For many arrhythmia syndromes, catheter ablation has replaced pharmacologic therapy. Multicenter studies over the past 3 decades have demonstrated disappointing efficacy, frequent nuisance, and even life-threatening side effects of antiarrhythmic drug therapy, particularly in patients with structural heart disease. Antiarrhythmic drugs are still used as part of a rhythm control strategy for atrial fibrillation (AF) and for the reduction of implantable cardioverter-defibrillator (ICD) shocks in patients with these devices. For most other syndromes, catheter ablation has become the first-line treatment in patients with significant symptoms ( Box 21-1 ).
First-Line Therapy in Symptomatic Patients
AV node reentry
Potentially Helpful in Patients with Symptoms Despite Pharmacologic Therapy
VT in structural heart disease
Anatomic ablation of poorly tolerated VT
AV junction ablation for rate control of AF
Inappropriate sinus tachycardia
AF, atrial fibrillation; AV, atrioventricular; VT, ventricular tachycardia.
This chapter provides an arrhythmia-specific overview of the available techniques, current efficacy, procedural side effects, and future considerations of nonpharmacologic therapy. Although broadly speaking, this topic could well include a discussion of surgical ablation and pacing therapy, the predominant focus is on catheter ablation. Discussion of the use of implantable electrical devices for the management of sudden cardiac death (SCD) is found in Chapter 22 .
Catheter Ablation for the Treatment of Tachyarrhythmias
The results of catheter ablation are syndrome specific. Although it can be curative for many paroxysmal supraventricular arrhythmias, catheter ablation is largely palliative for ventricular tachycardia (VT) in the setting of structural heart disease and is rapidly evolving as a method for treatment of AF ( Table 21-1 ). Cost, efficacy, and patient preference are important considerations in determining the role of catheter ablation versus drug therapy in specific arrhythmia syndromes.
|Accessory pathway mediated||>90|
|Atrioventricular nodal reentry||>97|
|Paroxysmal atrial fibrillation||>75|
|Atrioventricular junction ablation||>97|
|VT in structural heart disease||>70|
The general principle of ablation therapy, either surgical or catheter based, involves the selective destruction of a “vulnerable parameter” of the tachycardia circuit. Depending on the arrhythmia, this parameter can be identified electrophysiologically (e.g., bypass tract) or anatomically (e.g., slow pathway). Catheter positioning at this critical component is achieved based on electrical recording and fluoroscopic, echocardiographic, and/or magnetic resonance imaging (MRI) information, often in conjunction with three-dimensional (3D) electroanatomic mapping data. Ablation is performed by delivery of some form of energy to the tip of the catheter, resulting in focal destruction of the myocardium. Alternative energy sources—such as cryothermy, microwave, high-frequency ultrasound, and laser—are available for specific indications, but radiofrequency energy is the workhorse of catheter ablation at present because of its excellent efficacy and safety profiles. Radiofrequency energy damages tissue by resistive heating in the myocardium directly in contact with the distal catheter electrode. Irreversible tissue death occurs at temperatures in excess of 50° C. Radiofrequency lesions are homogeneous and precise, with necrotic centers 5 to 6 mm in diameter and 2 to 3 mm deep, surrounded by a hemorrhagic periphery ( Figure 21-1 ). Two biophysical considerations fundamentally limit the size of radiofrequency lesions: first, heat transmission diminishes by distance from the energy source to the fourth power and, second, temperatures greater than 100° C at the catheter/myocardial surface interface lead to coagulum and gas bubble formation that prevents subsequent current delivery. Although this is a fundamental limitation, the development of new ablation catheters—such as irrigated-tip radiofrequency ablation (RFA) devices, which allow for the production of larger and deeper lesions—is helpful in selected applications, particularly for VT in the setting of healed myocardial infarction (MI).
Catheter Ablation by Specific Arrhythmia Syndrome
Catheter ablation therapy for most paroxysmal supraventricular arrhythmias is safe, cost effective, and virtually curative. The success rate of catheter ablation for AF is more variable and depends on its paroxysmal or persistent nature (see Table 21-1 ).
