Interventional Therapy for Atrial and Ventricular Arrhythmias

	INTRODUCTION

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	HISTORICAL EVOLUTION

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The recording of intracardiac signals through electrodes, and subsequent stimulation of the cardiac tissue using these same electrodes, allowed for development of the concept of ablation. In 1967, Durrer and associates first described reproducible initiation and termination of tachycardia in a patient with atrioventricular re-entrant tachycardia (AVRT) using a bypass tract.¹ In 1969, the His bundle was first reproducibly recorded using a transvenous electrode catheter.² The continued advancements allowing localization of intracardiac signals led to the study of a variety of tachyarrhythmias.

The idea emerged that critical regions of cardiac tissue were necessary for the initiation and propagation of tachyarrhythmias. If these regions could be interrupted, the tachyarrhythmia could then be clinically cured. Once catheter mapping could localize arrhythmogenic foci, surgical excision was contemplated. In 1968, a description of such a surgical procedure for the elimination of an accessory pathway was first published.³ This heralded an era of nonpharmacologic treatment of tachyarrhythmias.

Surgical Ablation

A variety of arrhythmogenic foci and circuits were successfully mapped and ablated using surgical techniques in the 1970s. Resection of an atrial focus felt to be responsible for an atrial tachycardia was reported in 1973.⁴ Identification of re-entry circuits within the atrioventricular (AV) node allowed surgical dissection to treat AV nodal re-entrant tachycardia (AVNRT) without causing complete heart block.⁵ Although surgical ablation was therapeutic for a variety of tachyarrhythmias, the morbidity and mortality associated with thoracotomy and open-heart surgery limited its application. Because most supraventricular tachycardias (SVTs) are not life-threatening, the risk of the procedure was hard to justify. Rather, ablation procedures were an option of last resort in highly symptomatic patients refractory to medical therapy. With these limitations of the surgical approach, catheter-based ablation procedures were explored.

Catheter Ablation

In attempts to minimize the morbidity associated with ablation, a method of using a catheter to delivery energy to cardiac tissue to achieve local tissue injury was sought. In 1981, Scheinman and colleagues reported the first catheter-based ablation procedure, describing the ablation of the His bundle in dogs.⁶ This same group, in March 1981, performed the first closed-chest ablation procedure in a human. A patient with atrial fibrillation and rate control refractory to medical therapy was placed under general anesthesia and a catheter was advanced to the His bundle region. Using a standard external direct-current (DC) defibrillator, they attached one of the defibrillator pads to the intracardiac catheter and used the second defibrillator pad as a cutaneous grounding pad. A series of DC shocks was delivered between the two pads and complete heart block, and thereby rate control, was achieved.⁷

This closed-chest catheter-based procedure was quickly adopted to treat a variety of SVTs dependent on the AV node.⁸ However, to restore quality of life, these patients undergoing AV node ablation frequently required pacemakers, which at the time were not the small devices we are accustomed to today. As experience was gained and specific catheters were developed, energy could be more precisely directed to allow ablation of accessory pathways, atrial tachycardia, single limb of AVNRT, and ventricular tachycardia.

Although DC shock ablation allowed for the initiation of catheter-based ablation, it had its own limitations. The mechanism for DC shock ablation is such that a high-energy discharge from the catheter tip is developed. This results in the formation of a plasma ball at the distal electrode and subsequent "explosion" at the electrode tip. Because energy delivery was not titratable, such treatment had variable outcomes, including cardiac rupture and perforation. Since DC energy was delivered from the intracardiac electrode toward a cutaneous site, general anesthesia was required.

The introduction of RF energy as an ablative energy source heralded a new era in the nonpharmacologic, nonsurgical treatment of arrhythmias. RF energy had been used for decades by surgeons for surgical cutting and cautery and had a long history of safety and efficacy. Animal studies using RF energy were first described in 1987.⁹ Intracardiac RF energy produces controlled lesions at the catheter tip over a period of 40 to 120 seconds. The improved safety and efficacy of RF catheter-based ablation procedures quickly replaced DC shock ablation techniques.

