DIAGNOSIS OF PAF
by Dr Adam Fitzpatrick
Consultant Cardiologist and Electrophysiologist
Manchester Royal Infirmary
Paroxysmal AF, (PAF), lasts less than 7 days, with the majority of episodes terminating within 48 hours. AF lasting for more than 7 days is "persistent AF" 1.
The natural history is for PAF to become persistent.
Persistent AF becomes less likely to revert to sinus rhythm the longer it persists. The longer persistent AF persists the lower the chances of a return to sinus rhythm, and the more likely that chronic AF will result.
When PAF is suspected, symptom/ECG diagnosis is essential. Patients may attend general practice with PAF, (and the Quality Outcomes Framework, QOF, allows payment for diagnosis of AF), attend A&E, or have PAF detected with ambulatory monitoring. Because PAF leads on to chronic AF and the increased mortality, health-care costs and stroke-risk, confirming PAF is an important priority in patients with symptomatic palpitations.
PAF and chronic AF are associated with ischaemic heart disease, mitral valve disease, hypertension, cardiomyopathy, alcohol excess and thyrotoxicosis. These should be sought and treated. Electrocardiography is important for the diagnosis of AF and any other related condition. Echocardiography should always be undertaken to look for left ventricular dysfunction secondary to ischaemic heart disease, dilated cardiomyopathy, left ventricular hypertrophy (caused by hypertension), septal defects, mitral valve disease and myxoma can all precipitate AF.
The history may establish if there is a pattern to PAF. The physician should ask if attacks occur with exercise (adrenergic PAF) or at rest/with food (vagally mediated PAF), or if excessive alcohol use is a contributory factor.
MANAGEMENT OF PAF
Treatment for PAF should alleviate symptoms and aim for chronic AF to be avoided, preventing the risk of thromboembolic stroke, heart failure and cognitive dysfunction.
Anti-arrhythmic drugs to suppress AF may have important side-effects 1.
Physical treatments, such as Catheter Ablation have yet to be proven to improve the long-term outcome by influencing the natural history of deterioration in AF 3-5.
Symptom-control with antiarrhythmic drugs, pacemakers or catheter ablation 6, is accepted practice.
Treatment is also need for ventricular rate-control in prolonged paroxysms of AF.
Infrequent PAF may need no treatment, but does require review. The natural history of PAF is progress to persistent or permanent AF and maintenance of sinus rhythm may prevent this 1.
DRUG TREATMENT FOR PAF
In PAF the aim of drug treatment is the suppression of AF to relieve symptoms and to prevent or delay progression to established AF.
Progression of PAF to established AF is likely 7.
In PAF, there is a role for the use of all four Vaughan-Williams classes of antiarrhythmic drug; sodium channel, (flecainide, propafenone), and potassium channel, (amiodarone, sotalol), blocking drugs, b-blockers and calcium-channel blockers 8-10.
However, flecainide and amiodarone are by far the most effective drugs for suppression of PAF, and b-blockers are relatively ineffective 11.
Amiodarone is very toxic, especially with prolonged use 12, so flecainide is the drug of choice for PAF in structurally-normal hearts 13 14 .
All classes of anti-arrhythmic drugs have pro-arrhythmic side effects 15, and may be responsible for causing abnormal heart rhythms. However, the risk of pro-arrhythmia is low in patients with lone PAF and structurally normal hearts.
Flecainide should be started with caution and combined with atrio-ventricular nodal blocking agents where atrial flutter is a concern. Flecainide may encourage PAF to settle into common atrial flutter. Very rapid ventricular rates due to the anti-cholinergic effects of flecainide, and deaths have been reported as a result 16. This is much more likely with intravenous use of flecainide. Where PAF is clearly exercise-related, it makes sense to opt for ß-blockade as a first drug trial.
In patients where ß blockers, flecainide or other sodium-channel blockers are ineffective, amiodarone can be tried.
Amiodarone is very effective in maintaining sinus rhythm 17.
Long term use of amiodarone risks important side effects which have a cumulative incidence over time, e.g. photosensitivity, thyroid dysfunction, hepatic and neuro-toxicity, corneal microdeposits and pulmonary fibrosis 17.
Amiodarone has a low risk of proarrhythmia 17.
Amiodarone is a sensible choice for suppression of PAF in elderly patients, and patients with previous myocardial infarction or other structural heart disease 18.
ANTICOAGULATION IN PAF
Whereas the evidence from several large randomised placebo-controlled trials have provided guidance for the use of anticoagulation in persistent or established AF, there is less conclusive evidence in PAF because of the wide variation in the burden of arrhythmia in PAF, and hence difficulty in matching patients for enrolment into trials.
International Guidelines from the AHA/ACC/ESC advise the same rules for antithrombotic therapy for all types of AF.
In lone AF where drug or other treatment suppresses PAF effectively, the need for anticoagulation may be removed, and aspirin or no antithrombotic therapy may be the correct approach.
CATHETER ABLATION FOR PAF
Catheter ablation for PAF is growing in importance.
Techniques are directed at cauterising areas of high irritability that give rise to frequent ectopy and trigger PAF 19, or cauterisation of the substrate that maintains PAF 34, (predominantly left atrial tissue), or both. Usually this is done with radiofrequency energy delivered percutaneously by steerable catheters, (RFCA). In the UK, recent Guidance from NICE approved catheter ablation for PAF on the NHS for patients who have failed treatment with two antiarrhythmic drugs 19. Similar guidelines exist in the USA.
Success rates of 70-80% can be achieved, with multiple procedures being needed in many cases.
RFCA for PAF carries significant risks. These are; stroke (<1%), cardiac tamponade (2-6%), pulmonary vein stenosis (0.5-1%), a small risk of arteriovenous fistula (<0.5%), and a very small but important risk of oesophago-atrial fistula 19.
