Atrial Fibrillation Flashcards
Definition of atrial fibrillation
Supraventricular arrhythmia with uncoordinated atrial activation
Resulting in loss of effective atrial contraction
AF on ECG
- Absent of regular P waves +/- fibrillatory f waves
- Irregular activation of ventricles
- No specific RR interval pattern
- Absent of atrioventricular block
Temporal classification of atrial fibrillation
A. First diagnosed AF - never diagnosed before, regardless of symptoms, temporal pattern or duration
B. Paroxysmal AF - terminates spontaneously within 7 days or with intervention. (mostly terminates < 48 hours)
C. Persistent AF - not self terminating >7 days (longstanding persistent AF - at least 12 months duration where rhythm control still a treatment option)
D. Permanent AF - no further attempts at restoration to SR planned, after shared decision between patient and physician
Causes of AF
- Cardiac condition
- Non-cardiac condition
Cardiac related AF
1. Any condition that triggers LA enlargement, abnormal conduction pathways
- Eg: ACS, cardiomyopathy, heart failure, etc
2. Pericarditis, myocarditis, endocarditis
3. Congenital heart disease
Non-cardiac related AF
1. Sepsis and infection
2. Burns, severe trauma, shock
3. Alcohol consumption - alcoholic cardiomyopathy
4. Illicit drug - methamphetamine, cocaine, opiates, cannabis
5. Stress - interventions, procedures, surgery
6. Endocrine - thyroid, adrenal, pituitary, etc (see Endocrine in AF card)
7. Autoimmune - RA, SLE, IBD, coeliac, psoriasis, etc
8. Obesity
9. COPD
10. OSA
11. Malignancy
12. Fatty liver disease
Endocrine disorders and AF and considerations in MRCP PACES
- Thyroid disorder (hyper and hypo) causing cardiomyopathy
- Amiodarone induced thyroiditis
- Hyperparathyroidism and hypercalcaemia causing AF
- Primary aldosteronism (Conn’s) causing hypertension and aldosterone vascular effect
4 Acromegaly and growth hormone excess leading to cardiomyopathy - Diabetes as cardiovascular risk factor
Pathophysiology of AF
Pulmonary veins prone to atopy
1. Smaller L-type calcium-current and inward-rectifier potassium current, larger delayed-rectifier potassium current
- Reduced action potential duration -> incraesing likelihood of re-entry and spontaneous ectopy due to delayed after-depolarisation
2. Located adjacent to major cardiac autonomic ganglia that modulates electrical properties of atrium
Pathophysiology
1. Ectopic activity occurring in pulmonary veins
- Predisposing factors: CVRF, ion channel abnormalities, structural abnormalities
2. Altered atrial structure and function (electrical and fibrotic remodelling)
Clinical presentation of AF
- Mostly asymptomatic
- Symptomatic - chest pain, SOB, palpitations, reduced ET, giddiness, fatigue, syncope, depression, sleep disturbance
- Specific triggers leading to AF with RVR
- Complications of AF - heart failure, stroke, thromboembolism, cognitive decline (vascular dementia), depression
Modified European Heart Rhythm Association (mEHRA) Symptom Classification
1 - None
2a - Mild
2b - Moderate: ADL unaffected but patient troubled by symptoms
3 - Severe - ADL affected by symptoms
4 - Disabling - ADL discontinued
Diagnostic evaluation of new AF
Initial Evaluation
1. Medical history - AF pattern, family history, comorbids
2. CHADsVASc and HASBLED score
3. Electrocardiography
4. Bloods
- FBC
- Troponin, NTpBNP
- Electrolytes (Na, K, Ca, Mg, Phos)
- CVRF (lipid, HbA1c)
- Thyroid function test
5. TTE - for LAA thrombus, valvular heart disease
Further Evaluation
1. Holter monitoring - AF burden and ventricular rate control
