ATRIAL FIBRILLATION

Rate control Vs Rhythm

control
Department CME
18 Aug 2020

Team E
  Introduction
 What is AF, pathophysiology,
classification
 Causes of AF
 ECG features
Content  Diagnosing AF
 Management step-wise & principle
 Assessment for anticoagulation
 Rate control therapy vs. rhythm control
therapy
  Increase prevalence in advanced age
(1% AF patient <60 years old. ⅓ are
above 80 years old)
 Associated with structural heart
disease, IHD, HPT, DM,
Hyperlipidemia.
Introduction  Symptoms range from
asymptomatic to
hemodynamic instability.
 Risk of getting stroke
(thromboembolism), heart failure,
dementia, frequent hospitalization and
hence morbidity and mortality.
  The most common sustained arrhythmia
– featuring disorganized atrial electrical
activity and contraction.
What is AF,  AF requires an initiating event (ectopic
pathophysio, foci in atria/ pulmonary vein that rapidly
firing)
classification  and substrate for maintenance
(abnormal atria tissue, e.g. dilated
left atrium)
 ECG Features of Atrial
ECG features of atrial fibrillation
Fibrillation

• Irregularly irregular rhythm.

• No P waves.
• Absence of an isoelectric baseline.
• Variable ventricular rate.
• QRS complexes usually < 120 ms unless pre-existing bundle branch
block, accessory pathway, or rate related aberrant conduction.
• Fibrillatory waves may be present and can be either fine (amplitude
< 0.5mm) or coarse (amplitude >0.5mm).
• Fibrillatory waves may mimic P waves leading to misdiagnosis.
  Ventricular response (rate) in AF depend
on vagal tone, other pacemaker foci, AV
node function, refractory period, and
medications.
 Commonly AF is associated with a
ventricular rate of 110 – 160.
ECG Features  ‘rapid ventricular
of Atrial response’ is once the
ventricular rate is >
Fibrillation 100 bpm.
 ‘Slow’ AF is a to describe AF
with a ventricular rate < 60 bpm.
 Causes of ‘slow’ AF - hypothermia,
digoxin toxicity, medications, and sinus
node dysfunction.
 Causes of AF

• Valvular AF • Non-valvular AF

An entity if the patient has All other AF without mod-

moderate to severe mitral severe MS or mechanical
stenosis or a mechanical heart valve.
heart valve.
  Ischaemic heart disease
 Chronic uncontrolled Hypertension
 Valvular heart disease (esp. mitral stenosis /
regurgitation)
 Acute infections

Causes of Electrolyte disturbance (hypokalaemia,


hypomagnesaemia)
Thyrotoxicosis
Atrial


 Drugs (e.g. sympathomimetics)

Fibrillation 


Pulmonary embolus
Pericardial disease
 Acid-base disturbance
 Pre-excitation syndromes
 Cardiomyopathies: dilated, hypertrophic.
 Phaeochromocytoma
ECG Features – Narrow QRS complex
Irregular
 Diagnosing
Diagnosing AF
AF
1 AF-related symptom Symptomatic AF, silent AF

2 Duration classification Paroxysmal, persistent, permanent

3 Thromboembolism risk Low risk, high risk

4 Ventricular rate Fast, slow, controlled.

5 Hemodynamic stability, Stable AF, unstable AF

heart failure (LV dysfunction)

6 Causes To determine
MANAGEMENT of AF : Step-wise
approach

 Diagnosis of atrial fibrillation.