In older patients, (>70 years), patients with structural heart disease and patients with persistent or prolonged AF, there is significantly less chance of success with RFCA.
RFCA for PAF is a technique in development.
So-called "electroanatomic mapping systems" (a form of mini-"GPS", or "Sat-Nav" system), are becoming increasingly sophisticated at telling an electrophysiologist exactly where a catheter is within the heart, and exactly where anatomical structures are located relative to it. This is important for avoiding complications. Centres performing RFCA for AF should have these systems, should be undertaking regular RFCA procedures, and should have skilled technicians to support the doctors.
A CT Scan or MRI scan of heart chambers is useful for obtaining the detailed anatomy of the heart for RFCA procedures.
RFCA for PAF has resulted in fewer patients with drug-refractory PAF being offered RFCA of the AV-junction followed by implantation of a pacemaker.
RFCA of the AV-junction followed by implantation of a pacemaker provides good control of symptoms, reduced drug and healthcare consumption, and reduced hospital admissions 37. However, AV-junctional ablation is not reversible, and allows atrial fibrillation to continue, albeit without allowing it to produce rapid, irregular ventricular rates, so that patients may be unaware of being in PAF.
RFCA of the AV-junction followed by implantation of a pacemaker is increasingly reserved for patients with established/chronic AF in whom ventricular rate-control cannot be achieved with AV-nodal blocking drugs. In these patients AF persists in spite of treatment anyway, and RFCA of the AV-junction with permanent pacing can give excellent symptom control.
Fig 1. CT or MRI tomography can be reconstructed in 3D, (right of picture) and imported into eletroanatomic mapping systems that create a virtual anatomy, (left of picture).
THE ROLE OF PACING IN PAF
Permanent pacing has a role in suppression of PAF. The pacing mode selected must including pacing and sensing of the atrium, since ventricular pacing alone will make matters worse. Pacing the atrial septum, rather than the right atrial appendage, and multi-site atrial pacing have been claimed to achieve better control of PAF.
- Kopecky SL, Gersh BJ, McGoon MD, et al. The natural history of lone atrial fibrillation. A population-based study over three decades. N Engl J Med 1987;317:669-74.
- Levy S, Camm AJ, Saksena S, et al. International consensus on nomenclature and classification of atrial fibrillation: A collaborative project of the Working Group on Arrhythmias and the Working Group of Cardiac Pacing of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. J Cardiovasc Electrophysiol 2003;14:443-5.
- Wyse DG, Waldo AL, DiMarco JP, et al. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 2002;347:1825-33.
- Pappone C, Santinelli V. Atrial fibrillation ablation: state of the art. Am J Cardiol 2005;96:59L-64L.
- Jais P, Sanders P, Hsu LF, Hocini M, Haissaguerre M. Catheter ablation for atrial fibrillation. Heart 2005;91:7-9.
- NICE. Percutaneous radiofrequency ablation for atrial fibrillation. National Institute for Health and Clinical Excellence/www.nice.org/IPG168 2006;Guidance 168.
- Echt DS, Liebson PR, Mitchell LB, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. N Engl J Med 1991;324:781-8.
- Haissaguerre M, Shah DC, Jais P, et al. Electrophysiological breakthroughs from the left atrium to the pulmonary veins. Circulation 2000;102:2463-5.
- Jais P, Shah DC, Haissaguerre M, Hocini M, Garrigue S, Clementy J. Atrial fibrillation: role of arrhythmogenic foci. J Interv Card Electrophysiol 2000;4 Suppl 1:29-37.
- Lin WS, Prakash VS, Tai CT, et al. Pulmonary vein morphology in patients with paroxysmal atrial fibrillation initiated by ectopic beats originating from the pulmonary veins: implications for catheter ablation. Circulation 2000;101:1274-81.
- Chen SA, Hsieh MH, Tai CT, et al. Initiation of atrial fibrillation by ectopic beats originating from the pulmonary veins: electrophysiological characteristics, pharmacological responses, and effects of radiofrequency ablation. Circulation 1999;100:1879-86.
- Wazni OM, Marrouche NF, Martin DO, et al. Radiofrequency ablation vs antiarrhythmic drugs as first-line treatment of symptomatic atrial fibrillation: a randomized trial. Jama 2005;293:2634-40.
- Cappato R, Calkins H, Chen SA, et al. Worldwide survey on the methods, efficacy, and safety of catheter ablation for human atrial fibrillation. Circulation 2005;111:1100-5.
- Kale M, Bennett DH. Atrial septal pacing in the prevention of paroxysmal atrial fibrillation refractory to antiarrhythmic drugs. Int J Cardiol 2002;82:167-75.
- Kale M, Bennett DH. Pacemaker prevention therapies for the control of drug-refractory paroxysmal atrial fibrillation. Europace 2003;5:123-31.
- Mitchell AR. 'The patient takes charge'--long term use of the atrial defibrillator. Eur Heart J 2003;24:2075-6.
- Spurrell P, Mitchell A, Kamalvand K, Higson M, Sulke N. Does sinus rhythm beget sinus rhythm? Long-term follow-up of the patient activated atrial defibrillator. Pacing Clin Electrophysiol 2004;27:175-81.
- Spurrell P, Mitchell A, Kamalvand K, Sulke N. Quality of life after use of the patient activated atrial defibrillator. Int J Clin Pract 2003;57:30-4.
- Flaker GC, Blackshear JL, McBride R, Kronmal RA, Halperin JL, Hart RG. Antiarrhythmic drug therapy and cardiac mortality in atrial fibrillation. The Stroke Prevention in Atrial Fibrillation Investigators. J Am Coll Cardiol 1992;20:527-32.