Atrial Fibrillation

Introduction

  • Atrial fibrillation is a common supraventricular tachycardia with incidence in Canada is up to 4.5% per year, with lifetime risk estimated at 25% among those older than 40 years
  • The prevalence of atrial fibrillation is 1-2% in the general population in developed countries
  • Evaluation of the patient involves
    • Determining the underlying cause of atrial fibrillation
    • Rate or rhythm control strategy
    • Role of anti-coagulation

Definitions

  • Atrial fibrillation (AF) is a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation with consequent deterioration of atrial mechanical function.
  • On the electrocardiogram (ECG), AF is described by the replacement of consistent P waves by rapid oscillations or fibrillatory waves that vary in size, shape, and timing, associated with an irregular, frequently rapid ventricular response.
  • Different types of AF:
    • Paroxysmal AF is recurrent atrial fibrillation that terminates spontaneously, lasting possibly up to 7 days, but usually < 48 hours.
    • Persistent AF is atrial fibrillation that is sustained > 7 days or requires termination by cardioversion.
    • Longstanding persistent AF is atrial fibrillation that is persistent for > 1 year.
    • Permanent AF refers to atrial fibrillation where the patient and physician agree to stop additional attempts to restore normal sinus rhythm because atrial fibrillation cannot be converted anymore.
    • Lone AF is historic term used to describe atrial fibrillation in younger patients (such as patients < 65 years old) with no clinical history or echocardiographic evidence of cardiovascular disease, hypertension, or diabetes, but lacks standard definition and may be paroxysmal, persistent, or permanent.
    • Non-valvular AF is  AF in the absence of mechanical heart valves, rheumatic mitral stenosis, or moderate to severe non-rheumatic mitral stenosis.

Differential Diagnosis

Risk Factors

Cardiac

  • Hypertension
  • Coronary artery disease with prior myocardial infarction
  • Heart failure
  • Left ventricular dysfunction (systolic and diastolic; Including hypertrophic, dilated and
    restrictive cardiomyopathies)
  • Valvular heart disease
  • Congenital heart disease (early repair of atrial septal defect)
  • Pericardial disease
  • Post-surgical (particularly cardiac surgery)
  • Sick sinus syndrome
  • Atrial fibrillation as a result of ventricular pacing
  • Supraventricular tachycardia (including Wolf-Parkinson White syndrome, atrial tachycardia, atrial flutter or other)
  • Genetic/familial

Non-Cardiac

  • Excessive alcohol ingestion (acute or chronic)
  • Hyperthyrodism
  • Vagally-mediated (i.e. habitual aerobic training)
  • Pulmonary disease (pneumonia, COPD, pulmonary embolism, pulmonary hypertension)
  • Obstructive Sleep Apnea
  • Obesity
  • Chronic Kidney Disease
  • Tobacco Use
  • Diabetes

History and Physical

History

  • May have symptoms or be completely asymptomatic 
  • Symptoms may include
    • Palpitations
    • Shortness of breath (with heart failure)
    • Chest pain
    • Lightheadedness/dizziness (presyncope/actual syncope uncommon)
    • Focal neurological deficit (with embolic stroke)
  • Heterogenous history, symptoms vary according to ventricular response and overall functional status of individual patient
  • Establish pattern – new onset, paroxysmal, persistent, permanent
  • Establish severity, including impact on quality of life
  • Identify potentially treatable or reversible causes such as: endocrine abnormalities (hyperthyroidism), obstructive sleep apnea, excessive alcohol consumption
  • Identify risk factors for recurrence or poor prognosis (as listed above)
  • Establish bleeding risk and bleeding symptoms
  • Past Medical History: focusing on any previous cardiac problem, HTN, diabetes
  • Social history including tobacco, alcohol and drug use
  • Family History
 
Physical Exam:
  • Irregular jugular venous pulsations (JVP)
  • Elevated JVP with concomitant heart failure
  • Irregularly irregular rhythm detected by palpation of a pulse or auscultation
  • Heart sounds heard during auscultation may include
    • variable intensity of first heart sound (S1)
    • absence of a fourth heart sound (S4) heard previously during sinus rhythm
  • Pedal or sacral edema
  • Bibasilar rales/crackles (with concomitant heart failure)

Diagnostic Work-up

Testing Overview

  • Baseline evaluation should include:
    • EKG to document presence of atrial fibrillation
    • Transthoracic Echo in order to assess cardiac function
    • Blood tests indicated at least once in evaluation of atrial fibrillation
    • Chest x-ray if clinical findings suggest pulmonary abnormality
      • useful to detect underlying concurrent pulmonary disease and evaluate for signs of heat failure
      • as baseline testing in patients taking amiodarone
  • Other tests to consider:
    • Ambulatory electrocardiogram (Holter monitor, event monitor, loop monitor) 
    • Ambulatory blood pressure monitoring (if borderline hypertension)
    • 6-minute walk test (if adequacy of rate control uncertain)
    • Exercise treadmill testing
      • if adequacy of rate control uncertain
      • to reproduce exercise-induced atrial fibrillation
      • for suspected myocardial ischemia
    • Electro-physiological study (for consideration of curative ablation)
    • Sleep study (ambulatory oximetry or polysomnography)
    • Genetic testing in rare cases of apparent familial disease (especially if onset at young age)3

