Medicine

Last updated on: November 5th, 2020

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Atrial fibrillation

Clinicals - History

Introduction

Atrial fibrillation (AF) is an arrhythmia characterized by irregular and rapid atrial contractions. This leads to excessive signalling of the ventricles and therefore, a rapid heart rate. AF remains one of the major causes of stroke, heart failure, and cardiovascular morbidity in the world.

Patterns of atrial fibrillation

AF can be paroxysmal i.e. occur as arrhythmia episodes that terminate spontaneously or are resolved within 7 days of onset. If an AF episode does not terminate spontaneously and lasts >7 days it is referred to as persistent AF; and if it lasts continuously for over one year it is classified as long-standing persistent AF. AF is permanent only if a decision has been made jointly by the physician and patient to stop any attempts at restoring sinus rhythm.

Palpitations

Patients with AF may present with palpitations or increased awareness of rapid, irregular or uncomfortable heartbeat.

Shortness of breath

AF can cause shortness of breath with or without exercise. This is due to left atrioventricular asynchrony or ventricular dysfunction.

Chest pain

Chest pain can often be a symptom of an AF episode. It may be nonspecific or it may resemble angina pectoris.

Dizziness

When AF causes circulatory insufficiency in a person, they will present with dizziness, syncope or presyncope.

Reduced functional capacity

Over half of people living with AF have reduced functional capacity due to non-specific symptoms such as fatigue and lethargy, or have some degree of disability as a result of their intolerance to physical activities.

Asymptomatic patients

About one-third of people with AF remain completely asymptomatic.

Triggers

AF episodes may be triggered by various precipitating factors such as alcohol and caffeine intake, exercise, infection, surgery, thyrotoxicosis, electrolyte imbalance, and underlying cardiovascular conditions which affect the atrium.

Risk factors

The more risk factors that an individual has, the more likely they are to develop AF and the more likely it is to be persistent. AF risk factors include increasing age, hypertension, heart failure, coronary artery disease, valvular heart disease, obesity, diabetes mellitus, chronic kidney disease (CKD), alcohol consumption, obstructive sleep apnea (OSA), congenital heart defects, hyperthyroidism, channelopathies (abnormal QT and Brugada syndromes) and genetic predisposition to abnormal atrial excitation.

Thromboembolism

Most AF patients are at risk of developing thromboembolism due to stasis, endothelial dysfunction, and hypercoagulability at the level of the atrium. This can lead to a systemic embolic event with symptoms of stroke, transient ischemic accident (TIA), mesenteric ischemia or peripheral ischemia.

Clinicals - Examination

Irregular pulse

People with AF have an irregularly irregular peripheral pulse, varying in rate and amplitude. This is because the chaotic impulses in the atria disturb the normal sinoatrial node conduction, resulting in irregular ventricular beats.

Rapid heart rate

AF is a type of tachyarrhythmia and is associated with a rapid heart rate that varies between 100 and 180/min.

Low blood pressure

AF patients may develop hypotension as a result of inadequate ventricular filling.

High blood pressure

As hypertension is the most common cardiovascular comorbidity in AF, high blood pressure can be found in up to 90% in people with AF. It has been proposed that hypertension does not only co-exist with AF, but also predisposes to the development of AF. This is probably through the mechanisms of atrial remodeling and activation of renin—angiotensin–aldosterone system (RAAS).

Abnormal JVP waveform

The "a" wave of the jugular venous pulse (JVP) is lost in patients with AF, due to the disorganized atrial activity.

Signs of heart failure

If AF is accompanied with heart failure in a patient, the clinical findings may include S3 gallop and bi-basal crepitations on auscultation, peripheral edema, distended neck veins, or cardiogenic shock.

Signs of hyperthyroidism

When AF is associated with thyroid dysfunction, the findings on examination may include exophthalmos, lid lag, lid retraction, and tremor.

Differential Diagnoses

Sinus tachycardia

Sinus tachycardia is similar to AF in that it arises in response to a variety of physiologic, pathologic, and/or pharmacologic stimuli. However, it is distinguished from AF by its regular rhythm. On ECG, there is sinus rhythm.

