Catheter Ablation Therapy for Supraventricular Arrhythmias

DR MARINE: You’ve generally been healthy all your life and have been very active. When did you first notice something was amiss with your heart?

MS R: Well, it was around the year 2000. I was born in 1935, so you can do the math. It started with some “blips” or extra beats. And it didn't really bother me much at first, but they soon became more prolonged and bothersome. I had more and more arrhythmia and was getting desperate. The symptoms during palpitations progressed to almost passing out, and I also had a choking sensation in my neck when they occurred.

DR MARINE: How frequently was this happening?

MS R: Weekly at first, and then they became almost daily. It got to the point where I was falling and I was scared to walk. That's when the doctors started trying different medications. The medications would tend to work for a little while and then wear off. The arrhythmia got so strong that it would start at 4 in the afternoon and last for hours almost every day. At that time my palpitations were making my heart beat so hard and fast, like, you know, those cartoon shows where the heart goes out of the chest? That's what it was like. The first time it happened, I called for an ambulance. The second time, I drove myself to the nearest firehouse. By the fourth time, I couldn't even drive the car to the hospital. I was just on the verge of collapse all this time. And when I would go to sleep, the thought passed through my mind a few times: Am I going to wake up?

DR MARINE: At the time we met, Ms R was 69 years old and in very good health other than severe paroxysmal palpitations. During one of her visits to an emergency department, she had a 12-lead electrocardiogram (ECG) (Figure 1), which showed atrial fibrillation with a rapid ventricular response. She had multiple emergency department visits and physician visits as she described.

Her physical examination was unremarkable, and she appeared very healthy. Her workup included an echocardiogram showing a structurally normal heart. She underwent anticoagulation treatment with warfarin and started diltiazem and digoxin as an initial rate-control strategy. She was successively treated with propafenone and amiodarone, with failure of rhythm control therapy after about 6 months in each case. When she came to see me, she was taking warfarin and metoprolol and enduring the debilitating symptoms she described.

Ms R underwent a catheter-based ablation for treatment of atrial fibrillation and achieved relief of symptoms for several months before having recurrent episodes. She underwent a second procedure during which several pulmonary veins had to be reisolated. Since this second procedure, she has been free of documented atrial fibrillation for 18 months. Holter and event monitoring have demonstrated single premature beats, without recurrence of atrial fibrillation.

Herein, I present a brief overview of supraventricular arrhythmias ( Article ) and their treatment, then discuss the treatment of atrial fibrillation in particular. Supraventricular arrhythmias can cause a variety of symptoms, including palpitations, neck fullness, chest pain or pressure, dyspnea, and fatigue. Some patients may be entirely asymptomatic, even with rapid ventricular rates, while others are debilitated by their arrhythmia. While supraventricular arrhythmias may cause serious symptoms, such as syncope and congestive heart failure, they are rarely immediately life-threatening. However, they may cause severe morbidity, including syncope with the potential for significant physical injury. Diagnosis is best made with a 12-lead ECG taken during an episode of arrhythmia. Holter monitoring and event monitoring are useful in making the diagnosis in a patient with episodic symptoms.

Classical paroxysmal supraventricular tachycardia

      Atrioventricular reentry tachycardia

      Atrioventricular nodal reentry tachycardia

      Focal atrial tachycardia

Atrial flutter

Atrial fibrillation

Wolff-Parkinson-White (WPW) syndrome was first described by the 3 eponymous physicians in Boston and London in 1930.¹ The disorder is caused by an abnormal cardiac muscle bundle, called an accessory pathway or bypass tract, which provides a functional electrical connection between atrium and ventricle in a region outside the normal atrioventricular (AV) node. Accessory pathways have been described almost everywhere in the regions of the tricuspid and mitral valves.² In WPW syndrome, an ECG is abnormal due to fusion of ventricular activation from 2 sources: the accessory pathway (delta wave) and the His-Purkinje system. The size and morphology of the delta wave and QRS complex depend on the location of the accessory pathway, relative speed of conduction over the pathway vs the normal AV conduction system, and presence or absence of intrinsic conduction disease. In some patients, the accessory pathway may lose antegrade (atrium to ventricle) conduction and so may be associated with a normal ECG.