Catheter Ablation for Supraventricular Tachyarrhythmias
Accessory Pathway–mediated Tachycardias
Accessory pathways are microscopic muscular bundles that connect the atrium and ventricle, providing a “bypass” of the normal conduction system. Manifest pathways, those capable of antegrade conduction, are present in the Wolff-Parkinson-White (WPW) syndrome. Concealed pathways are not apparent on the surface electrocardiogram (ECG) but can still mediate reentry. Most symptomatic arrhythmias in patients with accessory bypass tracts are associated with a narrow QRS complex—that is, orthodromic supraventricular tachycardia, conducted antegrade through the atrioventricular (AV) node and retrograde through the bypass tract. Less frequently, circus movement tachycardia occurs in the reverse order: the bypass tract serves as the anterograde limb of the reentrant circuit. The QRS complex during this tachycardia is fully preexcited, resulting in a wide QRS, or antidromic supraventricular tachycardia . Importantly, in patients with AF, rapid antegrade conduction over the accessory pathway can lead to ventricular fibrillation (VF) and cardiac arrest (estimated annual risk, 0.05% to 0.5%).
The target for ablation in accessory pathway–mediated reentry is the accessory pathway itself ( Figure 21-2 ). The AV node is another vulnerable site, but its ablation may ultimately necessitate pacemaker therapy if antegrade bypass tract conduction fails, a phenomenon that can occur in up to 20% of patients. Accessory pathways can occur at any location along the tricuspid and mitral annulus, except between the left and right fibrous trigones, where the left atrial myocardium is not in direct juxtaposition with the left ventricular (LV) myocardium, the region of the aortomitral continuity. The distribution of bypass tracts along the AV groove is not homogenous: 46% to 60% of bypass tracts are found within the left free wall space; 25% are within the posteroseptal space; 13% to 21% are within the right free wall space; and 2% are within the right superoparaseptal (formerly called the anteroseptal ) space. Right-sided pathways are ablated by a venous approach, typically at the atrial insertion of the pathway. Left-sided pathways are ablated either by a retrograde aortic approach or a transseptal approach to the left atrium. A small percentage of posterior septal accessory pathways can be successfully ablated with a catheter positioned within the proximal coronary sinus, often within the middle cardiac vein or within a venous malformation.
Ablation is a highly effective and curative therapy (>90%) for accessory pathway–mediated tachycardia. Acute success is usually persistent, and late recurrence of bypass tract conduction after ablation is rare (4%), typically observed during the first month after ablation. In a contemporary survey of 6065 patients undergoing ablation of an accessory pathway between 1997 and 2002, the long-term success rate was 98%, and a repeat procedure was necessary in 2.2% of cases. Serious complications—cardiac tamponade, AV block, coronary artery injury, or stroke—occurred in 0.6% of patients, with one fatality (0.02%). The highly favorable risk/benefit ratio justifies the use of catheter ablation as first-line therapy for any patient with accessory pathway–dependent tachycardia that requires treatment. This is particularly true for young patients who want to avoid long-term pharmacologic therapy.
Treatment of asymptomatic patients with incidentally detected accessory pathways is controversial. Most patients with asymptomatic preexcitation have a good prognosis; cardiac arrest is rarely the first manifestation of the disease. Prior studies have reported that approximately 20% of asymptomatic patients will demonstrate a rapid ventricular rate, but in AF, that is induced during electrophysiology (EP) testing. However, during clinical follow-up, few patients developed symptomatic arrhythmias, and none had cardiac arrest. An EP study can be useful to risk stratify patients with asymptomatic preexcitation. One study reported the follow-up of 212 patients with asymptomatic preexcitation, all of whom underwent a baseline EP study. After a mean follow-up of 38 months, 33 patients became symptomatic; 3 of these patients had VF, and 1 died. The most important factors in predicting outcome were the inducibility of AF during the study and the short bypass tract anterograde refractory period. Despite this study, the positive predictive value of invasive EP testing is considered to be too low to justify routine use in asymptomatic patients. The decision to risk stratify patients and possibly ablate pathways in asymptomatic individuals with high-risk occupations—such as school bus drivers, pilots, and scuba divers—is made on the basis of individual clinical considerations.
