Clinical Review: Atrial fibrillation

Contributed by Dr Andrew Money-Kyrle, consultant cardiologist, Buckinghamshire Healthcare NHS Trust.

ECG of a patient with AF, the most common sustained cardiac arrhythmia (Author image)
ECG of a patient with AF, the most common sustained cardiac arrhythmia (Author image)

Section 1: Epidemiology and aetiology

AF is the most common sustained cardiac arrhythmia, affecting 2% of the population and more than 10% of people aged over 80 years in the UK.

Apart from causing symptoms such as breathlessness and palpitations, its main importance is its association with increased thrombo-embolic stroke risk (approximately fivefold higher).

There are 12,500 strokes per year in the UK attributable to AF. Appropriate anticoagulation in all patients would prevent an estimated 4,500 strokes and 3,000 deaths a year.

AF may be defined as a loss of co-ordinated atrial electrical activity, with consequential loss of atrial mechanical activity.

Irregular depolarisation through the atrioventricular (AV) node results in intermittent depolarisation of the ventricles, resulting in the classical 'irregularly irregular' pulse.


The aetiology of AF is multifactorial, although in some cases no particular factor is identified (lone AF).

Apart from the increasing incidence of AF with advancing age, the most important triggers and associations are:

  • Hypertension
  • Toxic insults, such as chronic or acute alcohol intake
  • High caffeine intake
  • Thyrotoxicosis
  • Sepsis (particularly chest infections)
  • Pulmonary emboli
  • Cardiac valve disease, especially mitral valve disease
  • Coronary disease
  • Pericarditis
  • Electrolyte disturbances
  • Cardiac surgery
  • Infiltrations, such as amyloid


AF is classified as:

  • First onset
  • Paroxysmal (PAF) if it lasts for more than 30 seconds and reverts spontaneously within seven days
  • Persistent if it lasts more than seven days but is capable of being cardioverted, either chemically or electrically
  • Longstanding persistent if it lasts more than one year but is considered suitable for attempts to restore sinus rhythm

Permanent if it cannot be cardioverted or a decision is made not to attempt cardioversion

Patients with PAF also need to be considered for anticoagulation using CHA2DS2-VASc criteria because they also have a substantial risk of stroke.

Atrial flutter

Atrial flutter occurs when a reentrant pathway within the atria results in rapid atrial conduction, usually about 300 beats per minute (bpm).

Conduction through the AV node is often in a 2:1 ratio (giving a ventricular rate of 150bpm) or slower.

Atrial flutter is closely related to AF in terms of stroke risk and general management.

Section 2: Making the diagnosis

A third of patients with AF will not present with symptoms. Those who do have symptoms most commonly report tiredness, irregular palpitations and exertional breathlessness.

Occasionally, patients will present with collapse, angina or decompensating heart failure.

Even if an irregular pulse is picked up on examination, the diagnosis can only be confirmed with an ECG. This will show the absence of P waves with a rather irregular isoelectric line (fibrillation waves) and irregular QRS complexes.

Atrial flutter may look similar to sinus tachycardia, but the regular rate of 150bpm and flutter waves (a saw-toothed appearance of the baseline) in the inferior leads should suggest the diagnosis.

Other clinical features may include a mismatch between the apical and radial rates (the latter being reduced because some of the faster AF beats have a low pulse pressure and are impalpable).

There may be signs of valvular heart disease (especially mitral valve disease) and heart failure, sepsis or thyrotoxicosis.

BP readings with automated devices may be inaccurate and manual assessment is recommended.


ECG confirms the diagnosis of AF. Blood tests include FBC, U&Es, glucose, TFTs and LFTs.

Other investigations include echocardiography for left ventricular function, screening for valvular disease and assessing the size of the atria, because the chance of successful cardioversion diminishes with increasing left atrial dimension.

Ambulatory ECG monitoring may be needed to diagnose PAF.

Section 3: Managing the condition

Treatment divides into strategies for managing symptoms (rate control versus rhythm control) and those for preventing stroke.

Many patients need oral anticoagulation (OAC) if efforts are to be made to restore sinus rhythm, or their risk of stroke is elevated on the CHA2DS2-VASc score.

Rate control

Patients with breathlessness, palpitations or chest tightness often have poor ventricular rate control. Fast rates may be controlled with beta-blockers, rate-limiting calcium antagonists or digoxin.

Combinations, such as bisoprolol and digoxin, are often required to keep the rate at 60 to 100bpm. Digoxin on its own is often insufficient to control the rate with exercise.

Patients with fast AF may be in heart failure. Diuretics and ACE inhibitors may be required in addition to rate-limiting drugs. Slow AF may require pacing.

