The New Eng l a nd Jour na l of Me dic i ne

Drug Therapy A L A S T A I R J . J . W O O D , M. D. , Editor

R ADIO -F REQUENCY A BLATION AS T REATMENT FOR C ARDIAC A RRHYTHMIAS FRED MORADY, M.D.

R

ADIO-FREQUENCY catheter ablation has replaced antiarrhythmic-drug therapy for the treatment of many types of cardiac arrhythmia. This article reviews the biophysics and results of radio-frequency catheter ablation and the clinical indications for its use. Catheter-ablation procedures are performed in an electrophysiology laboratory. Usually both the diagnosis and the catheter ablation can be accomplished in a single session.1 Three or four electrode catheters are inserted percutaneously into a femoral, internal jugular, or subclavian vein and positioned within the heart to allow pacing and recording at key sites. The efficacy of catheter ablation depends on the accurate identification of the site of origin of the arrhythmia. Once this site has been identified, an electrode catheter is positioned in direct contact with it and radiofrequency energy is delivered through the catheter to destroy it. BIOPHYSICS OF RADIO-FREQUENCY ABLATION

Radio-frequency current is alternating current that is delivered at cycle lengths of 300 to 750 kHz when used for catheter ablation. It causes resistive heating of the tissue in contact with the electrode.2 Because the degree of tissue heating is inversely proportional to the radius to the fourth power,3 the lesions created by radio-frequency energy are small. Typical ablation catheters, which are 2.2 mm in diameter (7 French) and have a distal electrode 4 mm long, create lesions approximately 5 to 6 mm in diameter and 2 to 3 mm deep.4,5 Larger lesions are possible with larger electrodes or saline-irrigated ablation catheters.6 Although electrical injury may be a contributing factor, the primary mechanism of tissue destruction by radio-frequency current is thermal injury.7 Irreversible tissue destruction requires a tissue tempera-

From the Division of Cardiology, Department of Internal Medicine, University of Michigan Medical Center, 1500 E. Medical Center Dr., Box 0022, Ann Arbor, MI 48109-0022, where reprint requests should be addressed to Dr. Morady. ©1999, Massachusetts Medical Society.

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ture of approximately 50°C.8 In most ablation procedures, the power output of the radio-frequency generator is adjusted manually or automatically to achieve a temperature of 60 to 75°C at the electrode–tissue interface.9,10 If the temperature at the electrode–tissue interface reaches 100°C, coagulated plasma and desiccated tissue may form on the electrode, preventing effective delivery of the current, predisposing the patient to thromboembolic complications, and necessitating the removal of the catheter so that the coagulated material can be wiped off the electrode.11 The acute lesion created by radio-frequency current consists of a central zone of coagulation necrosis surrounded by a zone of hemorrhage and inflammation. Chronic lesions are characterized by coagulation necrosis and have a discrete border (Fig. 1).12 Changes that occur in the border zone explain why arrhythmias may recur several days to several weeks after apparently successful ablation. The arrhythmia may recur if the target tissue is in the zone bordering a lesion instead of in the central area of necrosis and if the inflammation resolves without residual necrosis.13 Conversely, the site of origin of an arrhythmia that has not been successfully ablated may later become permanently nonfunctional if it is within the border zone of a lesion and if microvascular injury and inflammation within this zone result in progressive necrosis.14,15 When introduced into clinical use in 1982, catheter ablation was performed with direct-current shocks.16,17 Radio-frequency ablation has replaced direct-current ablation because it has several advantages over direct current. These include the absence of skeletal- and cardiac-muscle stimulation; minimal discomfort during delivery of energy; the possibility of performing the procedure in conscious patients; the absence of barotrauma; the absence of damage to the catheter and the discrete nature of the resulting lesions; and the delivery of energy over a period of 30 to 60 seconds, which allows potential complications to be avoided by terminating the application of energy early. ARRHYTHMIAS THAT CAN BE TREATED WITH RADIO-FREQUENCY ABLATION Paroxysmal Supraventricular Tachycardia

The most common mechanism of paroxysmal supraventricular tachycardia is atrioventricular nodal reentry, which is responsible for approximately 60 to 65 percent of cases. In most patients with this arrhythmia, posterior atrionodal input to the atrioventricular node serves as the anterograde limb, or “slow pathway,” of the reentry circuit, and anterior atrionodal inputs serve as the retrograde limb, or “fast pathway” (Fig. 2).18,19 In typical atrioventricular nodal reentrant tachycardia, discrete P waves are not visible on the electrocardiogram, because the atria and ventricles are usually depolarized simultaneous-

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Compact: atrioventricular: node Fast-pathway: ablation sites

Right: atrium

Bundle of His

Tricuspid: annulus

Coronary-: sinus: ostium

Slow-pathway: ablation sites

Right: ventricle

Typical Atypical

Figure 1. Photomicrograph of the Mitral Annular Region of the Heart of a Dog Four Weeks after Delivery of Radio-Frequency Energy through an Ablation Catheter Positioned at the Ventricular Aspect of the Mitral Annulus (Hematoxylin and Eosin, ¬10). The left ventricular free wall, left atrial wall, and atrioventricular sulcus are shown in cross section. The radio-frequency lesion (arrow) is homogeneous and sharply demarcated. The lesion has a diameter of approximately 3 mm and a depth of 3 to 3.5 mm. (Photomicrograph courtesy of Dr. Jonathan Langberg.)

