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          Patterns, pearls and practical medicine

Atrial Fibrillation & Flutter

The Stats

  • Around 1.3 million people are living with AF in the UK (incidence increasing due to aging/comorbidities/awareness/technology)
  • Up to one-third of patients with AF are asymptomatic at diagnosis
  • AF drops the cardiac output by about 20%
  • Prevalence of AF is around 15% for those in their 80s
  • Lifetime risk was 1 in 5, but probably now 1 in 3
  • One third have no evidence of cardiac disease (in these, AF likely precipitated by rapid burst activity within pulmonary veins)

Forms

  • Paroxysmal AF – AF that terminates spontaneously (or with an intervention) within 7 days. Most self-terminating AF lasts <48 hours
  • Persistent AF – AF that lasts for > 7 days, with no upper limit, but where rhythm control is still a treatment option
  • Permanent AF – AF in which no further attempts at restoring sinus rhythm are planned
  • Generally speaking, paroxysmal, persistent and permanent AF should be treated equally, as all similarly bad. Often begins as paroxysmal but progresses to permanent
  • AF is very often a consequence of other pathology

Risk factors and precipitants

  • Commonest risk factor is hypertension
      • This also increases risk of CVA, HF and bleeding
      • A 10mmgHg drop in systolic BP reduces risk of AF by 17%
  • The strongest risk factors are
    • Rheumatic valve disease
    • HF
  • DM is present in 25% of AF, and carries worse prognosis
  • OSA is an important and underappreciated risk
  • Obesity is an independent risk factor and weight loss reduces risk of AF recurrence. Sustained weight loss of >10% can be almost as effective as ablation in treating AF. GLP1 drugs useful here (if a patient qualifies)
  • ETOH increases risk, even with lowish levels of consumption. Much less likely to recur if you abstain
  • Smoking
  • Physical activity moderately reduces risk, however high intensity exercise increases risk (U shaped curve), especially in men (endurance athletes have >2.5x risk of AF compared to non-athlete controls)
  • Caffeine does not increase risk
  • In new AF – consider potential underlying triggers (in susceptible patients)
      • Often none identifiable
      • Infections (incl COPD exacerbation)
      • Ischaemia
      • Mitral valve disease
      • HF / cardiomyopathies
      • Thyrotoxicosis
      • Acute ETOH / drugs
      • Electrolyte abnormalities – esp K+ and Mg2+
      • Rarer – rheumatic heart disease, sick sinus syndrome, HTN, PE, pericarditis, cancer, WPW, ASD, pheochromocytoma, pulmonary disease, exercise

Symptoms

  • Around 10% asymptomatic at all times
  • May be more prevalent in women
  • Presence of symptoms does not correlate to risk of complications
  • May include
    • Fatigue (common)
    • Palpitations (often impair quality of life) and anxiety
    • Chest pain
    • SOB and reduced ET
    • Dizziness
    • Syncope
    • Disordered sleep
  • Symptoms need to be evaluated after changes in treatment, and to guide treatment

Diagnosis and investigation

  • ECG
      • Typically AF is an irregularly irregular rhythm, with no P waves, small baseline undulations (F waves), an erratic baseline and variable ventricular rate
      • Particularly chaotic activity seen best in V1 (And if it only looks like flutter in V1 and nowhere else – that’s AF, not flutter with variable block)
  • Can be picked up on wearable devices like Apple watches or loop recorders (esp if post-CVA and suspicion of paroxysmal AF)
  • Can be diagnosed on devices that provide a single lead ECG but not on non-ECG wearables that can detect rhythm abnormalities
  • 30 seconds of AF needed to make a diagnosis of paroxysmal AF if it’s noted on a device (If possible intermittent AF – consider a Reveal device)
  • Holter can be used to diagnose AF, assess AF burden, or decide on rate-control strategy
  • Bloods – trop, BNP, TFTs, CRP, LFTs, lipids, HbA1c. Consider d-dimer.
  • Echo (sometimes TOE if LA thrombus suspected). Should not delay decision to start anticoagulation.
  • Consider CTCA / invasive angiogram / CMR
  • CT head if cognitive decline, confusion, neurology
  • Sleep study if OSA suspected
  • BP diary
  • Can be picked up on PPM interrogation – if asymptomatic, always discuss management of AF diagnosed in this scenario with cardiology