	BIOPHYSICS OF ABLATION

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Ablation using RF as an energy source involves the delivery of sinusoidal alternating current between the catheter tip at the endocardial surface and a large grounding pad on the skin. The current has a frequency of 350 to 700 kHz. The principal method of tissue injury with RF delivery is thermal. As the RF energy passes through the tissue at the distal electrode of the ablation catheter, resistive heating produces coagulation necrosis. The lesions produced are well demarcated and are 5 to 6 mm wide by 2 to 3 mm deep when a standard catheter tip is used. To achieve irreversible tissue injury, a tissue temperature of about 55° to 58°C is required.¹⁰ At temperatures above 100°C, plasma reaches the boiling point and coagulates on the catheter tip. Coagulum and desiccated tissue act as an insulating barrier to energy delivery, resulting in a rise in impedance and the prevention of tissue heating. If subendocardial tissue temperature exceeds 100°C, steam may be formed within the tissue, resulting in a rapid expansion and crater formation and an audible "pop" during ablation. Much like DC shocks, such steam "pops" can cause unpredictable injury (e.g., to surrounding normal conduction tissue) as well as rupture of thin-walled structures. Thus it is important to regulate the temperature of the catheter-tissue interface by regulating the energy delivered. Contemporary RF ablation catheters have a thermistor or thermocouple that allows for automatic adjustment of the temperature at the electrode tip–tissue interface through adjustment of power. This allows the maximal energy delivery without the buildup of excessive temperature that results in coagulum and increases in impedance.

A limitation in lesion size places some epicardial foci and arrhythmia circuits out of reach of endocardial ablations. One method to increase lesion size and depth uses the principle of limiting coagulum size by increasing the electrode-tissue interface by increasing tip size. In vitro studies have shown that 8-mm catheter tips produced lesions that are twice as deep and four times larger than lesions produced by standard 4-mm tips.¹¹ A limitation of larger catheter tips is that the larger surface area makes it difficult to regulate power delivery and achieve even temperatures. High current densities develop at the edges of the electrode resulting in higher temperatures and coagulum formation. The larger catheter tips have been shown clinically to significantly reduce procedural and fluoroscopy time for some types of ablation.¹²

Cooling the ablation catheter tip with saline irrigation, either through the catheter or external to the catheter, can also prevent coagulum formation at the tissue interface. This prevents a rise in impedance and allows for more energy delivery deep into the tissue, resulting in deeper and larger lesions.¹³ Irrigated RF catheters bathe the catheter tip internally using recirculating saline (Chilli II, Boston-Scientific, Natick, Mass) or externally through a porous electrode tip (Navistar Thermocool, Biosense-Webster, Inc., Diamond Bar, Calif). These catheters continue to utilize RF as an energy source; however, maximization of power delivery has demonstrated deeper lesions with a greater volume than with standard RF.¹⁴

Since the effects of RF ablation are usually irreversible, some ablations, such as for AVNRT, carry a 1% risk of complete heart block. Because of this concern, alternative energy sources have been developed that allow for reversible tissue injury prior to placement of permanent lesions.

One such catheter system (Freezor MAX, CryoCath, Montreal, Quebec, Canada) relies on gradual cooling of tissue to allow for an estimation of injury effect, and can be followed up by a more permanent cryoablation. Hypothermia has been the preferred method of delivering linear lesions in surgical ablation. This technique utilizes pressurized nitrogen or nitrogen oxide flow through a catheter tip nozzle. As the gas expands beyond the obstruction, there is a temperature drop to as much as –90°C. The advantage to the system rests entirely in its ability to deliver both transient and permanent injury to the tissue. The "cooling" phase (CryoMapping) allows one to assess not only the impact on pathologic tissue (e.g., anteroseptal accessory pathways, the slow limb of a dual AV node), but also to assess the impact of potential lesion placement on surrounding normal conduction tissue.¹⁵ If the CryoMapping phase yields desirable results, then the temperature is lowered even further to a "freezing" stage. Of interest is that during the "cooling" phase, an ice ball actually forms on the tip of the catheter and becomes mildly adherent to the tissue. This enhances stability of the catheter despite cardiac motion. The ability to deliver reversible injury and catheter stabilization has made CryoCath increasingly popular in those cases in which the pathologic lesion is in close proximity to the AV node and in younger patients in whom a pacemaker would be less than desirable.¹⁶

A second potential disadvantage to RF as an energy source is the risk of extracardiac tissue injury. Although constantly evolving, the inclusion of pulmonary vein (PV) isolation for treatment of atrial fibrillation is increasingly common.¹⁷ There were early reports of PV stenosis following PV ostial RF ablation and concerns about atrioesophageal fistula following RF ablation in the left atrium.^18,19 Interestingly, the rate of intraoperative atrioesophageal perforation was as high as 1.3% in one open-chest series of patients undergoing linear lesions between PV ostia, to include the posterior wall overlaying the esophagus.^20,21 This has led to less anatomic, more functional, approaches in some centers, with the intent of avoiding extracardiac structures placed at risk by older techniques.^22,23