ly (Fig. 2).20 In the uncommon, atypical form of atrioventricular nodal reentrant tachycardia, the fast pathway is the anterograde limb, and the slow pathway is the retrograde limb of the reentry circuit. In this type of tachycardia, P waves precede each QRS complex and are inverted in the inferior leads (Fig. 2). Either form of atrioventricular nodal reentrant tachycardia can be eliminated by radio-frequency ablation of either the fast or the slow pathway. Fastpathway ablation sites are usually located near the anterior and superior aspect of the tricuspid-valve annulus, whereas slow-pathway ablation sites are usually located near the ostium of the coronary sinus (Fig. 2).21 Because fast-pathway ablation sites are closer to the compact atrioventricular node, the risk of inadvertently creating atrioventricular block is higher with fast- than with slow-pathway ablation. Fastpathway ablation has been associated with a long-

Figure 2. The Reentry Circuit of Typical Atrioventricular Nodal Reentrant Tachycardia. Posterior input to the atrioventricular node (dashed arrow) serves as the anterograde slow pathway of the reentry circuit, and anterior input to the atrioventricular node (solid arrow) serves as the retrograde fast pathway. The shaded areas indicate the target sites for radio-frequency ablation of the fast and slow pathways. Also shown are examples of typical and atypical atrioventricular nodal reentrant tachycardia, at rates of 188 and 170 per minute, respectively, recorded in lead II. Discrete P waves are not present on the electrocardiogram in typical atrioventricular nodal reentrant tachycardia. In atypical atrioventricular nodal reentrant tachycardia, there is a deeply inverted P wave preceding the QRS complex in the inferior leads. In this type of tachycardia, the anterior input to the atrioventricular node serves as the anterograde fast pathway of the reentry circuit, and the posterior input serves as the retrograde slow pathway.

term success rate of 82 to 96 percent, a recurrence rate of 5 to 14 percent, and an incidence of highdegree atrioventricular block of 0 to 10 percent.1,22,23 In comparison, slow-pathway ablation has been associated with a long-term success rate of 98 to 100 percent, a recurrence rate of 0 to 2 percent, and an incidence of high-degree atrioventricular block of 0 to 1.3 percent.24-29 With appropriate technique on the part of the operator, the risk of inducing atrioventricular block during slow-pathway ablation can be reduced to less than 1 percent without compromising the success rate.30 For example, among 990 consecutive patients who underwent slow-pathway ablation, the success rate was 99 percent, and the prevalence of high-degree atrioventricular block was 0.5 percent (unpublished data). Therefore, slow-pathway ablation is preferable to fast-pathway ablation for the treatment of atrioventricular nodal reentrant tachycardia. Vol ume 340

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Atrioventricular: node Right: atrium Coronary-: sinus: ostium Accessory: pathway

Right: ventricle

Tricuspid annulus

Figure 3. The Reentry Circuit of Orthodromic Reciprocating Tachycardia. The atrioventricular node serves as the anterograde limb of the reentry circuit, and an accessory pathway serves as the retrograde limb. In this case, the accessory pathway is located in the free wall of the right ventricle. The wave of depolarization travels from the atrioventricular node to the accessory pathway through the ventricle, and from the accessory pathway to the atrioventricular node through the atrium. Because the ventricles are depolarized by the normal conduction system, the QRS complexes are narrow unless there is a bundle-branch block. Also shown is an example of orthodromic reciprocating tachycardia, at a rate of 210 per minute, recorded in lead III. A P wave is present in the left half of the RR cycle (arrow) because retrograde conduction through the accessory pathway is more rapid than anterograde conduction through the atrioventricular node.

Approximately 30 percent of paroxysmal supraventricular tachycardias are attributable to orthodromic reciprocating tachycardia, in which the atrioventricular node serves as the anterograde limb of the reentry circuit and an accessory atrioventricular pathway serves as the retrograde limb (Fig. 3). In this type of tachycardia, the electrocardiogram may show a P wave in the left half of the RR cycle (Fig. 3).20 Because the accessory pathway may not be capable of anterograde conduction, the electrocardiogram during sinus rhythm may not show a Wolff–Parkinson–White pattern. Radio-frequency ablation of accessory pathways is associated with a high success rate, as discussed in detail below. Approximately 5 to 10 percent of cases of paroxysmal supraventricular tachycardia arise in the atria and are caused by reentry, abnormal automaticity, or triggered activity.31,32 In atrial tachycardias, the P waves are often in the right half of the RR cycle.20 Unless the tachycardia is due to sinus-node reentry, the P waves during atrial tachycardia differ in configuration from the sinus P waves. Atrial tachycardias 536 ·

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arise more often in the right atrium than in the left atrium, and the chamber of origin can usually be identified by analysis of the P-wave configuration.33 Right atrial tachycardias are mapped with use of a venous approach, and left atrial tachycardias with use of a transseptal approach. If the tachycardia is not multifocal and either is inducible or occurs spontaneously in the electrophysiology laboratory, localization and radio-frequency ablation of the site of origin of atrial tachycardia are usually feasible. Among 146 patients in 10 studies who underwent radiofrequency ablation for atrial tachycardia, the overall short-term success rate was 92 percent, with late recurrence of the ablated tachycardia in 8 percent, the onset of a new tachycardia in 3 percent, and complications of venous or arterial access in 1.4 percent.32,34-42 Because of a very favorable risk–benefit ratio, radio-frequency ablation is appropriate first-line therapy for paroxysmal supraventricular tachycardia caused by atrioventricular nodal reentrant tachycardia or an accessory-pathway tachycardia in any patient who has sufficient symptoms to justify therapy. Atrioventricular nodal reentrant tachycardia and accessorypathway tachycardias are ideally suited for radio-frequency ablation, because critical components of their reentry circuits can usually be permanently eliminated with discrete applications of radio-frequency current. Atrial tachycardia is somewhat less well suited to radio-frequency ablation because of its unpredictable potential for multifocality. If there is adequate evidence that an atrial tachycardia is not multifocal, radio-frequency ablation of the atrial tachycardia may be appropriate either because the tachycardia is refractory to drug therapy or because the patient prefers radio-frequency ablation. In patients with multifocal atrial tachycardia that is refractory to drug therapy, atrioventricular-node ablation (discussed below) may be appropriate. The Wolff–Parkinson–White Syndrome