The most common tachycardia associated with WPW is AV reentry tachycardia. This arrhythmia results when a premature beat blocks in the accessory pathway, travels down the AV node, through the ventricle, up the accessory pathway, then down the AV node in what is termed circus movement or reciprocating reentry. When the circuit is down the AV node and up the bypass tract, it is called orthodromic and is associated with a normal QRS width and the absence of a delta wave during the arrhythmia. Less commonly, such a reentrant circuit may travel retrogradely up the AV node and down the accessory pathway (antidromic direction), producing a wide complex rhythm mimicking ventricular tachycardia.³

Wolff-Parkinson-White syndrome may be lethal when atrial fibrillation develops, either spontaneously or as a result of prolonged AV reentry tachycardia.⁴ With the loss of the normal buffering effect of the AV node, patients may achieve ventricular rates of more than 250/min, resulting in degeneration to ventricular fibrillation and death. The risk of this event is between 1 in 200 and 1 in 1000 WPW patients. Younger age, presence of multiple accessory pathways, and rapid pathway conduction and recovery (noted at invasive electrophysiology study) confer increased risk.^{5 - 6}

Treatment of WPW syndrome may first involve AV nodal blocking agents, though caution should be exercised if a history of atrial fibrillation is present. For antiarrhythmic drug treatment, type Ic sodium channel blocking agents such as flecainide are favored, as they effectively slow or eliminate conduction in the bypass tract as well as slow conduction through the AV node. These agents are safe and effective only in patients with structurally normal hearts. Medical therapy, however, is only moderately effective in rendering patients asymptomatic, and there is no evidence that medical therapy reduces the risk of sudden death.

Because of the limited efficacy of medical treatment, arrhythmia surgeons attempted to locate accessory pathways intraoperatively and then to surgically divide them. The first successful surgical procedure was reported in 1968.⁷ Soon thereafter, cardiac electrophysiologists began looking for ways to achieve similar results using minimally invasive catheter-based approaches. In 1982, Scheinman and colleagues⁸ described placement of an electrode catheter adjacent to the AV node in a patient with atrial fibrillation and refractory rapid ventricular response. The catheter was connected to an external defibrillator and DC current was applied to cause destruction (or “ablation”) of cardiac tissue immediately adjacent to the catheter. The technique was soon applied to ablation of other arrhythmias, including WPW syndrome, but its utility was limited by complications due to barotrauma and collateral damage to adjacent cardiac structures.

Use of radiofrequency energy for cardiac ablation was introduced in the late 1980s and rapidly gained supremacy in the field because of its ability to place a controlled lesion at any site within reach of a catheter tip with no risk of barotrauma and greatly reduced risk of collateral injury.⁹ When the tip of this catheter is placed against cardiac tissue and radiofrequency current is applied, a 3- to 5-mm circular area of localized cardiac necrosis is created within 10 to 30 seconds, mainly through effect of local heating.¹⁰ Its efficacy in curative ablation of WPW syndrome was demonstrated, and by the early 1990s it had become standard first-line therapy for almost all symptomatic patients.^{11 - 12}

Catheter ablation for WPW syndrome and most other supraventricular arrhythmias can now be performed on an outpatient basis, with procedure times of 2 to 4 hours, depending on the location of the pathway. In a multicenter trial of catheter ablation therapy for supraventricular tachycardia, a series of 500 patients with accessory pathways had a success rate of 93%, with a major complication rate of 3%.¹³ The North American Society of Pacing and Electrophysiology (NASPE) registry of catheter ablations performed in 68 US centers also found an acute success rate of 93% for accessory pathway ablation.¹⁴ Because of these results and the potential morbidity of the arrhythmia, catheter ablation therapy for symptomatic WPW syndrome and AV reentry tachycardia has become the standard approach.^{14 - 15} Treatment of asymptomatic individuals with preexcitation on ECG is controversial.^{6 ,16}

Atrioventricular nodal reentry tachycardia is the most common cause of presentation with a regular narrow-complex tachycardia. Patients with AV nodal reentry tachycardia are generally older (mean age, 44 years) and more predominantly female (70%) in contrast to those with WPW syndrome (mean age, 27 years; 40% female).¹³ Presentation of AV nodal reentry tachycardia is otherwise similar to that of WPW syndrome except that there is no increased risk of sudden death.