Complications

  • The risk of ischaemic CVA in AF is 5 times higher (more if co-existent HF) and CVAs from AF tend to be more severe
      • Risk of clot 5% / year in AF
      • 15%/year if AF and valvular HD (8% / year with mechanical valve and 40% / year if recent VTE).
  • Thromboembolism to other organs (esp arterial thromboses)
  • AF predisposes to dementia, mainly vascular dementia (unclear if associated with Alzheimer’s), and anticoagulation reduces this risk
  • HF – can be due to tachycardiomyopathy, can be a risk factor for AF itself. Develops in around 50% of all patients with AF eventually and those with AF have a 4-5 fold increased risk of HF
  • Anxiety and depression
  • Increased all-cause mortality (relative risk of 2)

 Three stage management overview

  • A – Anticoagulate / Avoid Stroke
      • Check CHA2DS2VASc and bleeding risk
  • B – Better symptom control
      • Rate and rhythm control (patients often require both)
      • Consider drugs, ablation, cardioversion, surgical ablation, ablate and pace
      • Rhythm control better for paroxysmal AF where patient more likely to be young and symptomatic
      • Rate control best for permanent AF
      • For persistent AF – control rate short term, consider DC cardioversion later, which is also a kind of diagnostic tool
  • C – Address CV risk factors, lifestyle and comorbidities
      • Including HTN, HF, obesity, OSA, DM, exercise and ETOH
  • Shared decision making and education/empowerment vital in all stages
  • Multidisciplinary approach is useful

Acute management of fast AF

  • Often this is a consequence of physiological stress (particularly if fast) – so look for the precipitant and treat if possible
  • Tasks
      • Correct electrolyte disturbance
      • Treat infections
      • Consider potential triggers (especially undiagnosed thyrotoxicosis, PE, ETOH/drugs, HF, IHD)
      • Anticoagulate (calculate CHASVASC and consider bleeding risk). Consider continuing long term even if trigger-associated AF, but on a case-by case basis
  • If unstable
      • Cardiovert +/- heparin
      • However AF rarely causes haemodynamic compromise unless there’s severe LV impairment
      • If rate < 150, unlikely that AF is causing hypotension alone. Compromise due to AF alone is rare
      • Very sick patients also won’t tolerate AF well – you might want to cardiovert earlier, perhaps with amiodarone
  • If AF present for < 24 hours
      • Urgent echo if symptoms of HF
      • Cardioversion, either DC or chemical (Eg amiodarone 5mg/kg over 1 hour, or if sure no structural heart disease use flecainide 2mg/kg (max 150mg) over 30 mins – success rate 55%)
      • Can also cardiovert if has taken > 3 weeks of anticoagulation (anticoagulate everyone if planning to cardiovert, independent of CHADVASC)
      • Success rate of shock is 80%
      • If can’t cardiovert and stable – move to rate control
      • Consider cardioverting after 3 weeks of anticoagulation – Prioritise rhythm control for new onset, young and symptomatic patients, those with tachycardiomyopathy, flutter, treated reversible cause
  • If unsure when AF started, or > 24 hours
      • Rate control (target <110). Options include:
      • Betablocker
          • Bisoprolol 2.5-10mg PO – Ask about asthma, might also avoid in hypotension or florid pulmonary oedema
          • Metoprolol 2.5mg (elderly) to 5mg IV – Up to max 15mg IV total. Usual maintenance is 25mg TDS PO
      • Calcium Channel Blocker (CCB)
          • Diltiazem 0.25mg/kg IV bolus over 5 minutes, then 10mg/hour. Maintenance is usually 180-300mg daily (so a low dose is 60mg TDS)
          • Verapamil 5mg IV or 40mg TDS PO maintenance
          • Avoid CCB if decompensated HF (or if EF <40%), but useful in severe asthma where you want to avoid a betablocker
      • Digoxin
          • 500mcg PO or IV loading, then repeat in 4 hours, then maintenance 62.5-250 mcg (depends on age, weight, renal function). Can give max 1.5 mg over 24 hours in divided doses.
          • Often first line if elderly, HF, immobile. Can be given if unstable.
          • Adjust dose in CKD
      • CCBs and betablocker are 1st line as they act faster than digoxin and have dose-dependent effects
      • Ineffective monotherapy – can use betablocker or diltiazem, plus digoxin
      • If beta blocker and digoxin not working – discuss with cardiology re: synchronised DCCV with TOE guidance (to look for thrombus in LA appendage) if not already anticoagulated for 28 days
      • Amiodarone
          • Often given if nothing else works (or in patients who do not qualify for atrioventricular node ablation and pacing)
          • Generally not given if not already anticoagulated for 28 days, as they can cardiovert and there’s a risk of stroke
          • Sometimes given if BP is low but patient not unstable, or if patient unstable and shock resistant.
          • Dose is 150-300mg IV over 20-60 mins, then then 900mg infusion over 24 hours (in 500ml-1L fluid)
          • Should not be given peripherally but often is in emergencies. Extravasation injury is common and can be severe
  • Can try magnesium too. Some suggest aiming to keep Mg2+ > 1.0
  • On discharge
      • Aim for HR < 110 for 2 hours
      • Outpatient echo if not had one
      • CV risk factor advice
      • Cardiology f/u and give patient copy of their ECGs
      • Anticoagulation clinic f/u if required