The Wolff–Parkinson–White syndrome may be associated with a regular narrow- or wide-QRS tachycardia or with atrial fibrillation or flutter and rapid ventricular rates.43 Ventricular rates exceeding 300 beats per minute may result in cardiac arrest or sudden death in patients with this syndrome.44 In the past, most patients with the Wolff–Parkinson–White syndrome were treated with drugs such as quinidine or procainamide, and surgical ablation was performed only in patients whose arrhythmias were refractory to drug treatment or were life-threatening. Today, radio-frequency ablation has eliminated the need for surgical ablation in almost all patients and the need for antiarrhythmic-drug therapy in many patients. Right free-wall accessory pathways and most septal accessory pathways are ablated with a venous approach by positioning an ablation catheter along the

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TABLE 1. COMPLICATIONS OF RADIO-FREQUENCY ABLATION OF ACCESSORY PATHWAYS.*

Left atrial wall

Accessory pathway

Mitral annulus

Atrioventricular sulcus Coronary sinus

Left circumflex coronary artery

Mitral valve

Left ventricular wall Ablation catheter

Figure 4. Placement of the Catheter for Radio-Frequency Ablation of a Left Free-Wall Accessory Pathway. An ablation catheter inserted into a femoral artery has been positioned at the ventricular aspect of the mitral annulus by a retrograde aortic approach. An alternative approach is transseptal catheterization and placement of the ablation catheter at the atrial aspect of the mitral annulus. The accessory pathway is shown in a typical location near the endocardial surface. Accessory pathways may occasionally traverse the atrioventricular sulcus close to the epicardial surface, necessitating ablation from within the coronary sinus.

tricuspid annulus or the right atrial septum, at the atrial or ventricular insertion of the accessory pathway. Left free-wall and left septal accessory pathways are ablated by positioning the catheter along the mitral annulus, at the atrial or ventricular insertion of the accessory pathway, with the use of a retrograde aortic or transseptal approach (Fig. 4). In a small percentage of patients, the accessory pathway can be ablated only by delivery of radio-frequency current within the coronary sinus or one of its branches.45 In studies of 100 to 363 patients, the early success rate of radio-frequency ablation of accessory pathways was 89 to 100 percent, the recurrence rate was 3 to 9 percent, and the long-term success rate after several months or years of follow-up was 85 to 100 percent.46-52 One of the determinants of success is the experience of the operator; after experience with accessory-pathway ablation in 250 patients, singlesession success rates of 95 percent or more and a

COMPLICATION

PREVALENCE %

Death Nonfatal complications Cardiac tamponade Atrioventricular block Coronary-artery spasm Mild mitral regurgitation Coronary-artery thrombosis Pericarditis Mild aortic regurgitation Transient neurologic deficit Bacteremia Femoral-artery complications Thrombotic occlusion Large hematoma Atrioventricular fistula

0.08 0.5 0.5 0.2 0.2 0.1 0.1 0.1 0.1 0.1 0.2 0.2 0.1

*The incidence of death is based on unpublished data from the University of Oklahoma, the University of Alabama, the University of Michigan, Duke University, and the University of California, San Francisco. The incidence of nonfatal complications is based on pooled data from seven published studies.46-52

mean duration of two hours or less for the procedure are possible.53 Twenty-nine of 1205 patients (2.4 percent) in seven large studies had complications of the ablation procedure.46-52 The most common complications were atrioventricular block in patients with a septal accessory pathway and nonfatal cardiac tamponade (Table 1). Transient repolarization abnormalities that mimic ischemia often occur after ablation of manifest accessory pathways. These abnormalities are due to cardiac memory, not injury,54 and do not require evaluation if there are no other clinical indications (Fig. 5). There were no deaths among patients treated with radio-frequency ablation in the initial studies,46-52 but there were deaths reported in later studies.55 Three of 3856 patients (0.08 percent) treated at five university centers died (unpublished data). In comparison, the annual risk of sudden death in patients with the Wolff–Parkinson–White syndrome and symptomatic tachycardia is estimated to be 0.05 to 0.5 percent.56 Radio-frequency ablation is an appropriate option for any patient with a symptomatic arrhythmia involving an accessory atrioventricular pathway (or the less common atriofascicular pathway57). It is particularly indicated if the arrhythmia is associated with severe symptoms or cardiac arrest. Although there is a risk of fatal complications, the risk is low in relation to the morbidity associated with the Wolff–ParVol ume 340

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I

*

II III Coronary-: sinus: ostium

1 sec

Figure 5. Radio-Frequency Ablation of a Posteroseptal Accessory Pathway. Shown are recordings from leads I, II, and III and the electrogram recorded by the ablation catheter positioned at the ostium of the coronary sinus. There is sinus rhythm at a rate of approximately 75 per minute, with a short PR interval and prominent delta waves. The onset of a 60-second application of radio-frequency current is shown by the arrow. Two seconds after the beginning of delivery of current, the PR interval normalizes and the delta waves disappear (asterisk). The prominent T-wave abnormality in lead III is caused by a cardiac-memory phenomenon, not by ischemia or infarction.54

Left atrium

Right atrium

Superior vena cava

Crista terminalis

Mitral annulus

Inferior vena cava

kinson–White syndrome. In asymptomatic patients whose electrocardiogram shows a Wolff–Parkinson– White pattern, radio-frequency ablation (or any other therapy) is usually not indicated.58