The characteristic 12-lead ECG features include a regular narrow-complex tachycardia with a rate typically between 140/min and 220/min. P waves are either entirely buried in the QRS complex and, therefore, not seen, or they occur at the end of the QRS complex, producing characteristic distortions known as a “pseudo-R′” wave in lead V₁ and “pseudo-S” wave in the inferior limb leads.¹⁷ The electrophysiologic mechanism of AV nodal reentry tachycardia is not completely understood, but the dominant model involves a reentrant circuit contained largely or completely within the AV node complex. In this model, patients with AV nodal reentry tachycardia have a “fast” and a “slow” AV nodal pathway, and arrhythmia typically results from conduction down the slow pathway and up the fast pathway, with nearly simultaneous conduction up to the atria and down to the ventricles.¹⁸

The arrhythmia often can be terminated with vagal maneuvers (Valsalva or carotid sinus pressure) and in nearly all cases with intravenous adenosine or verapamil. Long-term medical treatment includes oral β-blockers or calcium channel blockers (verapamil and diltiazem). These medications act by increasing AV nodal refractoriness and are generally well tolerated. However, they usually do not render patients asymptomatic and require lifelong administration.

The history of ablation for AV nodal reentry began with surgical approaches but was complicated by high rates of complete AV block and iatrogenic pacemaker dependence. Radiofrequency catheter techniques targeting the fast AV nodal pathway reduced rates of AV block to 5% to 8%. The currently used technique targeting the slow AV nodal pathway results in AV block in only 0.5% to 1.0% of patients.¹⁹ The ablation catheter is introduced through a femoral vein into the right atrium, where the tip is rotated against the interatrial septum just anterior to the coronary sinus ostium. After applying radiofrequency current for 1 to 2 minutes, usually inducing transient junctional rhythm, patients undergo a rigorous electrical stimulation protocol, without and then with isoproterenol or atropine, to ensure that the tachycardia has been eliminated. The procedure is successful in 97% of patients, with a 5% long-term recurrence rate.^{13 - 14} Patients who do experience recurrence may undergo a second ablation procedure safely, with similar long-term efficacy rates.

Because of the infrequent but serious complication of AV block, alternative techniques of ablation for this arrhythmia continue to be sought. Cryoablation, the creation of a controlled lesion using freezing rather than heating, has been used by arrhythmia surgeons for decades. Recently, transvenous catheters capable of administering cryoablation have been approved by the US Food and Drug Administration and appear to have an even lower risk of AV block, albeit at a lower short-term success rate and higher risk of long-term arrhythmia recurrence.²⁰

Atrial tachycardia is a focal arrhythmia that may originate from anywhere within the right or left atrium. The arrhythmia is less frequent than WPW syndrome and AV nodal reentry tachycardia and more commonly is associated with other cardiovascular disease in adults. On 12-lead ECG, the rhythm often looks like sinus tachycardia, except that the P-wave morphology and axis differ from that of sinus rhythm.²¹ Presentation, symptoms, and treatment are similar to that for AV nodal reentry tachycardia except that the arrhythmia is less responsive to vagal maneuvers and adenosine. In a study of 229 patients with supraventricular tachycardia, adenosine suppressed or terminated 45% of atrial tachycardias and 100% of AV reentry tachycardias and AV nodal reentrant tachycardias.²²

Medical treatment for atrial tachycardia usually begins with β-blockers, verapamil, or diltiazem. Digoxin is not effective and may exacerbate the arrhythmia because of the drug's ability to enhance automaticity. Patients who are symptomatic despite β-blocker or calcium channel blocker treatment are generally offered options of antiarrhythmic drug therapy with class I or class III agents (such as flecainide or sotalol, which suppress automaticity) or catheter ablation.