Atrioventricular Node Reentry
The most common mechanism of paroxysmal supraventricular tachycardia (PSVT) is atrioventricular node reentrant tachycardia (AVNRT). The slow pathway is the vulnerable parameter in AVNRT, and radiofrequency energy is applied at the posteroseptal right atrial sites near the ostium of the coronary sinus ( Figure 21-3 ). In a survey of a pooled sample of 8230 patients with AVNRT who underwent ablation between 1997 and 2002, the long-term success rate for AVNRT elimination was 99%. A repeat ablation procedure was necessary in 1.3% of patients, and high-grade AV block that required implantation of a pacemaker occurred in 0.4% of patients. These results confirm the highly favorable risk/benefit ratio of radiofrequency slow pathway ablation.
AVNRT is not a life-threatening arrhythmia, but many patients have bothersome symptoms of tachycardia. Because of a very favorable risk/benefit ratio, radiofrequency catheter ablation of AVNRT has become the treatment of choice for most symptomatic patients. Many patients elect to undergo catheter ablation as first-line therapy to avoid the need for antiarrhythmic drug therapy. A cost analysis study demonstrated that catheter ablation improved quality-adjusted survival and resulted in cost savings over pharmacologic therapy in symptomatic patients with AVNRT.
Atrial tachycardias may be focal or macroreentrant (also known as atrial flutter ). Focal atrial tachycardia is characterized by centrifugal spread of activation away from the site of origin and most commonly arises in the right atrium along the crista terminalis, near the tricuspid annulus, or near the coronary sinus ostium. Approximately 5% of focal atrial tachycardias arise in the left atrium, commonly along the mitral annulus. Experience gained during catheter ablation of AF revealed that focal tachycardias can also arise in the pulmonary veins, the superior vena cava, the vein of Marshall, or other atrial sites. Targets for ablation of focal atrial tachycardias are identified by the site of earliest activation, or activation mapping, or by pacemapping. Because focal atrial tachycardias are relatively uncommon, literature that describes results of catheter ablation is limited. In seven studies that included a total of 112 patients with focal atrial tachycardia, the short-term success rate of RFA was approximately 90%, with 7% late recurrence and no major complications. However, these success rates may overestimate the true efficacy of catheter ablation for focal atrial tachycardia, as these patients had uncomplicated diagnostic studies and reproducible atrial tachycardia amenable for mapping. Nonetheless, these studies did not use either a 3D mapping system or a cooled-tip ablation catheter, both of which are widely available today. With these advanced mapping tools, and with ablation catheters capable of creating larger lesions, clinical failures are more often related to the emergence of new foci rather than the inability to ablate a particular tachycardia.
Given the high probability of successful ablation and the low risk of serious complications, it is appropriate to consider the option of catheter ablation for any patient with a clinically significant atrial tachycardia that requires therapy. However, pharmacologic therapy is more appropriate if multiple atrial foci are present. In these patients, even if all the atrial tachycardia foci are mapped and ablated, new foci may emerge later. In older patients with multifocal atrial tachycardia who are highly symptomatic and drug refractory, AV node ablation and pacemaker insertion may be more appropriate.
Inappropriate sinus tachycardia is a nonparoxysmal tachyarrhythmia characterized by a persistent increase in resting sinus rate unrelated to, or out of proportion with, the level of physical, emotional, pathologic, or pharmacologic stress. These patients also exhibit an exaggerated heart rate response to minimal exertion. Sinus node modification targets the site of most rapid discharge, generally at the superior aspect of the crista terminalis. RFA is at best an only modestly effective technique for managing patients with inappropriate sinus tachycardia, and long-term success rate ranges between 23% and 83%.