Coronary sinus Tricuspid annulus

Atrial Flutter

Type I atrial flutter, the common variety of atrial flutter, has a “sawtooth” pattern of flutter waves in leads II, III, and aVF of the electrocardiogram (Fig. 6). This type of atrial flutter is generated by a large, counterclockwise reentry circuit in the right atrium and can be successfully eliminated by radio-frequency ablation of a critical isthmus of tissue between the tricuspid annulus and the inferior vena cava (Fig. 6).59 In initial studies, the early success rate was high, but the recurrence rate was 10 to 25 percent.39,59,60 In more recent studies the success rate was more than 90 percent and the recurrence rate was less than 10 percent when complete block of the isthmus was achieved.61,62 Complications should be rare and have yet to be reported.39,59-62 Because of a high success rate and low risk of complications, radio-frequency ablation of type I atrial flutter is appropriate not only in patients with atrial flutter that is refractory to drug treatment, but also in patients who desire an alternative to antiarrhythmic-drug therapy or repeated electrical cardioversion. However, even in patients who have not previously had episodes of atrial fibrillation, drug therapy for atrial fibrillation may be needed despite successful ablation of atrial flutter.63 Two other types of atrial flutter are also amenable to radio-frequency ablation: the clockwise version of type I atrial flutter, for which the success rate has been the same as for the counterclockwise atrial flutter described above,64 and atrial flutter caused by reentry around an incision after open-heart sur538 ·

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Figure 6. The Reentry Circuit of the Common Variety of Atrial Flutter (Type I). The right and left atria are shown in a left anterior oblique projection. The reentry circuit is confined to the right atrium and circulates in a counterclockwise direction within it (arrows). The shaded area between the tricuspid annulus and the inferior vena cava indicates the critical isthmus of tissue that is targeted for ablation of this type of atrial flutter. Also shown is a recording of counterclockwise atrial flutter in lead II, demonstrating the “sawtooth” pattern of flutter waves (rate, 250 per minute) characteristic of this type of atrial flutter.

gery.41,65 Because these types of atypical atrial flutter are not associated with specific electrocardiographic findings, catheter mapping in the electrophysiology laboratory is needed to establish their presence. Other types of atypical atrial flutter that arise in the right or left atrium are often difficult to map and ablate. Therefore, because of the lower probability of success in such cases, radio-frequency ablation is usually reserved for patients in whom atrial flutter is refractory to drug therapy when there is not the classic “sawtooth” pattern in the inferior leads. Atrial Fibrillation

An uncontrolled ventricular rate during atrial fibrillation is often responsible for uncomfortable symp-

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toms, functional limitation, and cardiomyopathy induced by tachycardia.66 If the ventricular rate cannot be controlled with digoxin, b-adrenergic–receptor antagonist drugs, or calcium-channel antagonist drugs, radio-frequency energy can be used either to ablate or to modify the atrioventricular node. The longterm efficacy of atrioventricular-node ablation is 98 to 100 percent.67,68 Complete atrioventricular block can usually be produced with radio-frequency current delivered on the right side of the heart; if not, a left ventricular approach is almost always successful.67,68 All patients require a pacemaker after atrioventricular-node ablation. Atrioventricular-node modification is performed by delivering radio-frequency energy in the right atrial posterior septum or mid-septum.69 The goal of atrioventricular-node modification is to control the ventricular rate without creating high-grade atrioventricular block. Long-term rate control without excessive bradycardia is achieved in approximately 75 percent of patients, with the remaining 25 percent requiring a permanent pacemaker because of atrioventricular block.70 Both ablation and modification of the atrioventricular node have been associated with an early risk of bradycardia-dependent polymorphic ventricular tachycardia that can be prevented by ventricular pacing at a rate of at least 75 beats per minute67,70 and a 1 to 2 percent risk of late sudden death that may well be attributable to preexisting heart disease rather than to the procedure.71 Symptoms, functional capacity, and left ventricular function improve after either radio-frequency ablation or modification of the atrioventricular node in patients with atrial fibrillation.70,71 The advantage of the modification procedure is that it often eliminates the need for a pacemaker; the disadvantages are an increased risk of polymorphic ventricular tachycardia in patients predisposed to bradycardia-dependent arrhythmias70 and less reliable rate control during atrial flutter,70 which often occurs in association with paroxysmal atrial fibrillation. The advantages of ablation are a much lower recurrence rate and the elimination of symptoms attributable to an irregular rate. A decision as to whether atrioventricular-node modification should be attempted before ablation is undertaken must be made on a case-by-case basis. Because all patients who undergo atrioventricularnode ablation and 25 percent of those who undergo atrioventricular-node modification become dependent on pacemakers, and because of the small risk of sudden death, these procedures are appropriate only when attempts at pharmacologic rate control have failed. In patients who cannot be maintained in sinus rhythm and who have severe symptoms from atrial fibrillation despite adequate control of the ventricular rate, a surgical “maze” procedure or one of its

variants has been used to restore sinus rhythm and prevent recurrences of atrial fibrillation.72 A catheter version of the maze procedure has been performed by creating several linear lesions in the left or right atrium.73,74 The safety and efficacy of this type of radio-frequency ablation to eliminate atrial fibrillation remain to be established, and therefore this procedure is indicated only on an investigational basis. Most cases of atrial fibrillation are due to multiple wavelets of reentry in the left and right atria. However, in some cases, idiopathic paroxysmal atrial fibrillation may have a focal source, often within one of the pulmonary veins, and may be amenable to focal ablation with radio-frequency energy.75 The proportion of patients with atrial fibrillation who have a focal site of origin is not known, and experience with radio-frequency ablation of this type of atrial fibrillation is limited.75 Idiopathic Ventricular Tachycardia