Atrial flutter

Atrial flutter, like AF, can lead to abnormal atrial impulses with unsynchronized ventricular contractions and rapid ventricular rate. Unlike AF, atrial flutter is caused by regular atrial contractions that tend to be faster than in AF, sometimes >240 bpm, producing varying rates of atrioventricular (AV) conduction. Atrial flutter can be distinguished by the typical ECG pattern of regular continuous undulation with dominant negative deflections in inferior leads II, III and aVF, often described also as a ‘saw tooth pattern’.

Atrioventricular nodal reentrant tachycardia (AVNRT)

AVNRT similarly to AF presents with episodes of palpitation, but unlike AF, AVNRT is regular. The cause of AVNRT is re-entrant circuit within the atrioventricular node, recognized on ECG by the short PR intervals and a pseudo R′ in lead V1 and a pseudo S in lead II for the typical or ‘slow-fast’ subtype of AVNRT; or by the long RP tachycardia (RP interval > PR interval) in the atypical or ‘fast-slow’ AVNRT.

Wolff-Parkinson-White (WPW) syndrome

Like AF, WPW can cause palpitations or syncope. However, it can be distinguished on ECG by the short PR interval and slurred R wave upstroke (delta wave).

Atrial tachycardia

Atrial tachycardia presents with palpitations and lightheadedness, similar to AF. On ECG, the P waves of atrial tachycardia have abnormal morphology, but unlike in AF, the heart rate in atrial tachycardia is regular.

Ectopic beats

Ectopic beats are triggered similarly to AF, by stimulants, stress, or an underlying cardiac pathology. Both can present with palpitations, but unlike AF, ectopic beats cause “skipped beats” followed by compensatory pause and palpitations which settle spontaneously. Ventricular ectopic beats on ECG are characterized by premature broad QRS complexes, followed by a full compensatory pause. Atrial ectopic beats can vary in their ECG appearance depending on the time of arrival during the heart cycle.

Anxiety disorders

AF and anxiety both present with palpitations, but in anxiety disorders there is no evidence of acute cardiovascular disease or AF traits on ECG.

Investigations - Diagnosis

Point of care screening

Opportunistic annual screening for silent AF is warranted in primary settings, in patients at risk or aged ≥ 65 years by simple pulse assessment followed by an ECG if the pulse is irregular.

ECG

AF is diagnosed with the help of an ECG. Irregular RR intervals and no discernible distinct P waves, lasting for at least 30 seconds is diagnostic for AF.

Electrolytes and renal function

The routine diagnostic work-up for new AF should include serum electrolytes, namely potassium, sodium, magnesium, and calcium, to detect for any underlying electrical dysregulation of the heart. Renal function tests are also required to guide fluid and electrolyte balance management and AF therapy dosing.

Thyroid stimulating hormone (TSH)

In primary care settings, the diagnostic work up for a new stable patient with AF settings should include TSH for hyperthyroidism associated AF. In the acutely ill patient however, TSH testing is of low value.

Transthoracic echocardiogram (TTE)

TTE should be performed in all patients with newly diagnosed AF to identify underlying causes of AF such as valvular heart disease, left ventricle dysfunction and atrial enlargement. TTE can also reveal intracardiac thrombi and predict the individual stroke risk according to the cardiac pathology revealed in a patient.

Screening of paroxysmal AF

There is no ideal type of continuous monitoring to detect PAF. The options include ambulatory mobile telemetry, Holter monitoring, external or implantable loop recorders, pacemakers and implantable cardioverter-defibrillators. The devices relying on skin contact electrodes can cause skin irritation, making it difficult for patients to wear such devices for a long time, leading to missing the diagnosis of PAF. Subcutaneous loop recorders allow continuous monitoring for up to 3 years and detect arrhythmias which last ≥2 minutes. Cardiac implantable electronic devices (CIEDs), implanted in people for prevention of sudden cardiac death for conditions other than AF, can be programmed to detect PAF and atrial tachyarrhythmias which carry the risks of clinical PAF.

Investigations - Management

Obstructive sleep apnea screening

Screening for OSA is recommended in patients with recurrent symptomatic AF.