Isthmus-Dependent Atrial Flutter
The most common type of atrial flutter is isthmus-dependent atrial flutter, in which the reentry circuit is confined to the right atrium, between the tricuspid annulus and the inferior vena cava, with the wavefront progressing either in a counterclockwise or clockwise direction across the cavotricuspid isthmus. This isthmus forms the vulnerable parameter of the circuit and is the target for ablation. Strategies for ablation have evolved in terms of procedural endpoint, from termination of atrial flutter to durable bidirectional block ( Figure 21-4 ), and technology that includes 4 mm to larger or irrigated RFA. In a randomized study that compared the 8-mm tip and irrigated-tip catheters, complete isthmus block was achieved in 99 of 100 patients, with equal efficacy between the two catheters. Early recurrence is unusual, although not well studied, in contemporary series, and complications are virtually absent. In light of the high efficacy and safety of RFA for isthmus-dependent atrial flutter, catheter ablation is an appropriate therapeutic option for drug-refractory patients and for those who prefer curative therapy over pharmacologic therapy. An important disadvantage to an ablation strategy for atrial flutter is the high incidence of AF in intermediate-term follow-up.
Other Atrial Flutters
Atypical atrial flutters—that is, noncavotricuspid isthmus-dependent flutters—are relatively uncommon and are usually related to atrial scarring (i.e., idiopathic or secondary to surgical incisions or incomplete ablation lines); it is increasingly seen after ablation of AF. The most frequent locations of right atrial ablation lines used to treat incisional flutters are between a lateral atriotomy scar and the inferior vena cava, superior vena cava, or tricuspid annulus. Success rates ranging between 80% and 85% were reported in early studies that did not use 3D mapping systems. A more contemporary study incorporated electroanatomic mapping and demonstrated that macroreentrant right atrial tachycardias often use relatively narrow channels between scars. Detailed voltage mapping has allowed identifications of these channels and elimination of the tachycardia with only a few applications of radiofrequency energy. Left atrial flutters may be a proarrhythmic complication of heart surgery, such as mitral valve surgery or a Maze procedure, or left atrial catheter ablation may be a proarrhythmic complication of AF. Many of these left atrial flutters use the isthmus between the mitral annulus and the left inferior pulmonary vein; hence, this is usually the target of ablation. In a series of 78 patients who underwent RFA of left atrial arrhythmias that occurred after pulmonary vein isolation (PVI), catheter ablation was successful in 85% of patients. After a mean follow-up of 1 year, 77% of patients were free of atrial arrhythmias without antiarrhythmic medications. Atrial arrhythmias that occur after RFA for AF are often persistent, difficult to suppress with rhythm control medications, and associated with rapid ventricular rates. Catheter ablation may therefore offer the best chance either to cure the arrhythmia or to render patients asymptomatic.
A landmark study by Haissaguerre and colleagues in 1998 focused attention on the importance of the pulmonary veins in the generation of AF. This began a period of rapid progress in the search for the optimal ablation strategy. Trigger-based strategies evolved from point-source ablation within individual veins to selective arrhythmogenic PVI ( Figure 21-5 ) to more proximal, four-vein antral isolation facilitated by 3D mapping systems ( Figure 21-6 ). This wider, circumferential ablation approach, originally developed to prevent pulmonary vein stenosis, has several potential advantages over segmental ostial isolation: 1) elimination of anchor points for “mother waves” or rotors near the pulmonary vein ostium; 2) ablation of other potential trigger sites, such as the vein of Marshall and the posterior left atrial wall; 3) atrial debulking, to provide less space for circulating wavelets; and 4) atrial denervation (i.e., vagal denervation by ablation lines).
Substrate-based strategies aim to prevent the atrium from sustaining fibrillation. Such strategies began as recapitulation of the surgical Maze and evolved to additional ablation of complex, fractionated atrial electrograms (CAFÉ) and developed to a stepwise ablation approach through to termination of AF. Comparisons between the two general strategies have been contentious and have led to variable results, depending on intensity of ECG monitoring, categorization of AF versus atrial tachycardia/flutter at recurrence, and the effect of repeat procedures and adjuvant antiarrhythmic drugs. In most contemporary studies, success rates of catheter ablation for paroxysmal AF are greater than 70%. Although many different techniques are used to achieve these results, most investigators acknowledge the primacy of PVI in patients with paroxysmal AF.
