Atrial fibrillation

From Ganfyd

Atrial fibrillation (AF) is an irregular heart rhythm due to chaotic electrical activity in the atria. AF predisposes to thrombus formation and embolic phenomena leading in some cases to stroke disease and other thromboembolic phenomena.

Contents 1 History 2 Aetiology 3 Causes 4 Treatment 4.1 Rhythm control 4.1.1 Cardioversion 4.1.2 Maintenance sinus rhythm 4.2 Rate Control 4.3 Embolism prevention 4.3.1 Anticoagulation 4.3.2 Antiplatelet agents 4.3.3 Triple therapy 4.4 Paroxysmal atrial fibrillation 4.5 Ablation 4.6 Surgery 5 NICE Key Recommendations 6 Other guidance and reviews 7 References

History

Aetiology

Seen with increasing age. Loss of normal atrial systole. Atria fibrillate at 400-500 bpm. Loss of any mechanical component to ventricular filling which then becomes entirely passive. Leads to stasis in atria and clot formation and increased incidence of thromboembolic disease. Warfarin may be indicated in those at risk.

Causes

• Ischaemic heart disease
• Hypertensive heart disease
• Valvular heart disease
• Congenital heart disease
• Atrial septal defect
• Thyrotoxicosis
• “Lone AF” (AF with no identified cause)
• Cardiomyopathy
• Possibly somatic mutations in a Connexin gene, mediated through distinctive gap junctions.

Treatment

Management is generally aimed at getting the heart back into sinus rhythm, by rhythm control. “AF begets AF” is the aphorism. The longer a patient is in AF the more difficult it will be to return them to sinus rhythm. Repeated cardioversions may be needed.

In long-standing AF or where cardioversion is unlikely to produce sustained sinus rhythm, treatment is aimed at ameloriating the symptoms and complications. In patients with a fast ventricular response rate, rate control improves the efficiency of the heart. The potential thromboembolic complications are addressed with anti-coagulation, though the choice of drug must be tailored to the patient.

There is no mortality advantage in using either a rate control or rhythm control strategy in patients with or without left ventricular failure. Cardiac symptom control tends to be better with rate control but it is usually the most resource intensive option.

Rhythm control

Cardioversion

• DC Cardioversion - Synchronised DC shock of 100-200 J given to a sedated patient. If the patient cannot be treated, as would be best, wihin a day or so of the condition developing then they should be anticoagulated for 4-6 weeks before and 4 weeks after.
• Chemical Cardioversion

Maintenance sinus rhythm

• Usually by amiodarone or sotalol. Dofetilide is also used.

Rate Control

An uncontrolled fast ventricular response rate can affect the efficiency of the heart and exacerbate pre-existing heart failure or ischaemic heart disease.

• digoxin
• beta-blockers

Embolism prevention

There is no drug based strategy directed towards embolism reduction that reduces total mortality^[4] although the trends in the RE-LY trial^[5] suggest this may be possible with the newer anticoagulants being developed. The aim is therefore to reduce significant morbidity which in AF is from systemic embolisation. There are likely to be rapid developments in this area as all present evidence suggests all other factors being equal there is a strong relationship between effectiveness of a therapy and bleeding risk. In other words any agent that reduces clotting or platelet function will work.

Anticoagulation

The purpose of anti-coagulation is to prevent embolic strokes and other systemic embolisations. Stroke is common in established AF in the elderly and also in paroxysmal AF in the elderly with benefit in otherwise well patients in non-rheumatic AF starting about 65 years. Stroke is not common in younger patients and so net benefit may not be seen. The moment when a younger patient should start anticoagulation requires individual consideration. Patients with a high risk of falling are at increased risk of serious adverse consequences from anticoagulation and this constitutes a reason to cease anticoagulation in some of them, again, the decision should be individual. For example the non adjusted risk of intracranial haemorrhage in fallers with AF on warfarin is about a third their stroke risk.

Warfarin has long been the anticoagulant of choice but dabigatran etexilate is non inferior at the doses of 110mg or 150mg twice a day^[5] and along with other new anticoagulants is likely to have an increasing place in therapy.