Management of AF in special circumstances

  • AF in context of acute infection / sepsis
      • AF is often transient and reversible in critical care, and often due to a non-cardiac cause like infection
      • Consider it a marker of illness severity
      • Most revert spontaneously
      • Reserve rate control for those with haemodynamic compromise. Amiodarone sometimes given. Betablockers can be used. Avoid diltiazem.
      • Ensure echo if not had one
      • If peri-arrest / unstable with AF but also sepsis and otherwise compromised – usually shock rather than simply treating cause of AF (but ideally anticoagulate first, or do TOE)
  • AF in context of ACS
      • Usually use anticoagulation and DAPT for one week, then stop aspirin after a week, and stop clopidogrel after 6 or 12 months (but could continue triple therapy for more than one week if ischaemic risks outweighs bleeding risks)
      • If high risk of bleeding, you can reduce dose of rivaroxaban from 20mg to 15mg OD
  • AF in the context of acute stroke
      • Jury is out on when to restart anticoagulation after ischaemic stroke, but probably wait at least 48 hours, and wait longer if larger stroke
  • Peri-op AF
      • Most commonly occurs after cardiac and thoracic surgery
      • Often self-terminating, however risk of recurrent AF is increased 5-fold in these patients
      • Manage as other forms of trigger-associated AF
      • Some will still need long term anticoagulation (started once acute bleeding risk has settled), esp if AF persists beyond 48 hours (but sometimes even if it doesn’t)
  • Pre-exited AF
      • Very fast, sometimes > 220
      • Avoid adenosine, betablocker, verapamil, digoxin (can cause VF)
      • Can potentially give flecainide, procainamide, ibutilide
      • But usually DC cardiovert and then ablate later
      • WPW on its own is usually asymptomatic, treat as an outpatient
  • AF with heart failure
      • Risk factors for HF and AF are closely aligned, and AF is both a cause and a consequence of HF. Acute AF commonly precipitates acute HF
      • All of the 4 pillars (prognostic medications, or GDMT) reduce risk of AF in HF
      • Avoid CCB for rate control, and be cautious with betablockers. Digoxin ok but takes time to work
      • Ablation can improve outcomes
  • AF with thyrotoxicosis
      • Risk of AF correlates to elevation of T4 and reduction of TSH
      • Risk of CVA higher in these patients.
      • Check whether patient has had amiodarone before, which may be the cause of the thyroid dysfunction
      • AF often reverts once euthyroid
  • AF in pregnancy
  • Exercise with AF
      • Moderate activity reduces risk of AF but risk of AF increased up to 5 fold in middle aged endurance athletes, especcially if tall, male, and exercising >20 years
      • But also rule out other underlying causes in athletes, including use of performance enhancing drugs
      • Ablation recommended
      • Check ventricular rate during exercise
  • Slow AF
      • Can be confused with complete heart block (which will be slow and regular and you might not be able to see P waves)
      • Often PPM required
  • AF with difficulty in rate control
      • Consider referring for AV node ablation and PPM
  • Myasthenia gravis and fast AF
      • Many of the usual rate limiting drugs are contraindicated eg betablockers, CCBs, digoxin. Options depend a bit on the echo, but could consider early cardioversion (+/- TOE if can’t wait for 3 weeks of anticoagulation), ablation, or ablate and pace