Persistent AF, especially long-lasting (>1 year since last episode of sinus rhythm) persistent AF, has proven more challenging to address, and the discussion regarding adjuvant substrate-based ablation is still topical. As reviewed by Brooks and coworkers, more extensive ablation appears to have an advantage in single-procedure efficacy, but efficacy is still fairly limited and variable, ranging from 21% to 74%. Alternative mechanisms perhaps are related to the significant structural and EP remodeling of the left atrium instilled by the long-standing arrhythmia. PVI alone is associated with a single-procedure, drug-free success rate ranging from 37% to 56% at 1 year. Repeat procedures (mean, 1.3 per patient) increases the drug-free success rate to 59%. Efforts to improve outcomes for persistent AF have led to investigation of alternative and adjunctive targets, such as fractionated electrograms, ganglionic plexi, extensive modification of the posterior and inferior wall, or ablation to the point of AF termination. As we continue to understand more about the persistent fibrillatory process, it is hoped that the evolution of more specific ablation techniques will improve the efficacy and safety of ablation in this patient population.
Compared with drug therapy, the available evidence supports the superiority of catheter ablation in terms of efficacy in maintaining sinus rhythm. Studies that directly compared catheter ablation and antiarrhythmic drug therapy confirmed that sinus rhythm is better maintained following catheter ablation. Moreover, in an intention-to-treat analysis, catheter ablation resulted in freedom of atrial arrhythmia in 79% of patients compared with only 32% in the antiarrhythmic drug group. These data were mostly driven by the larger number of patients with paroxysmal disease; however, favorable outcomes with ablation were also observed in the patients with persistent disease. In addition to being superior to drug therapy in maintaining sinus rhythm, catheter ablation resulted in better symptomatic relief and better exercise tolerance compared with drug treatment.
Complications of catheter ablation procedures are usually directly related to the intervention. Mortality rate following catheter ablation of AF is 1 per 1000 procedures according to a recently published international survey. Major complications occurred in 4.5% of procedures. The most frequently occurring complications included pericardial tamponade, pneumothorax, diaphragmatic paralysis, vascular complications (femoral pseudoaneurysm, arteriovenous fistula), atrioesophageal fistula, pulmonary vein stenosis, and transient and permanent embolic strokes (0.7%, and 0.3%, respectively).
With increasing success and concomitant use of catheter ablation for AF, a question of major importance is whether long-term maintenance of sinus rhythm after successful ablation eliminates the risk for stroke and thereby permits discontinuation of oral anticoagulation therapy. Unfortunately, only limited long-term outcome studies have been published. In a single-center study by Tzou and colleagues of 239 patients with both paroxysmal and persistent AF who underwent circumferential PVI and were free of AF at 1 year, the majority of patients (84%) remained free of AF after 5 years. Recurrence of AF occurred in 7% of patients per year, and the strongest predictors for recurrence were persistent AF and older age. Moreover, in the patients who underwent repeat ablation, the mechanism of late recurrence was overwhelmingly associated with pulmonary vein reconnection.
The management of anticoagulation in patients who have undergone AF ablation has largely been left to the judgment of the treating physician. However, several practice patterns have emerged based on the apparent presence or absence of AF, duration of recurrent episodes, and the CHADS 2 stroke risk stratification (congestive heart failure, hypertension, age >75 years, diabetes mellitus, and prior stroke or transient ischemic attack). In a multicenter study, Themistoclakis and colleagues studied the largest multicenter experience to date to address this issue. In this study, 3355 patients were monitored for a mean of 2.3 years. In 2692 patients (80%), warfarin therapy was discontinued 3 to 6 months after ablation (347 patients had a CHADS 2 score ≥2). Although the decision to stop warfarin was made on an individual basis, as a general rule, these patients did not have any recurrence of atrial arrhythmias. The annual incidence of stroke in the group off warfarin was 0.03%. This compared with an annual incidence of stroke of 0.2% in those continuing warfarin. Although this study suggests a very low incidence of stroke following successful ablation, caution must be exercised when applying these data to patients typically seen in practice, who may have only limited symptoms and for whom freedom of atrial arrhythmias after ablation is not as rigorously monitored. Current guidelines advocate continuing anticoagulation therapy guided by CHADS 2 score, at least until these data are confirmed by large, prospective, randomized trials.