Digoxin serum levels

Digoxin can accumulate and provoke adverse effects, especially in elderly and patients with kidney dysfunction. That is why when digoxin is used in the AF treatment, serum concentration of digoxin must be monitored and clinical response to lower doses evaluated. Lower doses of digoxin (≤250 μg once daily), corresponding to serum digoxin levels of 0.5–0.9 ng/mL, are recommended.

International normalized ratio monitoring

For AF patients anticoagulated by warfarin, international normalized ratio (INR) should be measured by routine laboratory tests at least once weekly initially, and then monthly. Recommended INR level is between 2-3 and the therapeutic warfarin dose should be modified accordingly. When switching from warfarin to a direct oral anticoagulant (DOAC), after warfarin is stopped, the DOAC can be started when the INR is less than 2.

Management - Supportive

Cardiovascular risk factor management

Identification and treatment of comorbidities and cardiovascular risk factors that have proven benefit in AF management include:


- Aerobic exercise for at least 210 min/week

- Blood pressure optimization to 130/80 mmHg or lower at rest

- HbA1c ≤ 6.5%

- Lipid targets per overall cardiovascular risk profile

- Smoking cessation

- Limitation of alcohol consumption to ≤ 3 standard drinks per week

- Reduction of body weight by 10%, aiming for BMI below 27 in the obese population

- Maximal compliance with continuous positive airway pressure (CPAP) therapy in people with OSA

Cardiovascular comorbidity management

To optimize AF treatment outcomes, any underlying heart disease needs appropriate management which may include diuretics for normalizing volume load, urgent catheter ablation of accessory pathways and timely recognition and responding to myocardial ischemia.

Stroke prevention

AF patients require stroke prevention treatment such as anticoagulation or left atrial appendage (LAA) occluding devices.


The CHA2DS2-VASc score is the most widely used tool to predict the stroke risk in a newly diagnosed AF and annually hereafter. It stands for:


C - Congestive heart failure.

H - History of Hypertension

A2* - Age ≥75 years

D - Diabetes

S2* - History of prior Stroke or TIA or systemic thromboembolism

V - Vascular disease, defined as prior myocardial infarction or peripheral arterial disease or atherosclerosis

A - Age 65–74 years

Sc – female gender


*The subscript 2 means adding 2, instead of 1 point for each positive finding. Female gender does not confer consistently increased stroke risk and can be omitted if other risk factors are not present.

Oral anticoagulation

Oral anticoagulation therapy reduces the risk of stroke in patients with AF by around 70%. Therefore, it is indicated in all valvular atrial fibrillation (VAF) patients, where mitral stenosis or prosthetic heart valve increase the risk of thromboembolism, irrespective of other risk factors; and in non-valvular atrial fibrillation (N-VAF) patients whose CHA2DS2-VA score is 2 or more. In patients with N-VAF whose CHA2DS2-VA score is 0, oral anticoagulation is not recommended.

Direct oral anticoagulants (DOACs)

Direct oral anticoagulants include direct thrombin inhibitors (e.g. dabigatran) and factor Xa inhibitors (e.g. apixaban, rivaroxaban). Unlike warfarin, they do not require routine anticoagulation monitoring, act rapidly and have a shorter half-life. They are recommended as first-line thromboembolism prevention therapy over warfarin in patients with non-valvular atrial fibrillation (N-VAF). They are contraindicated in patients with severe kidney failure.

Warfarin

Warfarin is still the recommended oral anticoagulant in patients with mitral stenosis, metallic valve replacement and severe kidney disease. However, warfarin interacts with several drugs and food products and requires adequate INR monitoring. In addition, it takes several days to achieve anticoagulation and has a longer half-life.

Reducing bleeding risk

Oral anticoagulation therapy increases bleeding risk. To minimize this risk, bleeding risk factors must be reversed or treated. Bleeding risk can be estimated by a variety of clinical scores including the most widely used HAS BLED, which stands for Hypertension, Abnormal renal and liver function, Stroke, Bleeding, Labile INR, Elderly, and Drugs.

Left atrial appendage (LAA) closure devices

The LAA is considered the “most lethal human appendage”. It is an embryonic left atrium remnant, but also has a role in the regulation of heart rate. LAA thrombus is present in up to 15% of patients in AF and 90% of thrombus formation in nonvalvular AF is in the LAA. Therefore, in patients intolerant to oral anticoagulation, LAA closure or occlusion devices are inserted to reduce the incidence of thrombus formation.