Anticoagulation

  • Reduces risk of stroke but there remains a residual risk (in part this may be due to non-adherence, or non-AF related stroke mechanisms)
  • If need to anticoagulate for cardioversion – use treatment dose LMWH, or IV bolus of heparin (continue heparin afterwards)
  • The SPARCtool helps estimate annual stroke risk and compare the potential benefits and risks of antithrombotic therapy in patients with non-valvular AF
  • The CHA2DS2-VASc score (or CHADSVA, which omits sex)
      • Based on – hx of HF or HTN, Age, prior stroke/TIA/arterial thromboembolism, DM, vascular disease, sex
      • Generally anticoagulation indicated by CHA2DS2VASc scores of two or more (and treatment should also be considered for males with a score of one or more).
      • Some clinicians will not score female sex on CHADSVASC unless pt > 65 years old
      • If patient cardioverted, still have to do CHA2DS2VASc score (may need 4 weeks of anticoagulation if score over 2)
      • HF includes those with preserved and reduced EF (anyone with signs and symptoms)
      • Score for age if >65, and 2 points if aged >75
      • Subclinical device-detected AF does not carry the same prognostic risk and must be interpreted in the context of AF burden, bleeding risk and stroke risk. Discuss with cardiology. Otherwsise pattern of AF should not determine decision to treat
      • CHA2DS2VASc of 1 gives CVA risk of 1-2% annually. Score of 4 gives risk of 4-9%. Score of 7 gives risk of 9-21%. DOAC reduces risk by about 2/3
      • Not validated in HCM or amyloidosis – these patients should be anticoagulated regardless of score if not contraindicated
      • Does not include other factors that are known to increase stroke risk eg atrial enlargement, smoking, cancer, CKD, hyperlipidaemia, obesity
      • Should be reassessed if low and anything changes
  • Bleeding risks
      • Can be reduced by controlling BP, limiting ETOH, avoiding NSAIDs if possible, prescribing PPIs, reducing trauma-risk (consider falls, hobbies, occupations)
      • The risk of CVA usually outweighs the risk of bleeding
      • Consider bleeding risk scores but do not use in isolation to decide on anticoagulation
      • Consider other factors which also contribute and are not included in risk scores – eg dementia, cancer, cirrhosis, intracranial pathology
      • Primary intracranial tumours or an intracerebral bleed related to cerebral amyloid angiopathy are examples where OAC should be avoided, many other contraindications are relative or temporary
      • 5% of patients have high risk of CVA and high bleeding risk and are not anticoagulated
      • There is still a significant risk of CVA if anticoagulated but much less
  • Choice of anticoagulant – consider:
      • Patient weight
      • Renal function
      • Presence of valve disease
          • Warfarin best in mod-severe MS, or mechanical valves
          • DOACs preferred in all other valve disease
      • Likely drug compliance
          • > 20% of patients on anticoagulation are probably non-adherent after 12 months
      • Bleeding risk  and CHA2DS2VASc
          • Bleeding risk is higher with VKAs
      • Drug interactions
          • Especially ASMs like carbamazepine and phenytoin, rifampicin. Also antifungals and NSAIDs
          • Generally speaking combining anticoagulation with anti-platelets should only occur in patients with acute vascular disease
      • Contraindications
          • History of intracranial bleed or intraocular haemorrhage
          • Severe GI bleed history
          • Cerebral amyloid angiopathy
          • High HASBLED score
  • DOACs
      • Non-inferior to warfarin in preventing stroke, but with an reduced risk of bleeding esp ICH
      • Apixaban BD – first line. Lower risk of major bleeding (esp intracranial) and better at preventing stroke than warfarin.
      • May need dose reduction if eGFR <30, weight <60kg
      • Inappropriate dose reduction in DOAC increase risk of stroke without decreasing bleeding risk
      • If a stroke occurs, switching DOACs is not advised
  • Dabigatran
      • An option in elderly patients with bleeding risk as there is a reversal agent but GI side effects common.
      • Contraindicated if eGFR <30
  • Warfarin
      • Target INR 2-3 for management of AF (consider changing to alternative if >70% of time is out of therapeutic range)
      • Sometimes used if co-existing valvular disease or LV thrombus
      • Avoid prescribing with some antifungals, NSAIDs, fluoxetine
      • If taking Carbamazepine, patients will require a higher warfarin dose (and vica versa if taking amiodarone, metronidazole, allopurinol)
  • Dual antiplatelet therapy (DAPT) of aspirin 75 mg daily plus clopidogrel 75 mg daily may be suitable for people who are unable or unwilling to take anticoagulants (Aspirin alone does not have a role in stroke prevention in context of AF). However this is controversial, and some guidelines advise against. DAPT is much less effective than anticoagulation and carries similar risks of bleeding.
  • New factor XI inhibitors – watch this space!
  • Duration
      • Anticoagulation is often continued after a precipitant for AF has been treated (eg infection) as patient has proven their tendency for AF.
      • It’s also often continued after ablation and for 4 weeks post cardioversion (though if onset if definitively within 24 hours can sometimes omit anticoagulation). However, latest data suggest anticoagulation could probably be stopped if successfully ablated, CHADVASC of 2, and especially if using a smart watch (data incoming)
      • Long term anticoagulation should now be considered if patient goes into AF post op
      • Anticoagulation should continue for at least 3 weeks before and 4 weeks after TOE-cardioversion
      • If AF present for > 48 hours and no adverse features, patient should be anticoagulated for > 3 weeks before attempting DC cardioversion (or do TOE)
  • If anticoagulation contraindicated consider a left atrial appendage occlusion device (90% of clots form here) or surgical closure of LA appendage (alongside anticoagulation) if patient undergoing ablation
  • LA occlusion device 
      • Success rate 95%. Major complication includes device dislodgment and pericardial effusion (1%).
      • Needs DAPT for 6 weeks. Continue single antiplatelet for 6 months or stop after a check CT/ TOE
      • Needs TOE in 6 weeks afterwards (for leak / thrombus)
      • Devices are MRI compatible
      • Superior to warfarin at preventing CVA. Similar to DOACs.
      • Can be performed in 10 centres across UK (3 in London)
      • Must have CHA2DS2VASc > 2 and contraindication to anticoagulation (previous bleed or HASBLED > 3). Also suitable if previous CVA despite anticoagulation.
      • Not suitable for very frail patients or those with expected survival < 3 years
      • Stroke risk reduction comparable to those on anticoagulation
      • Used most in those with previous haemorrhagic strokes or cerebral amyloid angiopathy or high CHA2DS2VASc and bleeding issues
  • If a stroke occurs on anticoagulation – check adherence, appropriateness of dose, and consider non-embolic causes