Left atrial appendage (LAA) closure devices have emerged as novel nonpharmacologic approaches to reduce the risk of stroke in patients with AF. The first device tested in humans was the percutaneous LAA transcatheter occlusion (PLAATO; ev3 Endovascular, Inc., Plymouth, MN) system, a self-expanding, membrane-covered, spherical nitinol cage inserted into the LAA transseptally to occlude it in patients with contraindications to chronic warfarin therapy. However, because of high complication rates, the device was withdrawn from the market. The Watchman device (Atritech, Inc., Plymouth, MN) is also composed of a self-expanding nitinol frame. It has fixation barbs and a permeable polyester fabric that covers the left atrial–facing surface of the device ( Figure 21-7 ). In the Watchman Left Atrial Appendage System for Embolic Protection in Patients with AF (PROTECT-AF) study, the Watchman device was compared with conventional warfarin treatment in patients with AF and a CHADS 2 score of 1 or higher. Patients were anticoagulated with warfarin in the postimplantation period and were switched to aspirin/clopidogrel for 6 months and then indefinite aspirin alone if transesophageal echocardiogram (TEE) at 45 days after implantation confirmed adequate LAA closure. The device was noninferior to warfarin in the primary efficacy outcome—stroke, systemic emboli, and cardiovascular or other death—with fewer hemorrhagic strokes, and 90% of patients were able to stop warfarin. However, 12.3% of patients had serious procedural complications, most often pericardial effusions, but these complications also included acute ischemic stroke as a result of air embolism or thromboembolism. In addition, 2.2% of attempted implantations resulted in the need for cardiac surgery because of device-related complications.
Importantly, all percutaneous techniques to date require transseptal puncture; deploy long, hollow sheaths in the left atrium (another source of thrombus); and deposit residual hardware in the left atrium, necessitating postprocedural anticoagulation. These factors may all contribute to procedural implant complications. Also, because of the complexity and variability of LAA anatomy, current devices may not always be suitable for deployment, and optimal positioning of the device to ensure complete closure may be difficult. Moreover, although LAA occluding devices may have a role in thromboprophylaxis in patients at high stroke risk with contraindications to warfarin, they will not prevent embolism that originates outside the atrial appendage, and long-term efficacy is uncertain.
Surgical techniques for treatment of AF began in the early 1980s. The majority of these have only historic significance now, as they were unable to address major detrimental sequelae of AF, including vulnerability to systemic thromboembolism and hemodynamic compromise. The prototype surgical ablation procedure for AF was developed in the late 1980s by James Cox. The Cox Maze procedure was an operation involving multiple incisions in both the left and right atria, designed to interrupt the macroreentrant circuits thought to be responsible for AF. The procedure appeared to be highly successful in preventing recurrent AF, although it was never subjected to modern ECG monitoring in follow-up; it appeared not to compromise atrial transport function and significantly reduced the risk of thromboembolism and stroke. After two iterations to address late complications and technical difficulty, the Cox Maze III emerged and become the gold standard for the surgical treatment of AF. In a long-term study of patients who had the Cox Maze III procedure, 97% of patients at late follow-up were free of symptomatic AF. Despite these excellent results, the Cox Maze procedure did not gain widespread acceptance because of its complexity and technical difficulty. In the most recent iteration of the procedure, the Cox Maze IV ( Figure 21-8 ), bipolar RFA lesions had replaced the surgical incisions. This iteration supported efforts to develop a limited set of lesions that can be performed less invasively through a small thoracotomy on a beating heart, without a need for cardiopulmonary bypass. However, the major shortcoming of this procedure is its inability to reliably create permanent transmural atrial lesions. Importantly, both incomplete and complete ablation lesions created during surgical ablation procedures can be proarrhythmic by promoting macroreentrant circuits. In a study of 50 patients who underwent minimally invasive PVI and were followed up for at least 1 year, 20 patients (40%) developed recurrent atrial tachyarrhythmias. Thirteen of these patients underwent EP study. Pulmonary vein reconnection was the most common finding in patients with recurrent AF and occurred in 50% of all pulmonary veins examined despite achieving entrance and exit block in the operating room. Macroreentrant atrial flutter was the second most common arrhythmia.