Catheter ablation therapy for atrial tachycardia has been aided by the recent development of sophisticated mapping systems for localizing the site of origin of the arrhythmia in the electrophysiology laboratory.²³ Electrical and anatomical information is acquired with the ablation catheter in the atrium over 10 to 20 minutes and then integrated by computer to provide a 3-dimensional cardiac image. Once an activation map is created for a patient with focal atrial tachycardia, the target for ablation becomes readily apparent as a region encoded in red, signifying early activation. When the ablation catheter is placed on the target site and the radiofrequency current is applied, tachycardia will usually terminate and sinus mechanism will resume. The atrium is then stimulated with rapid pacing at baseline and with isoproterenol to ensure that the tachycardia remains noninducible.

Atrial flutter was first accurately described by Lewis et al²⁴ in 1920. Although this arrhythmia has been commonly grouped together with atrial fibrillation, research in the 1980s and early 1990s showed that they have different electrophysiologic mechanisms. Typical atrial flutter is caused by a macro-reentrant electrical pathway around the tricuspid valve annulus.²⁵ Initial management of atrial flutter often consists of rate control with β-blockers, verapamil, diltiazem, or digoxin, plus anticoagulation.

Surgical ablation of atrial flutter by creating lesions in the low medial right atrium near the coronary sinus was first reported in 1986, and catheter ablation followed several years thereafter.^{26 - 27} Early attempts at this procedure were plagued with a high arrhythmia recurrence rate, and a key advance occurred in 1995 when the importance of creating a complete line of conduction block in the cavotricuspid isthmus (area between the tricuspid valve and inferior vena cava) was reported.²⁸

The current ablation technique involves passing an ablation catheter from the inferior vena cava, placing the tip on the inferior margin of the tricuspid annulus, and applying radiofrequency ablation current while slowly dragging the catheter tip back to the inferior vena cava. The operator then performs pacing stimulation on each side of the ablation line to determine whether conduction across the line is possible. If so, more ablation lesions are created to seal any conduction gaps in the line. This technique has a success rate of 92%, with a recurrence rate of 3% and complication rate of 1%.^{29 - 30} The chief limitation of ablation for atrial flutter is late development of atrial fibrillation in about 30% of patients, an event predicted by history of heart failure, left ventricular dysfunction, and preexisting history of atrial fibrillation.³⁰

Atrial fibrillation is the most common sustained arrhythmia, an important cause of stroke, and the object of intensive investigation by electrophysiologists over the past 10 years. Although some patients with AF may be asymptomatic, many patients, particularly those with paroxysmal AF, experience palpitations, malaise, dyspnea, and loss of exercise capacity.

The incidence and prevalence of atrial fibrillation increase markedly with age, reaching a prevalence of about 10% in patients older than 80 years.³¹ Estimates of the total US prevalence of atrial fibrillation in 2000 range from 2.3 million to 5.1 million persons, and projections for prevalence in 2050 range up to 15 million.^{32 - 33} Data from the Framingham Heart Study suggest that the lifetime risk of developing atrial fibrillation is approximately 1 in 4 persons aged 40 years or older.³⁴ In addition, the presence of atrial fibrillation has been associated with a shorter life expectancy in epidemiologic studies.^{35 - 36}

Despite decades of study, the fundamental mechanisms causing atrial fibrillation in humans remain incompletely understood ( Article ). Since the 1960s, the dominant model to explain atrial fibrillation has been the multiple wavelet hypothesis, which proposes that the atria must be able to sustain 6 to 8 circulating reentrant wavelets, which are constantly colliding and reforming, producing a chaotic pattern of atrial activation.^{37 - 38} Atrial enlargement and fibrosis, changes in autonomic innervation, and alterations in ion channel currents all appear to promote maintenance of atrial fibrillation in susceptible patients. More recent research has highlighted the role of triggers of atrial fibrillation, which may include paroxysmal supraventricular tachycardia, atrial flutter, and atrial tachycardia originating in the pulmonary veins.