The complexity of a nonanatomic approach to atrial fibrillation ablation has left many in search of alternatives allowing for PV isolation without risk of damage to extracardiac structures. One such approach may be through the use of energy-delivering balloons. Previous work with RF in delivery of linear ablations was limited by the exponential increase in the power supply necessary with increasing electrode length. However, the placement of a cryothermy balloon in a pulmonary vein ostium has been shown to cause a significant transmural lesion, without extracardiac injury.²⁴ However, the means by which extracardiac tissue is left uninjured is also a minor setback for this technology. The placement of a lesion is only in those areas with direct contact with the energy source. Since the target is unlikely to be the perfect circular shape built into a balloon, any flow around the balloon will be an area in which there will be no injury, and therefore acts as a potential source for continued atrial-PV electrical connectivity. Recent European approval and ongoing clinical trials in the United States of an endocardial deflectable catheter-based high-intensity focused ultrasound balloon (ProRhythm, Ronkonkoma, NY) may allow for the placement of transmural linear lesions without the need for direct tissue contact, and animal trials into the use of laser balloon therapy are ongoing.²⁵

	ELECTROPHYSIOLOGY STUDY PROCEDURAL PROTOCOL

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Catheter ablation of tachyarrhythmias is typically an elective procedure with the patient presenting on an outpatient basis. As with any invasive procedure, patients need to be thoroughly evaluated and informed of the risks, benefits, and alternatives regarding the specific planned procedure. Occasionally, electrophysiology procedures are performed on an emergency basis in patients with recurrent or incessant hemodynamically unstable arrhythmias (e.g., ventricular tachycardia or atrial fibrillation with a rapidly conducting accessory bypass tract) that are refractory to drugs or overdrive suppression through a temporary wire.

Electrocardiographic (ECG) recording of the clinical tachyarrhythmia is crucial to planning the procedure. In the absence of hemodynamic instability, every attempt should be made to obtain an ECG prior to pharmacologic arrhythmia suppression. A patient may present to a physician’s office or to an emergency department with the tachyarrhythmia, allowing the recording of a 12-lead ECG. A loop recorder or 24-hour Holter monitor is sometimes helpful to record symptomatic tachyarrhythmias.²⁶ The recording of onset and termination of the tachyarrhythmia, either spontaneously, with vagal maneuvers, or with drugs, is also very helpful in determining the mechanism of the tachycardia.^27–29

Additional studies to be considered when evaluating the patient with a known or suspected arrhythmia include an echocardiogram to identify the presence of structural heart disease; a graded exercise test to determine catecholamine sensitivity with possible imaging to assess for ischemic burden; and right heart and left heart catheterization and coronary angiography to assess for stability of known disease, or to further seek etiology of a new arrhythmia. Because a diagnostic study can invoke hemodynamically unstable arrhythmias, it is important to know beforehand if there is myocardium at risk for either demand-related ischemia or for low-flow conditions.

All antiarrhythmic medications are usually discontinued at least four half-lives prior to the procedure to allow for induction of tachyarrhythmias. In most cases, AV nodal– blocking medications (commonly beta blockers and nondihydropyridine calcium channel blockers like diltiazem and verapamil) should also be stopped when the AV node may be involved in the re-entrant circuit. Anticoagulation medications should also be stopped, and depending on the indication, the patient may be bridged for the procedure with subcutaneous low molecular weight heparin or admitted to the hospital for intravenous heparin. Because of the need for systemic anticoagulation for ablative procedures that require left heart access, premenopausal women should avoid scheduling procedures that conflict with the first day of menses. Routine complete blood count, electrolyte status, and coagulation profile should be obtained before undergoing the elective procedure. Additional laboratory tests that are sometimes useful are thyroid function tests in patients with a history suggestive of hyperthyroid state, and a pregnancy test in women of childbearing age.

Patients should present on the day of the procedure in a fasting state in preparation for intravenous conscious sedation. Drugs typically used include short-acting benzodiazepines and narcotics in combination (e.g., midazolam and fentanyl). Because sedation may suppress arrhythmias, or alter the conduction properties of the heart, administration of these agents should be at the discretion of the electrophysiologist. Although general anesthesia is rarely required, it may be used in those undergoing prolonged procedures or in high-risk unstable patients.

Patient Monitoring

Continuous monitoring is performed using surface ECG, noninvasive or invasive blood pressure monitoring, continuous pulse oximetry, and capnography. An external defibrillator is available and attached to the patient with "hands-free" patches throughout the procedure. Intubation and resuscitation supplies should be readily available. Electrophysiologic procedures are typically divided into diagnostic and ablative phases. The diagnostic phase involves obtaining venous access, passage of multiple catheters into the heart to record intracardiac electrograms, and induction and mapping of tachyarrhythmias. Only after mechanistic determination of a tachyarrhythmia is ablation considered.

