Clinical review: Atrial fibrillation

Diagnosing atrial fibrillation, managing rate control, rhythm control and reduction in stroke risk in patients with AF, prognosis and follow-up are covered in this clinical review.

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
Section 2: Making the diagnosis
Section 3: Managing the condition
Section 4: NOACs and prognosis
Section 5: Case study
Section 6: Evidence base


Section 1: Epidemiology and aetiology

AF is the most common sustained cardiac arrhythmia, affecting around 2.5% of the population, and this is set to rise to 3% by 2050 as the population ages. More than 10% of people aged over 80 years are affected in the UK.

Apart from causing symptoms such as breathlessness and palpitations, its main importance is its association with increased thromboembolic 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. This equates to over £100m saved with appropriate anticoagulation.

The physical and mental quality of life of patients with AF has been shown to be poorer than post-MI patients and indeed, those who suffer an AF related stroke are much more likely to be dependent on care than those whose strokes are non-AF related.

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.

Aetiology
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 cardiovascular disorders, pulmonary disorders and constitutional disorders (see box 1).

Classification
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)

Cardioversion is less likely to be successful in patients with long standing AF due to atrial remodelling, so a dilated left atrium is a marker of both chronic AF and a predictor of cardioversion failure.

Patients with PAF also need to be considered for anticoagulation using CHA2DS2-VASc criteria because they also have a substantial risk of stroke, and this has been demonstrated in the literature. These patients are, however, more difficult to identify and post-stroke patients should be considered for ambulatory monitoring to identify undiagnosed PAF.

Atrial flutter
Atrial flutter occurs when a re-entrant 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.

Flutter may also coexist with 3:1 block or 4:1 block with slower ventricular rates respectively. Patients with flutter are at risk of stroke and should be anticoagulated against CHA2DS2-VASc criteria.

Important! Patients with flutter are at risk of stroke and should be anticoagulated against CHA2DS2-VASc criteria.


Section 2: Making the diagnosis

A third of patients with AF will not present with symptoms, and opportunistic screening of high-risk patients, for example at blood pressure checks and flu clinics, has yielded positive results in many practices. 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 (if in 2:1 block) 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). This is why the ventricular rate should always be measured in patients with AF.

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. Patients with error messages on automated devices should have their pulse checked,

Investigations
ECG confirms the diagnosis of AF. Blood tests include FBC, U&Es, magnesium, 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.  Whilst current guidelines are moving away from echocardiography in AF, clinically this is hard to adhere to.

Ambulatory ECG monitoring may be needed to diagnose PAF.


Section 3: Managing the condition

Treatment divides into patient education, managing lifestyle (smoking and weight in particular), addressing risk factors such as hypertension, optimising the management of comorbidities such as heart failure, CKD and COPD, and strategies for managing symptoms (rate control versus rhythm control) and preventing stroke.

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 and it should be noted that there is a slightly increased mortality risk with digoxin. It is contraindicated in patients with Wolff-Parkinson-White syndrome as it will encourage fast fibrillatory wave propagation through the accessory pathway and risk malignant ventricular arrhythmias.

Important! Patients with breathlessness, palpitations or chest tightness often have poor ventricular rate control.

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 and there ought to be a good reason to cardiovert a patient. There is little difference in outcome for mortality and stroke prevention between rate and rhythm control.

Rhythm control
Symptomatic patients or those with HFrEF (see box 1) may require rhythm control. DC or chemical cardioversion, or electrophysiological or surgical ablation, are options.

Attempts to restore sinus rhythm are more successful with coexisting prescribing of antiarrhythmics such as beta-blockers, 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 the procedure.

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 as they often revert to AF.

Important! Patients presenting within 48 hours of a clear onset of AF may be cardioverted immediately.

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 artery 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 oral anticoagulation (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.

Men with a score of one and women with a score of two 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. Aspirin should be taken with caution given that it is an anti-platelet agent, whereas clots in AF are fibrin rich rather than platelet rich. Gastro-intestinal bleeding risk is also higher in patients with aspirin compared to warfarin. There are some reasons why patients may require both aspirin and OAC, for example if they have had a stent or MI within the last year. In general terms, patients in AF who are anti-coagulated should not need aspirin for a history of stoke or peripheral arterial disease.

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).

It should be noted that several of the HAS-BLED criteria are modifiable; these should be managed to reduce bleeding risk to favour the use of OAC where possible. Falls should not generally be used as a reason not to anticoagulate - the risk of stroke if a patient is not anticoagulated is generally far higher than the risk of harm if an anticoagulated patient does fall. The risk of falls should also be reduced by home risk assessment, medication optimisation, and balance classes.


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. Apixaban has been shown to have more favourable bleeding risk compared to warfarin.

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%. Patients with a poor TTR are at much higher risk of complications and should be managed proactively.

Important! Patients with a poor TTR are at much higher risk of complications and should be managed pro-actively.

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.

Prognosis
The prognosis for AF depends on the presence of other risk factors, such as age, coronary artery disease, hypertension, CKD 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. AF increases the risk of heart failure, CKD and all-cause mortality.

Follow-up
Patients managed with rate and rhythm control should be followed up at least annually once stable. Common problems include the development of heart failure, rate control, anticoagulation problems. Monitoring of drugs such as amiodarone should be considered, and BP controlled.

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 even 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.

Examination
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.

Guidelines

Resources

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

This is an updated version of an article that was first published in April 2015. This article was updated by Dr Raj Thakkar GP and cardiac lead for the Oxford Academic Health Science Network.

Suggested further CPD activity
These further action points may allow you to earn more credits.
  • 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.

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