The two most common varieties of idiopathic ventricular tachycardia are ventricular tachycardia arising in the right ventricular outflow tract,76 which has a left bundle-branch–block configuration and inferior axis, and verapamil-responsive left ventricular tachycardia,77 which usually arises in the inferoapical septum and has a right bundle-branch–block configuration and superior axis. Less commonly, idiopathic ventricular tachycardia arises in other areas of the right or left ventricle. When there is only one site of origin of ventricular tachycardia, as is usually the case in patients with idiopathic ventricular tachycardia, radio-frequency ablation is often curative. Longterm success rates have been 85 to 100 percent,76-79 and complications are rare.79 Because of its high efficacy and low risk, radio-frequency ablation of idiopathic ventricular tachycardia may be appropriate when the arrhythmia is refractory to drug treatment or when the patient prefers this treatment. Ventricular Tachycardia in Patients with Coronary Artery Disease

Sustained, monomorphic ventricular tachycardia in patients with coronary artery disease is most often generated by a reentry circuit that incorporates diseased myocardium adjacent to an area of infarction in the left ventricle. If the patient is hemodynamically stable during ventricular tachycardia, target sites for ablation may be identified in the electrophysiology laboratory with various catheter-mapping techniques.80,81 However, because ventricular tachycardia often causes hemodynamic compromise, only 5 to 10 percent of patients with coronary artery disease are suitable candidates for catheter ablation. Most patients with ventricular tachycardia and prior infarction have multiple types of monomorphic ventricular tachycardia, and elimination of all ventricular tachycardias is often not a realistic goal. FurVol ume 340

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thermore, because the recurrence of an ablated ventricular tachycardia or the onset of a new ventricular tachycardia may be fatal, radio-frequency ablation is rarely used as the sole therapy for ventricular tachycardia. Instead, it is usually used in patients with coronary artery disease as an adjunct to an implantable cardioverter–defibrillator or, less commonly, to antiarrhythmic-drug therapy. In selected patients with ventricular tachycardia and prior infarction, the long-term success rate of radio-frequency ablation of ventricular tachycardia ranges from 67 percent to 96 percent, with serious complications in less than 2 percent of patients.80-84 These success rates refer only to the particular ventricular tachycardia targeted for ablation, not to all ventricular tachycardias in a given patient. The most common indication for radio-frequency ablation of ventricular tachycardia in patients with coronary artery disease is ventricular tachycardia refractory to drug therapy that results in frequent discharges from an implantable cardioverter–defibrillator, is too slow to be detected by an implantable cardioverter–defibrillator, or is incessant (Fig. 7).85 As new types of mapping systems that allow the localization of hemodynamically unstable ventricular tachycardias come into clinical use, the indications for the ablation of ventricular tachycardia in patients with coronary artery disease may expand. Miscellaneous Arrhythmias

In a small percentage of patients with symptomatic tachycardias, the tachycardia is a nonphysiologic sinus tachycardia that is not due to a correctable cause such as hyperthyroidism.86 Radio-frequency energy directed at the sinus node attenuates the sinus tachycardia and diminishes the severity of symptoms in 90 percent of patients.87 However, because the procedure may induce symptomatic bradycardia and the need for a pacemaker in 10 percent of patients,87 it is indicated only when the symptoms are disabling and refractory to b-adrenergic–receptor antagonist drugs. Automatic junctional tachycardia is an unusual type of supraventricular tachycardia in which there is atrioventricular dissociation. The literature on radio-frequency ablation of junctional tachycardia is limited to case reports and a series of 11 patients in which the success rate was 82 percent and high-degree atrioventricular block developed in 1 patient (9 percent).88 Bundle-branch reentry is a mechanism of wideQRS tachycardia that occurs most often in patients with cardiomyopathy, a left-sided intraventricular conduction defect, and a prolonged His bundle–ventricular interval.89 The reentry circuit incorporates the right and left bundles and is reliably eliminated by radio-frequency ablation of the right bundle.90 Because of preexisting disease of the His–Purkinje system, a pacemaker may be necessary after right-bun540 ·

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V1

I

II

LV 1 sec Figure 7. Radio-Frequency Ablation of Ventricular Tachycardia (Rate, 200 per Minute) in a 65-Year-Old Man with a History of Inferior Myocardial Infarction Who Received an Implantable Cardioverter–Defibrillator because of Recurrent Ventricular Tachycardia Associated with Syncope. Despite drug therapy, the patient had multiple discharges from his implantable cardioverter–defibrillator directed at this ventricular tachycardia. Shown are recordings from leads V1, I, and II and an endocardial electrogram recorded by an ablation catheter positioned near the apical edge of an inferior-wall aneurysm in the left ventricle (LV). Within one second after the application of radio-frequency energy (arrow), the ventricular tachycardia was ablated and replaced by sinus tachycardia at a rate of 130 per minute; the sinus tachycardia was attributable to an isoproterenol infusion used to induce the ventricular tachycardia. During several months of follow-up, there was a marked reduction in the number of shocks that the patient received from the implantable cardioverter–defibrillator.

dle ablation, and because other types of ventricular tachycardia may coexist with bundle-branch reentry, an implantable cardioverter–defibrillator or drug therapy may also be needed.90 Nevertheless, because of the high success rate of ablation and the advantages inherent in eliminating a tachycardia that otherwise would require long-term therapy, right-bundle ablation is usually indicated in patients with bundlebranch reentry. An attempt at radio-frequency ablation may sometimes be indicated in patients with ventricular tachycardias refractory to drug treatment who have heart diseases other than coronary artery disease.91 However, because ventricular tachycardia is often multifocal and creates hemodynamic instability and because it may not be inducible in the electrophysiology laboratory, radio-frequency ablation has a very limited role in the treatment of such patients. Benign ventricular ectopy does not require therapy except in patients who have severe symptoms, in which case b-adrenergic–receptor antagonists usually are sufficient to produce improvement. Rarely, catheter ablation of frequent ventricular ectopy may