Blood Tests

  • Blood tests to be considered at least once in evaluation of atrial fibrillation
    • Electrolytes (including magnesium, phosphate and calcium)
    • Thyroid-stimulating hormone (TSH)
    • Renal function tests
    • Liver function tests
    • Complete blood count
    • Coagulation profile
    • Fasting lipid profile
    • Fasting glucose
    • Serum levels of B-type natriuretic peptide (BNP)
 

Management

Mainstay of treatment in patients with atrial fibrillation is rate control and reduction of stroke risk.

Two strategies to manage atrial fibrillation are rhythm and rate control.

  • Shown to be equivalent in AFFIRM and AF-CHF trial 

Rate Control: 

  • Goal is to minimize effect on quality of life
  • Aim for a resting hear rate of <100 beats per minute in permanent atrial fibrillation
    • RACE II: Among patients with permanent atrial fibrillation, lenient rate control (HR<110 bpm) is as effective as strict rate control (HR < 80 bpm) in preventing cardiovascular events
  • Initial therapy should be beta blockers or non-dihydropyridine calcium channel blockers
    • Beta Blockers should be used in patients with myocardial infarction or in patients with systolic dysfunction
    • Calcium channel blockers should be avoided in patients with systolic dysfunction
    • Digoxin should NOT be used as initial therapy
      • It can be used in individuals that are sedentary or those with systolic dysfunction
      • It can be used in individuals with contraindications, unable to tolerate or have inadequate response to beta blockers or calcium channel blockers
      • Dosing should be adjusted according to renal function and potential drug interactions should always be considered.

Rhythm control:

  • Recommend a rhythm-control strategy for patients with atrial fibrillation who are symptomatic with adequate rate control therapy or in whom rate-control therapy is unlikely to control symptoms
  • Classes of antiarrhythmic agents are listed below, these can be used in acute management of atrial fibrillation
  • AV blocking agent should be used in patients with AF or AFL being treated with a class I antiarrhythmic drug (eg, propafenone or flecainide) in the absence of advanced AV node disease
  • Intermittent antiarrhythmic drug therapy (“pill in the pocket” as shown in the figure below) in symptomatic patients with infrequent, longer-lasting episodes of atrial fibrillation as an alternative to daily antiarrhythmic therapy
  • To be avoided in patients with advanced sinus or AV nodal disease
  • Rhythm control agents in patients without CHF (Class I agents to be used in conjunction with AV nodal blocking agents and avoided in CAD)
    • Drodenadone (use with caution with digoxin)
    • Flecainide
    • Propafenone
    • Sotalol (use with caution in individuals at risk of Torsades – e.g. female, age > 65, etc.

Rhythm Therapy in individuals with CHF:

  •  Determine ejection fraction
    • If EF>35%: Amiodarone or Sotalol
    • If EF<35%: Amiodarone
  • If above strategies fail – can move to catheter ablation

Please refer to CCS Part 4 Rhythm Management guidelines, Table 7 for full details of “Pill-in-Pocket” Therapy.

Cardioversion: 

  • To be discussed below in anticoagulation section

Catheter Ablation:

  • Can be used in patients who are highly symptomatic despite adequate rhythm control trial (drug-refractory) and in whom rhythm control is desired
  • Can be utilized in select individuals are first line therapy (e.g. paroxysmal atrial fibrillation that is highly symptomatic) or individuals with pre-excitation atrial fibrillation with an accessory pathway
  • Can be utilized as first line therapy or as a reasonable alternative to pharmacologic rhythm or rate control therapy patients with symptomatic typical atrial flutter 
  • Since it is an invasive procedure, risks and benefit must of catheter ablation be balanced; the chart below will outline some risks and benefits of catheter ablation

Management of Atrial Fibrillation or Atrial Flutter in the acute setting:

  • Stable patients – proceed with rhythm or rate control
  • Hemodynamically stable patients with AF/AFL of known duration <48 hours in whom a strategy of control has been selected:
    • Rate-slowing agents alone are acceptable while awaiting spontaneous conversion to sinus rhythm
    • Synchronized electrical cardioversion (150-200 joules biphasic) or pharmacologic cardioversion may be used. If criteria below are met (please refer to diagram below – Figure 7)
      • Hemodynamically unstable (AF/AFL is the direct cause of instability with hypotension, acute coronary syndrome, or pulmonary edema)
      • Anticoagulation for at least three weeks before cardioversion (based on described criteria in Figure 7)
        • Trans-esophageal echo may be used instead of anticoagulation for three weeks to rule out intra-cardiac thrombus
        • Anticoagulation for patients post cardioversion for 4 weeks then use CHADS-65 score to determine need for long term anticoagulation
      • NOTE: Antiarrhythmic drugs may be used to pre-treat patients before electrical cardioversion (to decrease early recurrence of AF and to enhance cardioversion efficacy)
    • Aside Treatment of WPW/rapid response in patients with rapid ventricular preexcitation during AF (Wolff-Parkinson-White syndrome)
      • Electrical Cardioversion if unstable
      • Intravenous antiarrhythmic agents (procainamide or ibutilide) in stable patients
      • AV nodal blocking agents (digoxin, calcium channel blockers, beta-blockers, adenosine) are contraindicated (can degenerate into v.fib spontaneously or it can be facilitated by the
        administration of specific agents)