The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial showed that attempts to control atrial fibrillation with antiarrhythmic drugs are hampered by low efficacy and absence of improvement in survival.³⁹ The AFFIRM trial therefore supports conservative treatment with rate-controlling medication and anticoagulation for most older patients with minimally symptomatic atrial fibrillation. However, a significant number of patients with atrial fibrillation, like Ms R, have very bothersome symptoms that may not respond to medical therapy.

Medical treatment for patients with atrial fibrillation is discussed in a comprehensive practice guideline published in 2006 by the American College of Cardiology, the American Heart Association, and the European Society of Cardiology.⁴⁰ In patients for whom a rate control strategy is chosen, β-blockers, nondihydropyridine calcium channel blockers, and digoxin, alone or in combination, may be used. The practice guideline endorses the use of warfarin anticoagulation for patients with a CHADS₂ risk score of 2 or greater, while patients with a CHADS₂ score of 1 may be treated with either aspirin or warfarin, depending on clinical circumstances.⁴¹ Patients with a score of 0 (“lone” atrial fibrillation) generally may be treated with aspirin; however, patients undergoing cardioversion require anticoagulation regardless of CHADS₂ score.

Patients who require a rhythm control strategy because of atrial fibrillation symptoms are first evaluated for electrical or pharmacologic cardioversion if persistent atrial fibrillation is present. Choice of antiarrhythmic drug therapy is guided by presence of cardiac comorbidities and renal/hepatic function. Patients with “lone” atrial fibrillation may be treated with flecainide, propafenone, or sotalol. Amiodarone or dofetilide may be used in patients with coronary disease or heart failure. Although amiodarone has been shown to be the most effective agent for maintaining sinus rhythm, a variety of adverse effects may limit its use.^{42 - 44}

The first invasive treatment for atrial fibrillation was ablation of the AV node to create permanent complete AV block followed by implantation of a permanent pacemaker (the “ablate and pace” method). This procedure is straightforward to perform and is highly effective in controlling palpitations.^{45 - 46} Its chief disadvantages are that it renders patients permanently pacemaker-dependent for life and does not prevent the atria from continuing to fibrillate. Patients may remain symptomatic because of reduction in cardiac output and face the same risks of thromboembolism and need for lifelong anticoagulation.

Taking a novel approach, Cox and colleagues⁴⁷ ambitiously sought to eliminate atrial fibrillation with a surgical technique based on the multiple wavelet hypothesis. They reasoned successfully that by dividing the atria into sufficiently small segments, no one area of the atria would be able to sustain atrial fibrillation wavelets, so a sinus rhythm mechanism would take over. The operation was tested in animal models before the first application in humans in 1987. The operation went through several iterations, the latest being the Maze III procedure, and several centers have reported long-term maintenance of sinus rhythm in 75% to 95% of patients.^{48 - 49} Because of the complexity of the operation and potential complications of open-heart surgery, it is not commonly performed today unless the patient is undergoing concomitant surgery for coronary or valvular heart disease. Nonetheless, it still serves as a “gold standard” for what can be achieved with interventional treatment for atrial fibrillation.

With the demonstrated success of the Maze III procedure, cardiac electrophysiologists began attempting to reproduce the operation with a minimally invasive, catheter-based approach.⁵⁰ These early attempts to produce a “catheter Maze procedure,” however, were marked by limited success and high complication rates.⁵¹

A breakthrough in this field occurred in 1998 when Haïssaguerre et al⁵² published a finding that 95% of atrial ectopic beats that initiate paroxysmal atrial fibrillation originate in the pulmonary veins. They studied a highly selected group of 45 otherwise healthy young patients with very frequent paroxysmal atrial fibrillation episodes and more than 1000 premature atrial contractions daily on Holter monitoring. After demonstrating the pulmonary venous origin of the premature atrial contractions with careful invasive catheter mapping, they proceeded to ablate the premature atrial contractions with radiofrequency ablation, which resulted in short-term freedom from atrial fibrillation in most patients.