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be appropriate in patients with ventricular ectopy that is refractory to drug therapy and with severe symptoms if the ectopy is uniform and has a left bundle-branch–block configuration and inferior axis indicative of an origin in the right ventricular outflow tract. A success rate of 100 percent has been reported, with no complications.92 USE IN CHILDREN

Because the risk of complications is higher in patients with small hearts, and because some arrhythmias may resolve spontaneously with age, a more conservative approach is warranted in children than in adults.93 In small children, radio-frequency ablation is usually performed only for serious arrhythmias that cannot be treated successfully with drugs. EXPOSURE TO RADIATION

Radio-frequency–ablation procedures require fluoroscopy, and the amount of radiation exposure depends on the equipment and the technique used. Acute skin injury is rare and can be avoided by minimizing radiation exposure.94 In one study, it was estimated that each hour of fluoroscopy was associated with a lifetime risk of fatal cancer of 0.1 percent and a risk of a genetic defect in the patient’s offspring of 20 per 1 million births.95 Radio-frequency ablation usually can be accomplished with less than 60 minutes of fluoroscopy. COST CONSIDERATIONS

Except for ablation of ventricular tachycardia and modification or ablation of the atrioventricular node, radio-frequency ablation can be performed on an outpatient basis.96,97 The total charges for an outpatient ablation procedure are typically $10,000 to $12,000.96,97 In 1997 the approximate range of Medicare reimbursement to physicians for radio-frequency ablation was $950 to $1,350. Accessory-pathway ablation has been demonstrated to be cost effective in patients with paroxysmal supraventricular tachycardia or atrial fibrillation; the cost is $6,600 to $19,000 per quality-adjusted year of life gained.56 Other ablation procedures have been found to result in long-term reductions in health care expenditures. For example, the cost of radiofrequency ablation is less than the long-term costs associated with management of paroxysmal supraventricular tachycardia that is refractory to treatment with drugs,98 and in patients with atrial fibrillation and an uncontrolled ventricular rate, atrioventricular-node ablation reduces the consumption of health care resources.99 QUALITY OF LIFE

Although most arrhythmias that are treated with radio-frequency ablation are not life-threatening, they often impair functional capacity and the pa-

TABLE 2. INDICATIONS FOR RADIO-FREQUENCY ABLATION OF CARDIAC ARRHYTHMIAS. Arrhythmias cured by radio-frequency ablation Ablation indicated for reasons of the patient’s preference or refractoriness of arrhythmias to drug therapy Paroxysmal supraventricular tachycardia Atrioventricular nodal reentrant tachycardia Accessory-pathway–mediated tachycardia Unifocal atrial tachycardia Wolff–Parkinson–White syndrome and variant preexcitation syndromes Common variety (type I) atrial flutter Idiopathic ventricular tachycardia Bundle-branch reentry tachycardia Ablation indicated for arrhythmias refractory to drug therapy Atypical atrial flutter Inappropriate sinus tachycardia Automatic junctional tachycardia Idiopathic ventricular premature depolarizations arising in the right ventricular outflow tract associated with severe symptoms Arrhythmias palliated by radio-frequency ablation; ablation indicated for arrhythmias refractory to drug therapy Atrial fibrillation with uncontrolled ventricular rate (atrioventricular-node ablation or modification) Sustained, hemodynamically stable, monomorphic ventricular tachycardia in patients with coronary artery disease Sustained, hemodynamically stable, monomorphic ventricular tachycardia in patients with heart diseases other than coronary artery disease Ablation procedures that are investigational or whose clinical indications are undefined Linear atrial lesions to eliminate atrial fibrillation Ablation of focal source of atrial fibrillation Ablation of hemodynamically unstable monomorphic ventricular tachycardia Ablation not indicated Multifocal atrial tachycardia (can be palliated with atrioventricular-node ablation) Polymorphic ventricular tachycardia Ventricular fibrillation

tient’s sense of well-being.100 Radio-frequency ablation for a variety of supraventricular arrhythmias has been demonstrated to improve the health-related quality of life.100 The quality of life also improved after radio-frequency ablation of ventricular tachycardia in patients who had frequent discharges from an implantable cardioverter–defibrillator.85 CONCLUSIONS

The indications for the radio-frequency ablation of arrhythmias are summarized in Table 2. Its advantages include relief of symptoms, improvement in functional capacity and the quality of life, elimination of the need for lifelong antiarrhythmic-drug therapy, and long-term cost savings. The principal disadvantage is the risk of complications, which varies depending on the type of ablation procedure and the experience and skill of the operator. Therefore, the risk–benefit ratio for radio-frequency ablation should always be considered on an individual basis before the procedure is performed. Vol ume 340