One of the major obstacles for adaptation of surgical AF ablation, either as a combined or stand-alone procedure, has been the lack of controlled studies and the absence of postprocedure rhythm monitoring in particular. A recent prospective study of a minimally invasive surgical (MIS) approach for the treatment of paroxysmal AF used postprocedure long-term rhythm monitoring—24-hour Holter, 14-day event, or pacemaker interrogation—for a follow-up period of at least 1 year. The procedure consisted of circumferential PVI, partial autonomic denervation, and selective excision of the LAA. No major adverse events were reported, and average hospital stay was 5.2 days. Freedom from any atrial tachyarrhythmia was 80.8% at 1 year, and antiarrhythmic drugs were stopped in 90% of patients. These results are in line with the reported outcomes of percutaneous ablation procedures for paroxysmal AF, although important differences in patient selection may well exist.
Excision/exclusion of the LAA is a critical component of the surgical approach for the treatment of AF. However, the efficacy of this approach in preventing stroke has only recently been critically examined. In a meta-analysis of five clinical trials studying 1400 patients who underwent LAA exclusion, no clear benefit was shown. One reason for this may be the inability to achieve acceptably high occlusion success rates (55% to 93%). A study that examined success rates associated with different surgical techniques to exclude the LAA demonstrated that excision of the LAA was significantly more effective than exclusion of the LAA (73% versus 23%, respectively).
The indications in the 2011 American College of Cardiology Foundation (ACCF)/American Heart Association (AHA)/Heart Rhythm Society (HRS) Focused Update on the Management of Patients with Atrial Fibrillation for catheter or surgical ablation for AF include reduction in AF-related symptoms and improved quality of life in patients who had not responded to medical therapy with at least one antiarrhythmic drug.
Atrioventricular Junction Ablation for Ventricular Rate Control
Treatment of AF with either restoration of sinus rhythm or control of the ventricular rate can sometimes be difficult. Moreover, growing evidence suggests that uncontrolled ventricular rates during AF frequently cause tachycardia-related cardiomyopathy. This is of special concern in the presence of preexisting structural heart disease because these patients are at high risk of complications from antiarrhythmic therapy and are less likely to tolerate the negative inotropic effects of AV node–blocking agents. Catheter ablation of the AV junction was the first routinely successful strategy to use radiofrequency energy, and the overall success rate for AV junction ablation is essentially 100% in recent reports, although a recurrence of AV conduction occurs in about 3% to 5% of patients. Randomized comparisons of ablation versus medical therapy demonstrated better symptomatic control and improvement in LV function in patients with severe symptoms. Despite this success, there are two important limitations in regard to AV junction ablation: the requisite pacemaker dependency and the potential risk to develop right ventricular (RV) pacing–related cardiomyopathy. A large body of evidence has recently emerged that underscores the harmful effects of long-term RV pacing. LV dyssynchrony imposed by RV pacing can lead to LV remodeling with dilation and decreases in LV ejection fraction (LVEF). In response, the Left Ventricular–Based Cardiac Stimulation Post–AV Nodal Ablation Evaluation (PAVE) study investigated the prophylactic implantation of biventricular pacemakers in patients undergoing AV junction ablation and showed that patients treated with a biventricular pacemaker performed modestly better on a 6-minute walk test and had preserved LVEF compared with patients with RV pacing only.