Rate-control as a long term treatment

  • The choice of drug should be based on the person’s symptoms, heart rate, comorbidities, and preferences
  • Targets
      • During rest, a lenient target heart rate <110 is adequate
      • A strict target of <80 bpm is recommended if patients remain symptomatic, have suspected tachycardiomyopathy, symptoms or deterioration of LV function, or have a biventricular pacemaker.
  • Rate control can exacerbate bradycardia, particularly with concomitant sinus node dysfunction or AV block (ie tachybrady syndrome); therefore PPM implantation might be required in some cases to enable safe escalation of rate control therapy
  • Betablocker
      • Bisoprolol or metoprolol usually 1st line
      • If BP a bit low and you’re a bit nervous about it – give metoprolol rather than bisoprolol, it’s out the system quicker
      • Contraindicated in asthma, uncontrolled HF, sick sinus syndrome, heart block, hypotension, severe peripheral vascular disease
  • CCB
      • Diltiazem or verapamil
      • Useful in severe asthma
      • Contraindicated in heart failure, hypotension, sick sinus syndrome, heart block, AF with WPW, pregnancy/breastfeeding
  • Digoxin
      • An alternative in people with non‑paroxysmal atrial fibrillation who are sedentary (do no or very little physical exercise).
      • It can be better than betablockers in elderly patients for achieving rate control and works especially well in HF where it might be first line
      • Can add to a betablocker
      • Contraindicated in heart block, WPW, VT
      • Can be useful if rate not very fast
      • Can monitor levels
  • Amiodarone
      • Can assist with rate control too (but usually used for rhythm control).
      • Contraindications include thyroid disease, heart block, severe hypotension, CCF, pregnancy/breastfeeding
      • Numerous drug interactions
  • Flecainide
      • Contraindications: flutter, CCF, structural HD, recent MI
  • Sotolol
      • Check normal baseline QTC before starting, and recheck in 2 weeks after starting to ensure remains normal. Also monitor K+.
      • Contraindicated in HFrEF
  • Rate still uncontrolled
      • If they are taking the maximum drug dose, consider combination treatment with any two of the following drugs: a beta-blocker, digoxin, or diltiazem (but avoid giving both betablockers and CCBs)
      • If unable to rate control on drugs, consider PPM / AV node ablation