Management - Specific

Electrical cardioversion

In hemodynamically unstable patients, immediate electrical cardioversion is the first-line treatment. Generally, up to 3 shocks of 150J are delivered to restore sinus rhythm, alongside appropriate sedation, anticoagulation and treatment of precipitating cause of unstable AF.

AF <48 hours: ‘Wait and see’

For new onset AF with mild symptoms, a ‘wait and watch’ approach with rate control is a reasonable option due to the high spontaneous reversion rate to sinus rhythm for new-onset AF within 48 hours.

AF >48 hours: anticoagulation

Stable patients with atrial fibrillation persisting for longer than 48 hours or patients in whom the duration of atrial fibrillation is unknown, require immediate initiation of anticoagulation. These patients can be started on rate control treatment but cannot undergo cardioversion until 3 weeks of anticoagulation treatment or exclusion of left atrial thrombus by transthoracic echocardiogram (TTE).

Rate control

Rate control is often enough to control AF related symptoms. It is the first-line treatment of AF in patients who are asymptomatic or hemodynamically stable and require control of the ventricular rate. The choice of drug for rate control depends on patient’s individual characteristics, symptoms and LV-function. An acceptable heart rate goal is average resting heart rate <110 bpm.


Beta adrenoceptor blocker oral monotherapy is the preferred treatment for rate control due to the rapid onset of action and effectiveness at high sympathetic tone. When beta blockers are contraindicated, non-dihydropyridine calcium channel blockers diltiazem and verapamil can be used instead. However, due to their negative inotropic effect, they are contraindicated in patients with LVEF <40%.


Amiodarone is used when other drug options have been unsuccessful at rate control and should not be administered as a first-line agent for chronic rate control due to its extracardiac toxicity profile. It is reserved for highly symptomatic AF patients and in patients with known structural or LV systolic dysfunction.


Digoxin can be used as an add-on therapy in suboptimal rate control by beta blocker or calcium channel blocker. It is used as a stand-alone therapy only if all other rate-control agents are contraindicated.

Rhythm control

Rhythm control strategies include electrical cardioversion, pharmacological cardioversion and long-term treatment with anti-arrhythmic agents. Cardioversion is recommended in patients who are either: highly symptomatic; unable to achieve adequate rate control; with significant LV dysfunction; or having early persistent or paroxysmal AF without significant atrial enlargement.


Electrical cardioversion has the highest success rate of achieving sinus rhythm. The most widely used drugs for pharmacological sinus rhythm restoration are sodium channel blockers such as flecainide and propafenone; and the class III anti-arrhythmic agents sotalol, ibutilide and amiodarone.


Note that flecainide and amiodarone are the individual agents most effective at restoring sinus rhythm. However, the choice of drug depends on the patient’s comorbidities, cardiovascular risk, and risk for potential serious proarrhythmic and extracardiac toxic effects.

'Pill in the pocket' cardioversion

Some patients may be candidates for ‘pill in the pocket’ cardioversion. This entails the self-administration of an oral anti-arrhythmic drug for infrequent symptomatic episodes of paroxysmal AF, after successful pharmacological cardioversion by the same drug in hospital.

Catheter ablation

Percutaneous catheter ablation is recommended in AF patients with failed anti-arrhythmic drug treatment, intolerance to AADs, or left ventricular dysfunction. The most effective target for ablation is complete pulmonary vein isolation (PVI) on an atrial level and has higher rates of sinus rhythm maintenance compared with AADs. Up to 30% of ablation patients will require a second procedure within the first 12 months.

Atrial fibrillation surgery

AF patients undergoing aortic replacement or coronary artery bypass grafting (CABG) may be candidates for concomitant surgical ablation of AF because persistent AF is associated with increased post-operative morbidity and mortality.


Patients with symptomatic paroxysmal AF or long-standing persistent AF, who are intolerant of antiarrhythmic medication or who have failed percutaneous ablation; and patients for whom the likelihood of successful percutaneous ablation is low, may be eligible for stand-alone surgical and hybrid management of AF. This includes the ‘Cox-Maze procedure’ or modifications to the original procedure.

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