Catheter Ablation for Ventricular Tachyarrhythmias
Idiopathic Ventricular Tachycardia
Idiopathic ventricular tachycardias are VTs that occur in the absence of clinically apparent structural heart disease. The outflow tract is the most common origin of idiopathic VT, and approximately 70% to 80% of these arrhythmias originate from the RV outflow tract. Other origins include the pulmonary artery, the LV outfow tract; the aortic sinuses of Valsalva, near the bundle of His; the coronary sinus and cardiac veins; the mitral and tricuspid valve annuli; and the epicardium. These VTs can often be recognized by specific ECG characteristics. The typical QRS morphology during outflow tract VT shows a left bundle branch block (LBBB) configuration with an inferior (right or left) axis. Idiopathic focal outflow tract VT is typically seen between 20 and 50 years of age and occurs more frequently in women. The two typical forms are exercise-induced VT and repetitive monomorphic VT occurring at rest. Repetitive salvos of nonsustained VT (NSVT) are frequent and comprise 60% to 92% of reported series, but sustained VT occasionally occurs. RV outflow tract VTs are usually mapped to the area just below the pulmonary valve on the septal aspect of the outflow tract. In a case report series of RV outflow tract ablation, acute success rates typically exceeded 80%, and recurrence of arrhythmia was reported in up to 5% of cases. Complications are rare, but perforation, tamponade, and death have been reported.
One frequently seen reason for failed ablation of an RV outflow tract VT is incorrect mapping. VT with an LBBB configuration and inferior axis QRS morphology can also originate from the LV outflow tract, including the sinus of Valsalva, and the anterior epicardium. VT arising from the RV outflow tract typically shows an R/S transition zone in the precordial leads at V4, whereas an R/S transition at V1 or V2 indicates an LV origin. VTs originating from extension of ventricular myocardium above the aortic annulus are ablated from within the sinuses of Valsalva. These VTs account for about 20% of all idiopathic outflow tract VTs. Activation mapping typically shows a two-component electrogram with the earliest deflection preceding the QRS complex by an average 39-ms ablation. The majority are ablated from the left coronary cusp, followed in frequency by the right coronary cusp, the junction between the right and left coronary cusp, and rarely the noncoronary cusp.
Although idiopathic outflow tract VTs have a benign course, potentially malignant forms of VT that resemble idiopathic VT may also arise from the outflow tract region, including VT in arrhythmogenic RV dysplasia/cardiomyopathy, polymorphic catecholeminergic VT, Brugada syndrome, and also idiopathic polymorphic VT (PMVT)/VF. All patients who come to medical attention with outflow tract VT require an evaluation for organic heart diseases or genetic syndromes associated with sudden death.
Intrafascicular verapamil-sensitive reentrant tachycardia typically presents as exercise-related VT in individuals between the ages of 15 and 40 years, and 60% to 80% of patients are male. The QRS morphology has a right bundle branch block (RBBB) configuration with RS complexes in the midprecordial leads. The mechanism is reentry in or near portions of Purkinje fascicles of the left bundle, and often Purkinje fiber activation precedes local ventricular activation at the site of origin both in sinus rhythm and during VT. The overall success rate of intrafascicular VT ablation is greater than 95%. Although complications related to left-heart catheterization are expected, no serious complications were reported in these studies. Given its high efficacy and low risk, catheter ablation should be considered in patients with persistent symptoms despite the use of drug therapy (β-blockers or calcium channel antagonists) or in patients who prefer curative therapy over long-term drug therapy.
Ventricular Tachycardia in Patients with Structural Heart Disease
Sustained monomorphic VT can complicate several forms of heart disease, including coronary heart disease, nonischemic dilated cardiomyopathy, hypertrophic cardiomyopathy, RV dysplasia/cardiomyopathy, and sarcoid heart disease. The most frequent and well-understood anatomic substrate for VT is healed MI, in which slow, discontinuous conduction in the surviving border zone of the infarct allows the establishment of stable reentrant circuits. Sites of arrhythmia origin are recognized by low-amplitude, fractionated endocardial electrograms, an EP marker for the slow conduction necessary for reentry ( Figure 21-9 ). Similar endocardial electrogram abnormalities have been demonstrated in other forms of heart disease, however, the abnormal electrograms are typically localized to perivalvular areas and the epicardium. Because the majority of VTs are hemodynamically unstable, and patients usually exhibit multiple VT morphologies as a result of separate reentry circuits (or shared areas of slow conduction with variable exits from the scar), activation and entrainment mapping, which require mapping during ongoing VT, have been increasingly supplemented by substrate-mapping approaches ( Figure 21-10 ).