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locations: results in 100 consecutive patients. J Am Coll Cardiol 1992;19: 1303-9. 49. Calkins H, Langberg J, Sousa J, et al. Radiofrequency catheter ablation of accessory atrioventricular connections in 250 patients: abbreviated therapeutic approach to Wolff-Parkinson-White syndrome. Circulation 1992;85:1337-46. 50. Swartz JF, Tracy C, Fletcher RD. Radiofrequency endocardial catheter ablation of accessory atrioventricular pathway atrial insertion sites. Circulation 1993;87:487-99. 51. Kay GN, Epstein AE, Dailey SM, Plumb VJ. Role of radiofrequency ablation in the management of supraventricular arrhythmias: experience in 760 consecutive patients. J Cardiovasc Electrophysiol 1993;4:371-89. 52. Deshpande SS, Bremner S, Sra JS, et al. Ablation of left free-wall accessory pathways using radiofrequency energy at the atrial insertion site: transseptal versus transaortic approach. J Cardiovasc Electrophysiol 1994; 5:219-31. 53. Calkins H, el-Atassi R, Kalbfleisch SJ, Langberg JJ, Morady F. Effect of operator experience on outcome of radiofrequency catheter ablation of accessory pathways. Am J Cardiol 1993;71:1104-5. 54. Kalbfleisch SJ, Sousa J, el-Atassi R, Calkins H, Langberg J, Morady F. Repolarization abnormalities after catheter ablation of accessory atrioventricular connections with radiofrequency current. J Am Coll Cardiol 1991; 18:1761-6. 55. Kosinski DJ, Grubb BP, Burket MW, Durzinsky D. Occlusion of the left main coronary artery during radiofrequency ablation for the Wolff-Parkinson-White syndrome. Eur J Card Pacing Electrophysiol 1993;1:63-6. 56. Hogenhuis W, Stevens SK, Wang P, et al. Cost-effectiveness of radiofrequency ablation compared with other strategies in Wolff-ParkinsonWhite syndrome. Circulation 1993;88:Suppl II:II-437–II-446. 57. McClelland JH, Wang X, Beckman KJ, et al. Radiofrequency catheter ablation of right atriofascicular (Mahaim) accessory pathways guided by accessory pathway activation potentials. Circulation 1994;89:2655-66. 58. Zardini M, Yee R, Thakur RK, Klein GJ. Risk of sudden arrhythmic death in the Wolff-Parkinson-White syndrome: current perspectives. Pacing Clin Electrophysiol 1994;17:966-75. 59. Feld GK, Fleck RP, Chen PS, et al. Radiofrequency catheter ablation for the treatment of human type 1 atrial flutter: identification of a critical zone in the reentrant circuit by endocardial mapping techniques. Circulation 1992;86:1233-40. 60. Cosio FG, Lopez-Gil M, Goicolea A, Arribas F, Barroso JL. Radiofrequency ablation of the inferior vena cava-tricuspid valve isthmus in common atrial flutter. Am J Cardiol 1993;71:705-9. 61. Cauchemez B, Haissaguerre M, Fischer B, Thomas O, Clementy J, Coumel P. Electrophysiological effects of catheter ablation of inferior vena cava-tricuspid annulus isthmus in common atrial flutter. Circulation 1996; 93:284-94. 62. Poty H, Saoudi N, Nair M, Anselme F, Letac B. Radiofrequency catheter ablation of atrial flutter: further insights into the various types of isthmus block: application to ablation during sinus rhythm. Circulation 1996; 94:3204-13. 63. Philippon F, Plumb VJ, Epstein AE, Kay GN. The risk of atrial fibrillation following radiofrequency catheter ablation of atrial flutter. Circulation 1995;92:430-5. 64. Kalman JM, Olgin JE, Saxon LA, Lee RJ, Scheinman MM, Lesh MD. Electrocardiographic and electrophysiologic characterization of atypical atrial flutter in man: use of activation and entrainment mapping and implications for catheter ablation. J Cardiovasc Electrophysiol 1997;8:121-44. 65. Baker BM, Lindsay BD, Bromberg BI, Frazier DW, Cain ME, Smith JM. Catheter ablation of clinical intraatrial reentrant tachycardias resulting from previous atrial surgery: localizing and transecting the critical isthmus. J Am Coll Cardiol 1996;28:411-7. 66. Grogan M, Smith HC, Gersh BJ, Wood DL. Left ventricular dysfunction due to atrial fibrillation in patients initially believed to have idiopathic dilated cardiomyopathy. Am J Cardiol 1992;69:1570-3. 67. Trohman RG, Simmons TW, Moore SL, Firstenberg MS, Williams D, Maloney JD. Catheter ablation of the atrioventricular junction using radiofrequency energy and a bilateral cardiac approach. Am J Cardiol 1992;70: 1438-43. 68. Kalbfleisch SJ, Williamson B, Man KC, et al. A randomized comparison of the right- and left-sided approaches to ablation of the atrioventricular junction. Am J Cardiol 1993;72:1406-10. 69. Williamson BD, Man KC, Daoud E, Niebauer M, Strickberger SA, Morady F. Radiofrequency catheter modification of atrioventricular conduction to control the ventricular rate during atrial fibrillation. N Engl J Med 1994;331:910-7. [Erratum, N Engl J Med 1995;332:479.] 70. Morady F, Hasse C, Strickberger SA, et al. Long-term follow-up after radiofrequency modification of the atrioventricular node in patients with atrial fibrillation. J Am Coll Cardiol 1997;29:113-21. 71. Brignole M, Menozzi C. Control of rapid heart rate in patients with