This publication caused a number of investigators to ask why the pulmonary veins are so arrhythmogenic. It has been known for decades that the pulmonary veins are invested with bundles of atrial myocardium that extend from the left atrium into the pulmonary veins, likely reflecting their common origin in the sinus venosus (Figure 2A).^{53 - 54} Although there is believed to be something arrhythmogenic about the junction of atrial muscle with pulmonary venous tissue, why this is so remains obscure despite extensive study.⁵⁵ Likewise, it is not known why some individuals develop arrhythmogenic foci in their pulmonary veins while the majority do not.

After initial reports of ablative treatment of atrial fibrillation targeting foci of premature atrial contraction in the pulmonary veins, it became apparent that a high percentage of patients developed recurrence because of foci developing elsewhere in the same or other pulmonary veins.⁵⁶ Treatment evolved to electrical isolation of all 4 pulmonary veins guided by a circular electrode catheter placed at the ostium of each vein.⁵⁷ About this time, Pappone et al⁵⁸ began reporting excellent results using a single-catheter technique guided by electroanatomical mapping.

Details of technique vary somewhat, but most academic electrophysiology laboratories use a technique that combines the approaches of circumferential ablation around the outside of the pulmonary veins using electroanatomical mapping and demonstration of electrical isolation of the pulmonary veins^{59 - 60} (Figure 3). The procedure is generally reserved for patients with paroxysmal or persistent atrial fibrillation associated with significant symptoms who have recurrent arrhythmia despite a trial of at least 1 class I or class III antiarrhythmic drug.^{40 ,61} Patients are bridged from warfarin using enoxaparin and undergo preprocedure computed tomography or magnetic resonance imaging of the left atrium followed by transesophageal echocardiography to exclude left atrial thrombus. After placement of sheaths and catheters in the femoral veins, the computed tomographic scan or magnetic resonance image of the left atrium is imported into the cardiac mapping system to help guide ablation with fine anatomical detail of the left atrial anatomy⁶² (Figure 2B). Two transseptal punctures are performed and wide-area radiofrequency ablation is performed around both the right- and left-sided pulmonary veins using the technique described by Pappone et al.⁵⁸ A circular mapping catheter is then introduced and placed in each pulmonary vein (Figure 3C) and ablation continued outside the ostium of each vein until complete electrical isolation is demonstrated (Figure 4).

Results using the hybrid approach described above were reported recently in a series of 64 patients (which included Ms R) who had undergone the procedure with a minimum of 1 year of follow-up.⁶³ Allowing for use of repeat procedures, 62% of patients were free of symptomatic atrial fibrillation at 1 year without use of antiarrhythmic drugs. When use of previously ineffective antiarrhythmic drugs was factored in, 71% of patients achieved a good outcome.

Reported success rates of atrial fibrillation ablation at other centers have ranged from 37% to 95% and vary by technique used, patient characteristics, duration and intensity of follow-up, and definition of success used by the investigators.^{60 ,64 - 67} The mean overall success rate combining multiple studies in a recent review was approximately 70%.⁶⁰ In a worldwide atrial fibrillation ablation survey, freedom from atrial fibrillation without antiarrhythmic drugs was reported in 4550 of 8745 patients (52%), and overall success (including use of antiarrhythmic drugs and repeat procedures) was 75.9%.⁶⁴ Two randomized controlled trials comparing atrial fibrillation ablation with antiarrhythmic drug therapy have been reported, both showing significant reduction in atrial fibrillation in the ablation arm.^{68 - 69} Some factors associated with improved outcome after atrial fibrillation ablation are listed in Article .⁶¹ Patients with paroxysmal atrial fibrillation and structurally normal hearts have the best success rate, approximately 70% with a single procedure.⁶¹