 

Anticoagulation: 

  • See the CCS algorithm below for anti-coagulation in non-valvular atrial fibrillation and atrial flutter
    • Note: for individuals < 65 years of age and no risk factors, anticoagulation is not recommended, with anti-platelet therapy based on coronary or peripheral artery disease presence
    • NOACs preferred as first line anticoagulation in atrial fibrillation (non-valvular)
      • Greater ease of use of the NOACs vs warfarin
      • RCT data showing that the NOACs are either non-inferior or superior to warfarin in stroke prevention
      • NOACs have no more major bleeding or less bleeding vs warfarin and especially less intracranial hemorrhage.
      • Reduced dose Apixaban in individuals meeting 2/3 following criteria
        • Age >80
        • Creatinine > 133 micromol/L
        • Weight < 60 kg
    • Warfarin preferred over NOACs in individuals with valvular atrial fibrillation, mechanical valve, and CrCl <30
    • Patients whose risk of stroke warrants OAC therapy, but who refuse any OAC, should receive ASA 81 mg/day plus clopidogrel 75 mg/day
    • Renal function to be monitored on an annual basis in patients on OAC
  • Bleeding risk can be assessed with the HAS-BLED tool 

Anticoagulation based on renal function and appropriate adjustments

Anti-thrombotic therapy in patients with Atrial Fibrillation

  • 20-30% of patient with AF have CAD
  • Carefully balance the risk and benefits of anti-thrombotic therapy
  • A list of factors that may help with balancing risk and benefit of anti-platelet and anticoagulation therapy
  • Some recommendations to reduce bleeding risk
    • Avoid using Prasugrel and Ticagrelor in conjunction with oral anticoagulants
    • May need to target lower threshold  for warfarin (INR 2.0-2.5)
    • Avoid NSAIDs
    • Consider use of proton pump inhibitors
  • Management of antithrombotic therapy in patients with atrial fibrillation (AF) and coronary artery disease (CAD)/peripheral artery disease (PAD) (Figure Below)
    • Note that some NOAC doses differ
    • Note for patients with NVAF/AFL aged < 65 years with no CHADS2 risk factors, CCS suggests no antithrombotic therapy for stroke prevention unless any CAD/PAD
    • Ideally this should be discussed with interventional cardiologist
 
Anti-platelet and Anticoagulation -CCS Guidelines
Dosing of OAC+Antiplatelets

Peri-operative Atrial Fibrillation Management:

  • Continuing or stopping anticoagulation should be made based off risk of bleeding during procedure
  • Aspirin or Clopidogrel to be stopped 5-7 days before procedure, or if very high risk of bleeding 7-10 days before procedure
  • Warfarin
    • Hold 5 days before procedure
      • INR < 1.5 for low risk procedure
      • INR < 1.2 for intermediate or high risk procedure
    • Restart after discussion with surgeon
      • 24-48 hours if low risk of bleeding
      • 48-72 hours is intermediate or high risk of bleeding
  • NOACs
    • Hold 1-2 days prior if low risk procedure
    • Hold 2-3 days prior if intermediate or high risk procedure
    • No need for bridging
    • Can re-start one day after adequate hemostasis is established after discussion with surgeon
  • Heparin
    • Bridging therapy with LMWH or UFH be instituted when the INR is below therapeutic level only in patients at high risk of thromboembolic events (CHADS2 ≥4, mechanical heart valve, stroke/TIA within 3 months, rheumatic heart disease)
    • To be restarted after the procedure when hemostasis is established, discuss with surgeon
      • 24 hours for a procedure with a low risk of bleeding
      • 48-72 hours for a procedure with an intermediate or high risk of bleeding 
      • Should be done  prophylactic dosages for the first 24 to 72 hours and then increased to therapeutic dosages. Bridging is then continued until INR is in the therapeutic range

 

Further Reading

  • Cardiology: A practical handbook by David Laflamme
 

Authors

  • Primary Author: Dimitar Saveski (MD, Internal Medicine Resident)
  • Author/Reviewer: pending (MD, FRCPC, Cardiology Fellow)
  • Staff Reviewer: pending (MD, FRCPC[Cardiology])
  • Last Updated: June 24, 2020
  • Comments or questions please email feedback@cardioguide.ca
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