AF were used in the rhythm control group including anti-arrhythmic therapy, electrical cardioversion and pulmonary vein isolation, compared with rate control.
No conclusions could be drawn of differences in outcome between each of these therapeutic approaches as the study was not designed nor powered to address these questions.
There are a number of different treatment options available in the management of AF. What is not considered in the aforementioned trials is the need for individualised treatment.
Rate control may be inappropriate in highly symptomatic patients with frequent paroxysms of AF, and an aggressive interventional approach may result in little clinical benefit in asymptomatic patients and may be inappropriate in frail or elderly patients.
What is now evident is that with different treatment options available AF management has become far more complex than the traditional use of rate control alone.
Therapies for AF should be tailored to the individual patient, with particular emphasis on clinical risks and benefits.
As our understanding of this condition and strategies to treat it continue to evolve, our clinical approach should also change to provide the best possible patient care.
Choice of drugs used for rhythm control
for rhythm control
Agents with proven efficacy
Less effective or incompletely studied drugs
Source: AHA/ACC/ESC/NASPE guidelines