2. Treadmill ECG - monitor effects of 1C antiarrhythmias
3. TOE
4. CT CA or coronary angiogram - suspected CAD
5. MRI heart - cardiomyopathies, plan for interventional procedures
6. CT brain or MRI brain - cognitive assessment, dementia, stroke
Relationship between atrial flutter and atrial fibrillation
Atrial flutter - commonest tachyarrhythmias - 88 to 317 per 100,000 person
Risk factors of AFL and AF are similar
Complications of AFL and AF are similar - stroke, thromboembolism
50% AFL progresses into AF
The AF-CARE Pathway
Modalities for assessment in AF-CARE pathway
_C_ - Comorbidity and risk factor management
- Assess for CAD or ischaemia
- Determine etiology for heart failure and management
_A_ - Avoid stroke and thromboembolism
- Rule out thrombus, ensure safety of rhythm control strategy
- Guide left atrial appendage (LAA) occlusion procedure
_R_ - Reduce symptoms with rate and/or rhythm control
- Determine potential to maintain SR
- Determine potential to improve LVSF
- Assist in planning rhythm control
_E_ - Evaluation and dynamic reassessment
- Detect changes in heart structure and function
Modalities for assessment:
1. CT CA or coronary angiogram
2. MRI heart
3. TTE or even TOE
HF-CARE: Comorbidity and risk factor management
- What are the comorbidities/risk factor and their management evidence class?
A. Hypertension - BP target 120-129/70-79 (class I)
B. DM - glycaemic control (class I)
C. Heart failure
- Diuretics (Class I)
- GDMTs and SGLT2i (Class I)
D. Overweight/obesity
- Weight loss target 10% or more (Class I)
- Bariatric surgery in rhythm control (Class IIb)
E. OSA - CPAP (Class IIb)
F. Alcohol - reduction 3 drinks or less per week (Class I)
G. Exercise programme (Class I)
H. Others - managed aggressively (Class I)
HF-CARE: Avoid stroke and thromboembolism
A. Assess risk of thromboembolism
- CHADsVASc score: 2 or more (class I); 1 or 0 (Class IIa)
- Temporal pattern NOT relevant
B. Choice of anticoagulation
- DOAC except valvular AF (mechanical valve or MS) (Class I)
- VKA target INR 2-3 (Class I); >70% range (IIa)
- Antiplatelet NOT an alternative
C. Assess bleeding risk
- HASBLED score, but manage modifiable risk factors for bleeding (Class I)
- DO NOT use risk score to withhold anticoagulation
D. Prevention of bleeding
- DO NOT combine antiplatelets and DOAC for stroke prevention
- AVOID antiplatelets beyond 12 months in DOAC treated CCS/PVD with AF
(AUGUSTUS trial)
HF-CARE: Reduce symptoms by rate and rhythm control
- Patient pathways for different temporal classification of AF
First onset AF
- Wait for spontaneous cardioversion or if haemodynamic instability for electrical cardioversion
- AF < 24-48 hours NO NEED pre-procedure DOAC or TOE for thrombus exclusion
(RACE 7 ACWAS trial)
Paroxysmal and persistent AF
- Aim for rate control depending on LVEF and shared decision making on rhythm control
- AF > 24 hours to receive DOAC at least 3 weeks OR perform TOE to exclude thrombus
- Both AF class I for antiarrhythmics depending on LVEF and heart disease
(ATHENA trial)
- Paroxysmal AF class I for catheter ablation
- Persistent AF class IIb for catheter ablation
(CABANA trial, EAST-AFNET 4 trial)
(CASTLE-AF trial for AF with HF)
Permanent AF
- Aim for rate control depending on LVEF
- Intensify rate control therapy and evaluation for AVN ablation and pacemaker (Class IIa)
- Severe symptomatic or HF hospitalisation for AVN ablation and CRT (Class IIa)
Post-conversion
- DOAC for at least 4 weeks
(Optional only if AF < 24 hours)
HF-CARE: Evaluation and dynamic reassessment
- Thorough evaluation of comorbidities and risk factors.