Significant risks of atrial fibrillation ablation must be acknowledged and discussed with each patient for whom the procedure is proposed. The worldwide survey of atrial fibrillation ablation reported a 6% rate of major complications, which is higher than for catheter ablation procedures for other supraventricular arrhythmias.⁶⁴ Risks of catheter ablation for atrial fibrillation reported in this study included approximately 1% risk of stroke, 1.3% risk of pulmonary vein stenosis, 1.2% risk of pericardial tamponade, and 0.2% risk of phrenic nerve injury.⁶⁴ Other case series have reported higher rates of pericardial tamponade (up to 3%), pulmonary vein stenosis (up to 3.4%), and thromboembolism (up to 7%).^{61 ,70 - 71} Atrioesophageal fistula is usually fatal because of introduction of air into the systemic circulation and/or sepsis and occurs in approximately 0.1% to 0.2% of cases.^{61 ,72} Stroke and pericardial tamponade may also result in mortality. Pulmonary vein stenosis, although decreasing in incidence, may result in significant pulmonary limitation and need for catheter- or surgical-based intervention.⁷³ Vascular access complications are the most frequent problem but generally resolve with conservative treatment.

Current research efforts in the field of atrial fibrillation ablation are focused on further improving long-term efficacy and decreasing complications by refining catheter technique as well as by introducing new technology, such as delivering cryothermal, laser, or ultrasound energy through balloons placed in the ostia of the pulmonary veins. A better understanding of the long-term benefits and adverse effects of the ablation procedure is needed. Follow-up in most published series has been limited to 1 to 2 years, so it is not yet known if atrial fibrillation ablation can achieve lifelong elimination of atrial fibrillation. The long-term safety and efficacy of ablation for atrial fibrillation has not been well established. Finally, investigators are seeking a better understanding of the different types of atrial fibrillation and how therapy can be tailored to individual patients. A state-of-the-art review of atrial fibrillation ablation techniques and future directions in the field can be found in the expert consensus statement recently published by the Heart Rhythm Society.⁶¹

Supraventricular arrhythmias, while only rarely life-threatening, may cause significant symptoms that diminish quality of life. Considerable progress has been made in understanding the mechanisms of these arrhythmias over the past few decades. This understanding has led to application of interventional therapies that directly target the root cause by eliminating 1 or more critical pathways that allow the arrhythmia to occur. Arrhythmia surgeons operating on the exposed open heart have generally pioneered these interventions, and electrophysiologists have followed by reproducing the therapeutic effect with less invasive catheter-based treatment. Curative treatment for nearly all patients with WPW syndrome, AV reentry tachycardia, and AV nodal reentry tachycardia and for most patients with atrial tachycardia and atrial flutter is now routine, and catheter ablation has accordingly become first-line treatment for these arrhythmias, especially when the arrhythmias are associated with severe symptoms such as syncope. A general approach to consideration of ablation therapy for these arrhythmias, based primarily on the ACC/AHA guidelines published in 2003, is provided in Figure 5.¹⁵

Atrial fibrillation remains the last frontier for the interventional electrophysiologist, but this arrhythmia is also yielding to intensive investigation and therapeutic efforts. Understanding of the important role of the pulmonary veins and posterior left atrium has led directly to catheter-based and surgical procedures that provide prolonged freedom from atrial fibrillation in a majority of patients. While it may be too early to speak of cure of atrial fibrillation with these procedures, published reports with medium-term follow-up are encouraging. Because of the higher procedural risk and lower long-term success rates of atrial fibrillation ablation, it is not yet recommended as first-line therapy. However, it has become established treatment for atrial fibrillation in experienced centers for patients with significant atrial fibrillation symptoms in whom medical therapy fails. A general approach to consideration of ablation therapy for atrial fibrillation, based on professional society guidelines published in 2006 and 2007, is provided in Figure 5.^{40 ,61}

Significant challenges for this field remain. In particular, a more complete understanding of atrial pathophysiology, which leads to atrial fibrillation, will be required to better identify targets for intervention. Several questions remain: What is the role of atrial autonomic innervation? How does the atrial substrate for maintenance of atrial fibrillation develop? What explains the wide variation in symptoms that patients with comparable burden of atrial fibrillation may have? How can interventional therapy for atrial fibrillation be made safer and more effective? Determining the answers to these questions and applying this knowledge to treatment of patients with atrial fibrillation will likely occupy the efforts of electrophysiologists for years to come.