A rate control strategy without efforts to restore sinus rhythm may be optimal in asymptomatic patients. There is little difference in outcome for mortality and stroke prevention between rate and rhythm control.

Rhythm control

Symptomatic patients may require rhythm control. DC or chemical cardioversion, or electrophysiological or surgical ablation, are options.

Attempts to restore sinus rhythm are more successful with an antiarrhythmic such as a beta-blocker, flecainide or amiodarone. Normal-sized atria and a short period in AF are predictors of success. Without antiarrhythmics, many patients revert to AF within a few weeks.

Patients in AF for >48 hours can be offered DC cardioversion, but should be anticoagulated for at least three weeks before and four weeks after.

Continuation of OAC depends on the patient's stroke risk, estimated by CHA2DS2-VASc score. Patients restored to sinus rhythm with an elevated risk should continue OAC in the absence of contraindications.

Patients presenting within 48 hours of a clear onset of AF may be cardioverted immediately, chemically or electrically, with heparin cover. After 48 hours, patients may be cardioverted if a transoesophageal echocardiogram demonstrates a thrombus-free left atrial appendage.

They should be anticoagulated for a minimum of four weeks, or indefinitely if their CHA2DS2-VASc score is two or more.

Any clear trigger, such as thyrotoxicosis, a chest infection or high alcohol intake, should be treated.

Amiodarone can cardiovert and maintain sinus rhythm in AF. Although effective, potential side- effects have limited its use. It requires monitoring of the thyroid and liver, and awareness of potential complications, such as pulmonary fibrosis.

Dronedarone has an increased risk in patients with heart failure, but has a limited role in selected patients.

Flecainide is useful for cardioverting and maintaining sinus rhythm in patients with good left ventricular function with no coronary disease or deemed low-risk for it. Suitable patients with intermittent symptomatic PAF may use flecainide as and when symptoms arise.

Rhythm control in selected patients may include AF ablation. Rate control can sometimes only be achieved by ablating the AV node and implanting a pacemaker.

Stroke, thromboembolism

Assessment of stroke risk and need for OAC is most easily achieved using the CHA2DS2-VASc score, which is simple and well validated in a number of studies (see table 1).

Current NICE recommendations are that patients who have a CHA2DS2-VASc score of zero do not need OAC or antiplatelets.

Men with a score of one should be considered for OAC. Patients with a score of two or more should be offered OAC in the absence of contraindications.

Patients with valvular heart disease have a higher stroke risk and should be offered OAC.

A meta-analysis of warfarin showed an RR reduction of 64% in stroke.

Although NICE has stopped recommending aspirin as a sole agent for stroke prevention, the European Society of Cardiology guidelines indicate that aspirin may be considered rather than OAC in patients with one 'clinically relevant, non-major' risk factor.

In deciding whether to start OAC, consider the patient's bleeding risk, which can be assessed using clinical assessment tools such as the HAS-BLED (hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, labile INR, elderly, drugs/alcohol) score (see table 2).

Section 4: NOACs and prognosis

Warfarin has been the mainstay for stroke prophylaxis, but new therapies offer anticoagulation without repeated blood tests.

The thrombin inhibitor dabigatran and Xa inhibitors apixaban and rivaroxaban have been licensed in the UK for this indication. These drugs are known as NOACs (novel, new or non vitamin K antagonist OACs).

NICE recommends dabigatran as an option for patients with one or more of the following risk factors:

  • Previous stroke, TIA or systemic embolism
  • Left ventricular ejection fraction below 40%
  • Symptomatic heart failure of NYHA class II or above
  • Age 75 years or older
  • Age 65 years or older with one of the following: diabetes, coronary artery disease or hypertension

Dabigatran is contraindicated in severe renal impairment (eGFR <30mL/min), active bleeding and hepatic impairment.

The MHRA recommends renal function assessment in all patients before starting dabigatran, when a decline in renal function is suspected during treatment, and annually in patients aged over 75 years or with renal impairment. Rivaroxaban and apixaban have NICE appraisals for similar indications.

NOACs have an increasing role as a result of patient choice or problems with warfarin, such as having a time in therapeutic range (TTR) <65%.

About 90% of emboli that go on to cause strokes are thought to originate in the left atrial appendage. High-risk patients who cannot have OAC may be suitable for devices such as a left atrial appendage plug.

The prognosis for AF depends on the presence of other risk factors, such as age, coronary disease, hypertension and diabetes. Patients without risk factors aged under 60 years (lone AF) have a good prognosis, with a stroke risk of only 1.3% over 15 years. Those with a CHA2DS2-VASc score of six have an annual stroke risk of 9.8% without anticoagulation.  

Patients managed with rate and rhythm control should be occasionally followed up. Common problems include the development of heart failure, rate control, anticoagulation problems and sometimes monitoring of drugs such as amiodarone.