Rhythm control

  • Options are
      • Ablation
      • Anti-arrhythmic drugs
      • DC cardioversion
      • Wait and see if patient spontaneously cardioverts
  • Early rhythm control (within 12 months) improves heart outcomes and quality of life, and is generally considered better than rate control if feasible
  • Factors that favour rhythm control
      • Patients whose symptoms continue after heart rate has been controlled
      • Rate‑control strategy has not been successful
      • Suspected tachycardiomyopathy
      • A brief AF history
      • Non-dilated left atrium
      • Patient preference
  • Assess the symptom severity (AHRA symptom score), quality of life and patient preferences
  • Consider age of patient and likelihood of restoring SR long term when consider rate verses rhythm control
  • Better outcomes if used early (instead of just rate control approach) but often rate control used first
  • Ablation is more effective than drugs but still 40% relapse into AF at 12 months
  • Drugs
      • Less effective at restoring SR compared to DCCV
      • Generally avoid if sinus node dysfunction, AV conduction problems, prolonged QTC
      • Flecainide 1-2mg/kg over 10 mins IV, or 200-300mg PO
          • One of the most effective (55% at 3 hours, 80% at 8 hours)
          • Contraindicated in HF, significant CAD, Brugada, severe CKD, flutter, SN dysfunction, LVH
          • Stop infusion if QRS widening or BBB
          • Sometimes used as ‘pill in the pocket’ if recent onset paroxysmal AF
          • Maintenance dose 50-150mg BD (often used with a betablocker or CCB to prevent 1:1 conduction if rhythm transforms to flutter)
      • Amiodarone 300mg IV over 30-60 mins, then 900mg over 24 hours
          • Slower onset of action (can take 12 hours, or even several days)
          • Can be used in HF, LVH or CAD
          • Avoid in hyperthyroidism
          • Can cause hypotension, AV block, bradycardia, QT prolongation, phlebitis
          • Used long term to control rhythm (not rate) 200mg OD
      • Propafenone – similar contraindications to flecainide
      • Other options include Ibutilide, Vernakalant, Dronedarone, Sotolol
  • DC cardioversion
      • Consider electively if relatively recent onset (< 2 years) and very symptomatic
      • High recurrence rate (75% at one year without drugs, 40% at one year with amiodarone)
      • Ensure anticoagulated for > 3 weeks prior (or if more urgent, consider TOE. If thrombus present, anticoagulate for >4 weeks and repeat TOE)
      • Most patients should continue anticoagulation for 4 weeks after DC cardioversion (but sometimes can be omitted with SR restored within 24 hours of AF onset and no thromboembolic risk factors)
  • Ablation – see below

