Atrial fibrillation

Atrial fibrillation (AF) refers to irregular atrial contraction, caused by chaotic impulses.

AF is increasingly common, NHS studies indicate a prevalence of 1-2% in the UK. It is a major cause of morbidity, in particular stroke, which is largely preventable with appropriate anticoagulation.

Classification

AF can be classified as paroxysmal, persistent or permanent.

• Paroxysmal
  • Recurrent (more than 1 episode ≥30 seconds in duration).
  • Terminates spontaneously within 7 days (usually within 48 hours of presentation).
• Persistent
  • Lasts longer than 7 days or requires termination by pharmacological / electrical cardioversion.
• Permanent
  • Refractory to cardioversion.
  • Sinus rhythm cannot be restored or maintained.
  • AF is accepted as a final rhythm.

A large number of conditions may predispose to AF, the below list is not exhaustive.

Cardiac

• Hypertension
• IHD
• Valvular disease (RHD)
• Cardiomyopathy

Non-cardiac

• Respiratory
  • COPD
  • Pneumonia
  • Pulmonary embolism
  • Pleural effusion
  • Lung cancer
• Endocrine
  • Thyrotoxicosis 
  • Diabetes mellitus
• Infection
• Electrolyte disturbances
• Drugs
  • Bronchodilators
  • Thyroxine

Lifestyle

• Alcohol
• Caffeine (contribution is debated, there is no evidence that at normal levels of consumption caffeine causes AF)

Despite the range of risk factors and causative conditions, common changes to the electrophysiology of the heart may occur.

Atrial myocardium

Atrial myocardium has a number of interesting electrophysiological properties. It possesses a short action potential with a refractory period that reduces with an increasing rate. 

These properties permit rapid contraction.

Generation of arrhythmia

As mentioned, AF is caused by disruption of the electrophysiology in the atrial myocardium. Many mechanisms have been proposed with varying degrees of evidence to support their existence. Most likely, they occur simultaneously.

Two of the most commonly discussed mechanisms are:

• Multiple wavelets - proposes that wavefronts (spontaneous waves of excitation) become fragmented resulting in multiple daughter wavelets.
• Autonomic foci - these foci, located primarily in the pulmonary veins, act to initiate AF.

Ultimately, the physiological sinoatrial node rhythm is superseded by these rapid and chaotic impulses.

The only sign of AF may be an irregularly irregular pulse. Always consider the clinical features of potential underlying causes. AF may also present with an embolic event (stroke or mesenteric ischaemia) or signs of heart failure.

Symptoms

• Palpitations
• Shortness of breath
• Angina
• Presyncope

Signs

• Irregularly irregular pulse
• Tachyarrhythmias

Patients should be investigated for AF if clinically suspected or if presenting with complications of AF (e.g. syncope, strokes, TIA).

Bedside

• Observations
• Blood pressure
• ECG
  • ​No distinct p waves, fine fibrillation.
  • Irregular spacing of R waves (irregular RR interval).

Bloods

• FBC
• U&Es
• TFTs
• Cholesterol
• Bone profile (Ca²⁺)
• Mg²⁺

Imaging

• Echocardiogram
• CXR
• CT / MRI - if embolic event suspected.

Imaging

• Echocardiogram

The CHA₂DS₂-VASc score assesses stroke risk in patients with AF. 

NICE categorise CHA₂DS₂-VASc scores as:

• Low risk -  0 (if a woman has no other risk factors gender is no longer significant).
• Intermediate risk - 1
• High risk ≥ 2 - anticoagulation.

NICE recommend anticoagulation in all patients with a score of 2 or more. It should be considered in men with a score of 1. In women with a score of 1 due to gender, NICE do no consider this an indication for treatment.

The HAS-BLED score allows the identification of those at risk of significant bleeding on anticoagulation therapy. A point is given for each of the following factors:

Management of AF may be achieved with rate or rhythm control. 

Underlying causes should be identified and treated. Patients may be anticoagulated to reduce the risk of thrombo-embolic events.

1. Rate control

Most common type of management. Aimed at controlling rapid heart rate.

First line therapies: 

• Beta blockers (e.g. metoprolol)
• Rate-limiting calcium channel blockers (e.g. verapamil).

Other therapies:

• Digoxin monotherapy - may be used in sedentary patients (in active patients sympathetic action may easily overcome the effects of digoxin).
• Sotalol - should only be prescribed by a cardiologist due to life-threatening side effects.

2. Rhythm control

Cardioversion is aimed at reverting the heart back to a normal (sinus) rhythm. 

Decision made by specialists, may be indicated when:

• New onset
• Identifiable reversible cause.
• Heart failure (caused by or exacerbated by AF).

There are two forms of cardioversion:

• Electrical - typically indicated in AF that has been present > 48hrs.
• Pharmacological - amiodarone, sotalol.

In new-onset AF establishing time of onset is important.

Firstly, ventricular rate should be appropriately controlled with a beta blocker. If onset < 48hrs, immediate cardioversion can take place. If > 48hrs or timing is uncertain, anticoagulation (for at least three weeks) is required before cardioversion. This is due to potential thrombus generation in the atrial appendage.

3. Anticoagulation

Anticoagulation may take two main forms:

• Vitamin K antagonists (e.g. warfarin): has been the mainstay for many years. Regular INR measurements required. 
• Novel anticoagulants (NOACs): newer agents such as Rivaroxaban (direct Xa inhibitor) and Dabigatran (direct thrombin inhibitor). 

If the above are contraindicated dual anti-platelet therapy (aspirin and clopidogrel) may be used. Aspirin or clopidogrel monotherapy is no longer advised.

4. Ablation therapy

Catheter and surgical ablation therapy offers an additional treatment option.

NICE recommends its use when drug treatment has failed. The potential risks and benefits should be discussed with the patient. It is a complex procedure requiring mapping of circuits and can fail.