The rate may be too fast at times of activity but controlled at rest, leading to exertional breathlessness. Screening for this may require 24-hour ECG monitoring. Too many rate-limiting medications may lead to bradycardias, dizziness and syncope.

Section 5: Case study

A 76-year-old woman presents to her GP with exertional breathlessness and tiredness. She has noticed intermittent palpitations, mostly at night but also with some activities.

She has type 2 diabetes with hypertension, with no history of vascular disease or stroke, and normally takes ramipril 5mg, metformin, aspirin 75mg and simvastatin 40mg.


She has an irregularly irregular pulse, about 70bpm on palpation and 110bpm on auscultation. There are no murmurs and no overt signs of heart failure. The ECG confirms AF with a rate of 105bpm and no acute changes. Thyroid and kidney function are normal.

Her CHA2DS2-VASc score is five, giving an annual stroke risk of 6.7%. In the absence of contraindications, anticoagulation is recommended. Her HAS-BLED score is two, giving an annual bleeding risk of 1.88%.

She starts warfarin (stopping her aspirin) and the ventricular rate is controlled with digoxin 125 microgram and bisoprolol 2.5mg.

The patient continues to feel unwell and is referred to cardiology. She struggles with her warfarin control, with a TTR of only 50%. She has difficulty getting to the clinic for her INRs. The cardiologist recommends swapping from warfarin to rivaroxaban and increasing the bisoprolol to 5mg, and arranges a DC cardioversion, which restores sinus rhythm for seven months. The patient stops her digoxin but carries on taking rivaroxaban and bisoprolol.

She reverts to AF and reports palpitations, breathlessness and dizziness. She is referred to an electrophysiologist, who recommends AV nodal ablation and a pacemaker.

The patient remains on rivaroxaban, ramipril and her diabetes medications, and also finds benefit from furosemide 40mg.

Section 6: Evidence base

Clinical trials

  • Lip GY, Frison L, Halperin JL et al. Identifying patients at high risk for stroke despite anticoagulation. A comparison of contemporary stroke risk stratification schemes in an anticoagulated atrial fibrillation cohort. Stroke 2010; 41: 2731-8.

Validation of CHA2DS2-VASc scores.

  • Gage BF, Waterman AD, Shannon W et al. Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA 2001; 285(22): 2864-2.

Validation of CHADS2 score.


  • NICE. Atrial fibrillation: the management of atrial fibrillation. CG180. London, NICE, June 2014.
  • European Society of Cardiology. 2012 focused update of the ESC guidelines for the management of atrial fibrillation. Eur Heart J 2012; 33: 2719-47.
  • NICE. Patient decision aid. Atrial fibrillation: medicines to help reduce your risk of a stroke - what are the options? London, NICE, June 2014. cg180-atrial-fibrillation-update-patient-decision-aid2


These further action points may allow you to earn more credits by increasing the time spent and the impact achieved.

  • Hold a meeting with the clinical staff at your practice to discuss opportunistically identifying cases of AF by checking pulses of patients at risk of AF, and audit the effectiveness of this.
  • Write a protocol for counselling patients when starting a NOAC.
  • Arrange a clinical meeting with a local consultant cardiologist to discuss rational therapies for rate control in patients with AF, and create a local protocol.

Save this article and add notes with your free online CPD organiser at Take clinical tests and claim certificates for CPD at


  • NICE. Atrial fibrillation: the management of atrial fibrillation. CG180. London, NICE, June 2014.
  • NICE. Dabigatran etexilate for the prevention of stroke and systemic embolism in atrial fibrillation. TA249. London, NICE, March 2012.
  • European Society of Cardiology. 2012 focused update of the ESC guidelines for the management of atrial fibrillation. Eur Heart J 2012; 33: 2719-47.
  • Lip GY, Frison L, Halperin JL et al. Identifying patients at high risk for stroke despite anticoagulation. A comparison of contemporary stroke risk stratification schemes in an anticoagulated atrial fibrillation cohort. Stroke 2010; 41: 2731-8.
  • Gage BF, Waterman AD, Shannon W et al. Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA 2001; 285(22): 2864-2.
  • Pisters R, Lane DA, Nieuwlaat R et al. A novel user-friendly score (HAS-BLED) to assess one-year risk of major bleeding in atrial fibrillation patients: The Euro Heart Survey. Chest 2010; 138(5): 1093-100.
  • Connolly SJ, Ezekowitz MB, Yusuf S et al. Dabigatran versus warfarin in patients with atrial fibrillation – RE-LY trial (Randomized Evaluation of Long-Term Anticoagulation Therapy). N Engl J Med 2009; 361: 1139-51.

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