atrial fibrillation: drugs or ablation? Pacing Clin Electrophysiol 1996;19: 348-56. 72. Cox JL, Boineau JP, Schuessler RB, Kater KM, Lappas DG. Five-year experience with the maze procedure for atrial fibrillation. Ann Thorac Surg 1993;56:814-24. 73. Swartz JF, Pellersels G, Silvers J, Patten L, Cervantez D. A catheterbased curative approach to atrial fibrillation in humans. Circulation 1994; 90:Suppl 1:I-335. abstract. 74. Haissaguerre M, Jais P, Shah DC, et al. Right and left atrial radiofrequency catheter therapy of paroxysmal atrial fibrillation. J Cardiovasc Electrophysiol 1996;7:1132-44. 75. Jais P, Haissaguerre M, Shah DC, et al. A focal source of atrial fibrillation treated by discrete radiofrequency ablation. Circulation 1997;95: 572-6. 76. Klein LS, Shih HT, Hackett FK, Zipes DP, Miles WM. Radiofrequency catheter ablation of ventricular tachycardia in patients without structural heart disease. Circulation 1992;85:1666-74. 77. Nakagawa H, Beckman KJ, McClelland JH, et al. Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by a Purkinje potential. Circulation 1993;88:2607-17. 78. Wen MS, Yeh SJ, Wang CC, Lin FC, Chen IC, Wu D. Radiofrequency ablation therapy in idiopathic left ventricular tachycardia with no obvious structural heart disease. Circulation 1994;89:1690-6. 79. Coggins DL, Lee RJ, Sweeney J, et al. Radiofrequency catheter ablation as a cure for idiopathic tachycardia of both left and right ventricular origin. J Am Coll Cardiol 1994;23:1333-41. 80. Morady F, Harvey M, Kalbfleisch SJ, el-Atassi R, Calkins H, Langberg JJ. Radiofrequency catheter ablation of ventricular tachycardia in patients with coronary artery disease. Circulation 1993;87:363-72. 81. Stevenson WG, Khan H, Sager P, et al. Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circulation 1993;88:1647-70. 82. Kim YH, Sosa-Suarez G, Trouton TG, et al. Treatment of ventricular tachycardia by transcatheter radiofrequency ablation in patients with ischemic heart disease. Circulation 1994;89:1094-102. 83. Gonska BD, Cao K, Schaumann A, Dorszewski A, von zur Muhlen F, Kreuzer H. Catheter ablation of ventricular tachycardia in 136 patients with coronary artery disease: results and long-term follow-up. J Am Coll Cardiol 1994;24:1506-14. 84. Bogun F, Bahu M, Knight BP, et al. Comparison of effective and ineffective target sites that demonstrate concealed entrainment in patients with coronary artery disease undergoing radiofrequency ablation of ventricular tachycardia. Circulation 1997;95:183-90. 85. Strickberger SA, Man KC, Daoud EG, et al. A prospective evaluation of catheter ablation of ventricular tachycardia as adjuvant therapy in patients with coronary artery disease and an implantable cardioverter-defibrillator. Circulation 1997;96:1525-31. 86. Krahn AD, Yee R, Klein GJ, Morillo C. Inappropriate sinus tachycardia: evaluation and therapy. J Cardiovasc Electrophysiol 1995;6:1124-8. 87. Lee RJ, Kalman JM, Fitzpatrick AP, et al. Radiofrequency catheter modification of the sinus node for “inappropriate” sinus tachycardia. Circulation 1995;92:2919-28. 88. Hamdan M, Van Hare GF, Fisher W, et al. Selective catheter ablation of the tachycardia focus in patients with nonreentrant junctional tachycardia. Am J Cardiol 1996;78:1292-7. 89. Caceres J, Jazayeri M, McKinnie J, et al. Sustained bundle branch reentry as a mechanism of clinical tachycardia. Circulation 1989;79:25670. 90. Cohen TJ, Chien WW, Lurie KG, et al. Radiofrequency catheter ablation for treatment of bundle branch reentrant ventricular tachycardia: results and long-term follow-up. J Am Coll Cardiol 1991;18:1767-73. 91. Kottkamp H, Hindricks G, Chen X, et al. Radiofrequency catheter ablation of sustained ventricular tachycardia in idiopathic dilated cardiomyopathy. Circulation 1995;92:1159-68. 92. Zhu DW, Maloney JD, Simmons TW, et al. Radiofrequency catheter ablation for management of symptomatic ventricular ectopic activity. J Am Coll Cardiol 1995;26:843-9. 93. Van Hare GF. Indications for radiofrequency ablation in the pediatric population. J Cardiovasc Electrophysiol 1997;8:952-62. 94. Park TH, Eichling JO, Schectman KB, Bromberg BI, Smith JM, Lindsay BD. Risk of radiation induced skin injuries from arrhythmia ablation procedures. Pacing Clin Electrophysiol 1996;19:1363-9. 95. Calkins H, Niklason L, Sousa J, el-Atassi R, Langberg JJ, Morady F. Radiation exposure during radiofrequency catheter ablation of accessory atrioventricular connections. Circulation 1991;84:2376-82. 96. Kalbfleisch SJ, el-Atassi R, Calkins H, Langberg JJ, Morady F. Safety, feasibility and cost of outpatient radiofrequency catheter ablation of accessory atrioventricular connections. J Am Coll Cardiol 1993;31:567-70. 97. Man KC, Kalbfleisch SJ, Hummel JD, et al. Safety and cost of outpa-

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tient radiofrequency ablation of the slow pathway in patients with atrioventricular nodal reentrant tachycardia. Am J Cardiol 1993;72:1323-4. 98. Kalbfleisch SJ, Calkins H, Langberg JJ, et al. Comparison of the cost of radiofrequency catheter modification of the atrioventricular node and medical therapy for drug-refractory atrioventricular nodal reentrant tachycardia. J Am Coll Cardiol 1992;19:1583-7. 99. Fitzpatrick AP, Kourouyan HD, Siu A, et al. Quality of life and out-

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comes after radiofrequency His-bundle catheter ablation and permanent pacemaker implantation: impact of treatment in paroxysmal and established atrial fibrillation. Am Heart J 1996;131:499-507. 100. Bubien RS, Knotts-Dolson SM, Plumb VJ, Kay GN. Effect of radiofrequency catheter ablation on health-related quality of life and activities of daily living in patients with recurrent arrhythmias. Circulation 1996;94: 1585-91.

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