 Assessment of duration.
 Assessment for anticoagulation.
 Rate or rhythm control .
 Treatment of underlying / associated
diseases.
  Treat the symptoms
(palpitation,giddiness)
 Classification of AF (persistent, etc)
Management -  Prevent complication
Principle ( thromboembolism)
 Rate control or rhythm control
 Treat the precipitating factor
  Determine the 1 year risk of a
Thrombo- embolic event in a non-
Assessment for anticoagulated patient with non-
Anticoagulant - valvular AF.
CHA2DS2-VASc  Score 0 - low risk for TE events
score (none seen in cohort at one year)
(Birmingham  Score of 1 - intermediate risk (0.6%
rate at 1 year)
2009)
 Score >1 - high risk (3% rate at 1
year).
  OAC therapy can prevent the majority
of ischaemic strokes in AF patients
(reduces the relative risk of stroke by
around 70%) and can prolong life.
 Stroke risk (without OAC) often exceeds the
bleeding risk on OAC.
Assessment for  CHA2DS2-VASc score has simplified the
initial decision for OAC.
Anticoagulant  In general, patients without clinical stroke
risk factors do not need antithrombotic
therapy.
 In future, biomarker-based risk scores may
better stratify patients (e.g. those at a truly low
risk of stroke).
 Men: score => 1
 Women: score =>2
→ OAC should be
considered, balancing
the expected stroke
reduction, bleeding risk,
and patient preference.

 Female sex does not

appear to increase
stroke risk in the
absence of other
stroke risk factors.
Assessment for Anticoagulant
Assessment fAssessment for Anticoagulant -
DOAC or Anticoagulant - DOAC
• DOAC recommended
as first-line therapy
over warfarin in
patients with
nonvalvular atrial
fibrillation, unless
absolute
contraindications.
 Assessment for Anticoagulant – Bleeding Risk
Assessment for Anticoagulant –
Bleeding Risk
• Bleeding risk scores have been developed,
mainly for patients on VKAs (e.g. warfarin).
• Generally, high bleeding risk score should not
lead to withholding OAC.
• Rather, bleeding risk factors should be
identified and to correct the modifiable risk
factors.
• Several bleeding risk score: HAS-BLED, ORBIT (Outcomes Registry
for Better Informed Treatment of Atrial Fibrillation), ABC (age,
biomarkers, clinical history), HEMORR2HAGES, ATRIA.
• A systemic review and meta-analysis comparing the performance of
HAS-BLED, ATRIA and HEMORR2HAGES recommended HAS-BLED
for the assessment of atrial fibrillation patients’ major bleeding
risk.
 Assessment for Anticoagulant – Bleeding Risk
Assessment for Anticoagulant –
Bleeding Risk
• HAS-BLED estimate the 1-year risk for major
bleeding in patients with atrial fibrillation.
• Major bleeding is any bleeding that:
 requiring hospitalization, and/or
 causing a decrease in hemoglobin level > 2
g/L,
 and/or requiring blood transfusion
 Assessment of Anticoagulant – OAC
(VKA vs NOAC)

• VKAs - the only treatment with established safety in AF with rheumatic mitral
valve disease and/or a mechanical heart valve.
•Both VKAs and NOACs are effective for the prevention of stroke in AF.
Meta-analysis - studies of warfarin vs. NOACs (n=29 272 vs. n=42 411).
Result:
 NOACs significantly reduced stroke or systemic embolic events by
19%
 Mortality was 10% lower in patients randomized to NOAC.
 Intracranial haemorrhage was halved in NOAC.

• Greater relative reduction in bleeding with NOACs at centres with poor INR
control.
• Use of VKAs is limited by the narrow therapeutic interval, necessitating
frequent
monitoring and dose adjustments.
• VKAs are effective for stroke prevention in AF, when delivered with adequate TTR
(Time in Therapeutic Range - estimates the percentage of time a patient's INR is
within the desired treatment range or goal)
Assessment of anticoagulant – OAC vs Anti-Platelet

• Antiplatelet therapy bleeding rates are similar

to those on OAC.
• VKA therapy prevents stroke, systemic
embolism, myocardial infarction, and vascular
death better than single or dual antiplatelet
therapy (aspirin and clopidogrel).
• Antiplatelet therapy cannot be recommended
for stroke prevention in AF patients.
 Rate Control vs. Rhythm Control