Ablation

  • Very strong evidence of benefit, but especially in paroxysmal AF patients, or those with tachycardia-related cardiomyopathy (it can reverse LV dysfunction). A cornerstone strategy for AF rhythm control
  • The most established and evidence-based technique is pulmonary vein isolation using radiofrequency or cryoballoon ablation
  • Better than drug therapy in trials, and reduces mortality compared with drug treatment
  • Success rate 90% if no underlying structural heart disease. Also high success rate if AF is paroxysmal or recent onset
  • Improves LV function in heart failure, and can prolong survival
  • Day case. Takes 90 minutes.
  • Indications – HF, AF refractory to medications, patient preference, AF causing significant symptoms
  • If patient has an increased risk of thromboembolism, they should be anticoagulated for > 3 weeks before ablation (and cardiac imaging advised if patient also has amyloid, rheumatic HD or HCM as these patients have an increased risk of CVA even if anticoagulated)
  • It is not a way of getting off anticoagulation – they usually stay on DOAC afterwards if CHADSVASC suggests you need it. Some say all patients should be anticoagulated for 2 months afterwards
  • Not so good if LA>45 mm, MV disease, HCM, congenital heart disease, longer AF duration, high BMI, failed cardioversions and multiple comorbidities
  • The best candidates have a structurally normal heart (esp normal LA size) and more recent AF, and few/no comorbidities.
  • Biggest benefit in patients with short duration AF, AF induced cardiomyopathy suspected, class 1 and 2 HF, no atrial fibrosis, pAF, younger patients or those without comorbidities, those who show significant improvement in LV function after cardioversion
  • Can be considered in sinus node disease eg slow AF/pauses/tachy-brady syndrome, to avoid PPM insertion
  • Consider ablation first line if:
      • AF paroxysmal
      • Persistent AF and not high risk for recurrence (ie no enlarged LA)
      • AF is associated with HF with reduced EF (and AF likely cause)
      • New onset AF
      • Flutter
      • Patient preference
  • Types
      • Radiofrequency ablation – burn around pulmonary veins
      • Cryoballoon ablation
      • Both equivalent. Takes < 1 hour. Cryoballoon a bit quicker
      • Pulsed field ablation (PFA) newest method with fewer complications. Comparable efficacy.
  • Risks
      • Pulmonary vein stenosis
      • Phrenic nerve palsy
      • Atrio-oesophageal fistula (rare but serious, <1:1000, 80% mortality)
      • Tamponade (2%)
      • Stroke / TIA (CVA 0.25%)
      • Haemolysis and coronary artery spasm can occur rarely with PFA
      • Unsuccessful
      • Death (1:2500)
  • More ablation = more risk. Similar risk to drug therapy
  • Contraindicated if LA thrombus
  • Pacing and AVN ablation (‘ablate and pace’)
      • A useful strategy for managing drug-refractory permanent AF with high ventricular rates esp in older patients.
      • Can reduce mortality rate compared with medical treatment
      • Fairly low risk
      • Insert PPM a few weeks before ablation (the choice of PPM depends on patient, and LV function, CRT sometimes used in HF)

Atrial flutter

  • Circuits counter-clockwise around tricuspid annulus in 90% (in the RA)
  • Easily amenable to ablation (although rarer flutter circuits exist and often harder to ablate – these may not appear as typical saw tooth)
  • Usually arises in the right atrium and associated with diseases that affect the right heart
  • Risk factors are similar to those of AF, and around half of patients with flutter will go on to develop AF
  • Stroke risk probably similar to AF
  • Often occurs in patients who also get AF
  • Unlikely to be 2:1 flutter if rate > 160 but possible when rates 125-150 (especially if rate slowed by drug tx)
  • ECG
      • Saw-tooth pattern most obvious in inferior leads (negative flutter waves) and positive flutter waves in V1
      • Diagnosis often missed
      • Ventricular rate depends on 1:1 (300), 2:1 (150, two large squares between QRS) and 3:1 conduction (100), 4:1 (75)
      • Flutter waves can be behind the QRS (so if you see 3 flutter waves between QRS’s, it’s probably 4:1 conduction)
      • Usually negative flutter waves in inferior leads and positive in V1 (unless atypical flutter)
      • Lead I tends to look quite flat with no visible p wave
      • Variable conduction causes irregular rhythm, otherwise its regular
  • Treatment
      • Generally speaking, manage as AF (though bear in mind that rate control can be a bit more difficult to achieve, and rhythm control is often preferred)
      • Stroke risk same as AF so anticoagulated based on CHA2DS2VASc
      • Give rate control eg betablocker or CCB like verapamil or diltiazem. Can add digoxin if required.
      • Drugs don’t work well but ablation does. Cures 95% of typical flutter. Around 60% of patients will later develop AF though after CTI line ablation
      • If ablation not successful, consider DC cardioversion or medical cardioversion with amiodarone or sotalol but patient will need anticoagulation for 4 weeks prior, or TOE guidance
      • Avoid flecainide as ventricular rate can increase (unless also using rate control)
      • If unwell – cardiovert

 

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