In patients with AF the following risk factors increase stroke risk^[8]:

• Prior stroke/TIA (relative risk 2.5, 95% CI 1.8 - 3.5) - absolute stroke rates for nonanticoagulated patients 6 - 9%/annum
• Age (relative risk 1.5 per decade, 95% CI 1.3 - 1.7) - absolute stroke rates for nonanticoagulated patients 1.5 - 3%/annum if older than 75
• Hypertension (relative risk 2.0, 95% CI 1.6 - 2.5) - absolute stroke rates for nonanticoagulated patients 1.5 - 3%/annum
• Diabetes mellitus (relative risk 1.7, 95% CI 1.4 - 2.0) absolute stroke rates for nonanticoagulated patients 2.0 - 3.5%/annum
• warfarin
  • Adjusted dose warfarin. Relative Rate cf placebo - 0.35 (95% credible interval 0.24 to 0.52)
  • Low dose warfarin. Relative Rate cf placebo - 0.35 (95% credible interval 0.19 to 0.60)
• aspirin
  • Relative Rate cf placebo - 0.64 (95% credible interval 0.44 to 0.88)^[7]

Antiplatelet agents

This is much better understood following the ACTIVE A^[4] and ACTIVE K^[9] trials. ACTIVE K established that anticoagulation therapy is superior to clopidogrel plus aspirin for prevention of vascular events in patients with atrial fibrillation. ACTIVE A established that clopidogrel plus aspirin is superior to aspirin (at least in those aged between 65 and 75) for prevention of vascular events in patients with atrial fibrillation at high risk of stroke. The two trials suggest that there is a reasonable alternative in initiating therapy to anticoagulation if anticoagulation is contraindicated. However for those already taking oral anticoagulation therapy clopidogrel plus aspirin is definitely inferior to anticoagulation. The actual absolute rate of major vascular events in ACTIVE A was 7.6% per year on aspirin and 6.8% on aspirin and clopidogrel. The rate of major haemorrhage on aspirin and clopidogrel was 2.0% per year, an increase of 0.7% per year against the vascular event gain of 0.8% per year. Some might interpret this as needing to treat about 1000 in a year to get a gain over aspirin alone.

Triple therapy

ESC consensus guidelines on what to do in patients on prior antithrombotic therapy for atrial fibrillation, who present with acute coronary syndrome and/or undergo percutaneous coronary intervention/coronary stenting exist. ^[10] Essentially the antiplatelet agents are given as well as the anticoagulant for the period of highest thrombotic risk with some modification if the risk of haemorrhage is high.

Paroxysmal atrial fibrillation

In the first year after a cardioverted episode of paroxysmal atrial fibrillation the incidence of stroke or any thrombo-embolism is higher than persistent AF. This is seen as a strong argument for anticoagulation in this group of patients, which many physicians have been reluctant to do^[6].

Ablation

Pulmonary vein ablation is a proven and useful therapy especially for paroxysmal atrial fibrillation

Surgery

• Maze procedure

NICE Key Recommendations

In June 2006 NICE published guidance of which the key recommendations edited for brevity are:

• Identification and diagnosis
  • An electrocardiogram (ECG) should be performed in all patients in whom atrial fibrillation (AF) is suspected because an irregular pulse has been detected.
• Treatment for persistent AF
  • The indications for either an initial rate-control or rhythm-control strategy should not be regarded as mutually exclusive and the potential advantages and disadvantages of each strategy should be explained to patients before agreeing which to adopt
  • Comorbidities that might indicate one approach rather than the other should be taken into account
  • Appropriate antithrombotic therapy should be used.
  • In patients with permanent AF, who need treatment for rate-control:
    • Beta-blockers or rate-limiting calcium antagonists should be the preferred initial monotherapy
    • Digoxin should only be considered as monotherapy in the predominantly sedentary.
  • In patients with newly diagnosed AF for whom antithrombotic therapy is indicated, treatment should be initiated with minimal delay after the appropriate management of comorbidities.
  • The stroke risk stratification algorithm should be used.

Other guidance and reviews

• BMJ Clinical Review: Management of Atrial Fibrillation^[11]

References