• To date, RCT do not suggest superiority of one strategy

over another.
• AFFIRM trial (large RCT, published in 2002)
 Rhythm-control strategy offers no survival advantage
over rate-control strategy.
 Lower risk of adverse drug effects, with the rate-
control strategy.
Rate Control vs. Rhythm Control
 Rate Control Therapy
• Often sufficient to improve AF-related symptoms
• Evaluate causes of ↑ heart rate (infection,
endocrine imbalance, anaemia, pulmonary
embolism)
• Agent of choice: beta-blockers, digoxin, CCB-
diltiazem & verapamil.
• For acute rate control - beta-blockers and
diltiazem/verapamil are preferred over digoxin
(due to rapid onset of action and effectiveness at
high sympathetic tone).
• When unstable, consider urgent cardioversion.
Rate Control Therapy
 Rate Control Therapy
• Beta blocker – generally contraindicated in
acute HF and hx of severe bronchospasm.
• Esmolol - β1-selective, fast onset of action
(within 60 to 120 seconds), extremely short
duration of action (10 to 30 minutes).
• Diltiazem and Verapamil is contraindicated in
patients with HFrEF, as can have negative
inotropic effects.
Rate Control Therapy
 Rate Control Therapy
• Digoxin – contraindicated in patient with accessory
pathway, VT, HCM with outflow track obstruction.
• Digoxin - Adjust dose in CKD patient. Dig renal
excretion impaired → high plasma level increase risk of
death.
• Amiodarone have rate-limiting properties, and only be
used in patients needing rhythm control therapy.
• Critically ill patients and severely LV systolic
dysfunction, where excess heart rate leading to
haemodynamic instability → IV amiodarone can be
used.
• Beta-blocker monotherapy is often the first-line rate-
controlling agent. However, achieving a heart rate <110
b.p.m. will often require combination therapy.
 Rate Control Therapy - Target
HR
• Leneant target is <110 bpm.
• The optimal heart rate target unclear, note that
many ‘adequately rate-controlled’ patients
(resting heart rate 60–100 b.p.m.) are severely
symptomatic, calling for additional management.
• When medications fail to control rate and
symptoms, ablation of the atrioventricular
node/His bundle and implantation of a VVI
pacemaker can control ventricular rate.
 Rhythm Control Therapy
• Is indicated to improve symptoms in AF
patients who remain symptomatic on
adequate rate control therapy.
• Acute restoration of sinus rhythm for unstable
AF.
Electrical cardioversion Pharmacological cardioversion
-Restores sinus rhythm quicker and - does not require sedation or fasting
more effectively than pharmacological
cardioversion.
- Associated with shorter
hospitalization
 Electrical Cardioversion
• Method of choice in severely haemodynamically compromised
• Is for recent-onset AF with rapid ventricular response that is producing
hypotension, myocardial ischemia, or pulmonary edema.
• For long-standing AF, electrical cardioversion is not likely to succeed.
Instead, go for rate control treatment.
• Sedate patients with IV midazolam and/or propofol.
• Continuous monitoring of BP and oximetry
• Make available IV atropine or isoproterenol, or temporary transcutaneous
pacing, to mitigate post-cardioversion bradycardia.
• Biphasic defibrillators are more effective than monophasic waveforms.
• Anterior–posterior electrode positions generate a stronger shock field in
the left atrium thus restore sinus rhythm more effectively (than antero-
lateral electrode).
• 120 – 200 J
In ischaemic and/or structural heart disease, amiodarone is recommended for
cardioversion of AF. (Recommendation Class I , Evidence Level A).
 Rhythm Control Therapy -
Anticoagulation in patients undergoing
cardioversion
• Cardioversion carries risk of stroke in non-anticoagulated patients.
• Need to initiate anticoagulation for all patients scheduled for
cardioversion.
• Patients with AF longer than 48 h should start OAC at least 3 weeks
before cardioversion and continue it for minimum 4 weeks
afterwards (for patients at risk of stroke, of course OAC is continued
beyond 4 wk).
• For emergency cardioversion… If patient at increase risk for embolic
complications (CHADS2 or CHA2DS2-VASc scores ≥1, mechanical
heart value, or rheumatic valvular disease), consider
anticoagulation with heparin before or immediately after electrical
cardioversion and continue that as a bridge to oral anticoagulants.
Reference

• LIFTL
• ESC Guideline for management of AF 2016
• ACC/AHA Guideline for management of AF
2014
• Tintinalli