- Regular reassessment of patient’s condition and adjusting the treatment plan as needed.
- Timing: 6 months after the initial presentation and then at least yearly.
- Imaging: TTE, CMR, TOE, nuclear - Proactive in identifying changes that could impact patient well-being.
- Promoting patient education and empowerment to improve efficiency of care and allow patients to identify when management changes are needed.
- Assess QOL, functional status, symptoms, treatment burden
Management algorithm for first diagnosed AF
- Haemodynamics
- Unstable -> electrical cardioversion then AF-CARE bundle
- Stable -> AF-CARE bundle - Rate control agents depending on LVEF
- Watchful waiting for spontaneous restoration < 48 hours (pAF)
- Cardioversion of symptomatic persistent AF
Management algorithm for paroxysmal AF
- Rate control target < 110/min (lenient), or stricter with continuing symptoms
- Agents depending on LVEF - Shared decision making on rhythm control - antiarrhythmias vs ablation
- Anti-arrhythmias:
> HFrEF -> amiodarone +/- sotalol (mrEF);
> No heart disease -> dronedarone, flecainide, propafenone +/- sotalol
- Catheter ablation (class I) - Monitor for recurrence of AF and consider further ablation, anti-arrhythmias or surgical ablation
Management algorithm for persistent AF
- Rate control target < 110/min (lenient), or stricter with continuing symptoms
- Shared decision making on rhythm control - antiarrhythmias vs ablation
- Anti-arrhythmias:
> HFrEF -> amiodarone +/- sotalol (mrEF);
> No heart disease -> dronedarone, flecainide, propafenone +/- sotalol - Shared decision making on rhythm control
- Electrical cardioversion in haemodynamic instability, rhythm control, benefits of SR
- Anti-arrhythmias
- Catheter ablation (IIb) - Monitor for recurrence of AF and consider further ablation, anti-arrhythmias or surgical ablation
Management algorithm for permanent AF
- Severely symptomatic/HF hospitalisation - consider AV node ablation and CRT (IIa)
- Stable patients, depending on LVEF
- < 40%: beta blockers or digoxin -> rate control
- > 40%: BB, digoxin, diltiazem or verapamil -> rate control - Consider intensity rate control therapy
- Evaluate for AV node ablation and pacemaker (IIa)
CHA2DS2VASc Score for AF
C - congestive heart failure
H - hypertension
A2 - Age > 75 years
A1 - Age 65-75 years
D - Diabetes
S2 - Stroke / TIA / thromboembolism
V - MI, PAD, plaque
S - Sex (female 1)
HASBLED Score vs ORBIT for AF
HASBLED
H (+1) - Hypertension uncontrolled > 160
A (+1-2) - Abnormal liver and/or renal function
S (+1) - Stroke
B (+1) - Bleeding history or anaemia
L (+1) - Labile INR TTR < 60%
E (+1) - Elderly > 65 years
D (+1-2) - Drugs (antiplatlets, NSAIDs) and/or alcohol
3 or more (high risk); 1-2 (intermediate risk)
ORBIT Score
+1 Age > 74 years
+2 Bleeding history
+1 GFR < 60
+1 Antiplatlet
4 or more (high risk); 3 (intermediate); 0-2 (low risk)
Choice of anticoagulation in AF
What are the evidence for DOAC?
What are the evidence for VKA?
- DOAC preferred to VKAs except valvular AF
- Target INR 2-3
- Switch to DOAC for eligible patients that failed to maintain therapeutic VKA INR range
- DO NOT dose adjust DOAC unless met specific criterias (increase stroke risk without reducing bleeding risk)
Evidence for DOAC
1. Non-inferior in non-valvular AF (superior in ARISTOTLE-AF trial)
2. 50% reduction in ICH, but similar to higher risk of other bleed (ROCKET-AF)
3. UNSAFE in valvular AF (PROACT Xa trial)
Evidence for VKA
1. Reduces stroke risk by 64%, reduces mortality by 25%
2. MUST be on VKA for mechanical valve and MS
3. Target INR 2-3 (established in lower vs standard INR target for warfarin)
4. Higher intracranial bleeding and other types of bleeding (GARFIELD-AF)
Balancing bleeding risk in AF
- DO NOT use bleeding risk score to decide or withdraw OAC, or even underdose OAC
- Assess and manage modifiable bleeding risk factors
- PPI use individualised - RCT on pantoprazole in rivaroxaban/aspirin did not show any impact
Management of compressible bleeding on OAC
- Compress bleeding site mechanically
- Assess haemodynamics, coagulation panel, FBC and RP
- Determine OAC and last dose
- Hold off OAC until stabilised
VKA
Life threatening: resuscitation, transfusion, PCC preferred than Vit K (FFP if no PCC)
(PCC achieves faster coagulation with fewer complications compared to traditional antidote Vit K)
Major bleed: consider PCC, FFP or vitamin K
Minor bleed: hold VKA until INR < 2
DOAC
Life threatening: resuscitation, transfusion, antidote, PCC if no antidote, monitor DOAC level
(Antidote: andexanet alfa)
Major bleed: charcoal or gastic lavage if DOAC taken within 2-4 hours, consider PCC if needed
Minor bleed: hold DOAC for a few doses
Post-bleeding management
1. Re-discuss risk and benefits of restarting OAC (shared decision making)
2. Review choice and dose of OAC
3. Re-initiate OAC after source of bleeding controlled
4. Assess risk of rebleeding, modify bleeding risk factors
Acute AF with RVR heart rate control
- Look and treat reversible causes of rapid AF (eg: sepsis, fluid overload, cardiogenic shock)
- Choice of drug depends on clinical status, HF and EF
A. Beta blockers - selective > non-selective
B. Diltiazem/verapamil - avoided in EF < 40%
C. Digoxin - slower onset of action and less effective in HR control during acute onset, to consider in combination with beta blockers
(RATE-AF trial - low dose digoxin comparable to bisoprolol for QOL in AF, fewer adverse effects)
D. Intravenous amiodarone, landiolol, digoxin - haemodynamically unstable patients with reduced EF
An approach to cardioversion in AF
A. Consider rhythm control in:
1. Symptomatic patients, including HF
2. Haemodynamic instability
3. Suspected tachycardia-induced cardiomyopathy
4. Brief AF history
5. Non-dilated left atrium (best chance of maintenance of sinus rhythm)
6. Patient prefernce
B. Anticoagulation choice
1. AF < 24 hours: no need prior anticoagulation
2. AF > 24 hours: either
> therapeutic anticoagulation at least 3 weeks OR
> TOE to rule out thrombus
C. Choice of cardioversion
1. Wait-and-see approach
2. Electrical cardioversion
3. Chemical cardioversion
D. Post-procedure anticoagulation
- Continue at least 4 weeks after cardioversion
- Continue indefinitely in high stroke risk factors regardless whether SR is maintained
The only exception of anticoagulation is:
- SR restoration within 24 hours of AF
- NO thromboembolic risk factors
Pill-in-the-pocket approach for pAF
Single dose of flecainide or propafenone standby at home
For infrequent, symptomatic, recent-onset paroxysmal AF.
Selection criteria:
1. Excluded sinus node disease, AV conduction defect, Brugada syndrome
2. Tested in hospital prior to ensure safety and effectiveness
3. AV nodal blocking agent beforehand to prevent development of atrial flutter and rapid conduction
Antithrombotic therapy post-ACS and PCI
AUGUSTUS trial:
- Short-term triple therapy (≤1 week)
- OAC + a P2Y12 inhibitor (usually clopidogrel) for 1 year
- Then lifelong OAC
Longer duration triple therapy (up to 1 month) in patients at very high ischemic risk if the ischemic risk outweighs the bleeding risk:
- STEMI
- Prior stent thrombosis
- Complex PCI
Emerging studies: EPIDAURUS, WOEST-3