Diagnostic Electrophysiology Study

Diagnostic localization of tachyarrhythmias involves positioning catheters in strategic locations within the heart to obtain intracardiac recordings from all four chambers of the heart as well as from the His bundle. Venous access is typically obtained in the bilateral groins via the right and left femoral veins. Catheters of 4F to 6F in size are passed into the right atrium and right ventricle as well as positioned just across the tricuspid valve to obtain His bundle recordings under fluoroscopic guidance. To obtain recordings of the left atrium and ventricle, a catheter is guided into the coronary sinus, which passes posteriorly in the AV groove and drains into the right atrium. Because of the angle of the entrance into the coronary sinus, cannulation is easier via the superior vena cava and thus previously venous access has been obtained from the right internal jugular, left subclavian, or left antecubital vein. However, steerable catheters allow for reliable access from the inferior approach and are now being used more frequently (Fig. 58-1).

View larger version (128K): [in this window] [in a new window]   Figure 58-1 Radiograph in the right anterior oblique projection showing catheters positioned for a standard diagnostic electrophysiology procedure. Three nonsteerable diagnostic catheters are introduced from the inferior vena cava into the right heart. Two 4F catheters with four electrodes are positioned in the region of the right atrial appendage (RA) and right ventricular apex (RV apex). A 5F catheter with six electrodes is positioned across the tricuspid annulus to obtain a His bundle recording (His). A nonsteerable 6F catheter is introduced via the right internal jugular vein into the coronary sinus (CS) to obtain left atrial and ventricular recordings. Finally, a deflatable 7F ablation catheter is positioned in the region of the low right atrium.

Direct recordings of the left heart are sometimes necessary and accomplished either by transseptal cannulation via the intra-atrial septum from the right atrium, or via a retrograde approach from the femoral artery and across the aortic valve. Systemic anticoagulation with heparin is maintained during catheter manipulation in the left heart because of the risk of thromboembolic events. Animal models have determined that mural thrombus is evident in up to 50% of cases immediately following RF ablation.^9,30 The Multicentre European Radiofrequency Survey conducted from 1987 until 1992 revealed that 84% of institutions used unfractionated heparin during the procedure, and 56% used either postprocedural heparin for a mean of 3.4 ± 2.8 days, or warfarin for a mean of 29 ± 11 days following ablation.³¹ In addition to the risk of mural thrombus at the site of ablation, there is mounting evidence of a systemic prothrombotic condition following RF ablation.^32,33

Once diagnostic catheters are positioned, programmed electrical stimulation is performed to induce and study the tachyarrhythmia. Sometimes modulation of the autonomic nervous system is required to induce tachyarrhythmias with the infusion of atropine or isoproterenol.³⁴ As will be described later, there are specific pacing maneuvers to initiate and evaluate the mechanism of a variety of tachyarrhythmias. Once an optimal site for ablation is determined, steerable ablation catheters are positioned at the target site. These catheters come with a variety of curvatures. Specifically shaped long vascular sheaths may also be used to direct catheters. Once RF energy is delivered to the target site, re-induction of the tachycardia is attempted.

At the end of the procedure, all catheters and sheaths are removed and manual pressure held to achieve hemostasis. If the patient was heparinized for the procedure, sheath removal is delayed until anticoagulation reverses. The patient is placed on bedrest for 4 or more hours. During this recovery period, the patient is monitored for hemodynamic stability and recovery from sedation, and to assess for bleeding from puncture sites. The patient may be discharged to home the same day or be observed overnight in the hospital. Routine follow-up studies are not warranted unless required to assess for a complication. As mentioned previously, because of the risk of thromboembolic events, patients are frequently sent home on aspirin, thienopyridines, low molecular weight heparin, warfarin, or a combination of risk-appropriate antithrombotic therapies.

Complications Associated with Electrophysiology Studies

In referring patients for catheter ablation, it is important to weigh the risks and benefits of the procedure for the individual patient. Most tachyarrhythmias, although causing a variety of symptoms, are generally hemodynamically well tolerated and are not life-threatening. Thus an awareness of the potential complications of catheter ablation is necessary prior to referring a patient. Complications can be divided into those involving access, catheter manipulation within the heart, and ablation.

Access-related complications include pain, adverse drug reaction from anesthesia and sedation, infection, thrombophlebitis, and bleeding at the site of access. Complications associated with bleeding include hematoma or arteriovenous fistula formation. Arterial damage or dissection may also result. Systemic or pulmonary thromboembolism can occur, most seriously resulting in transient ischemic attack or stroke.

Complications associated with placement of intracardiac catheters can be more life-threatening. These include trauma of a cardiac chamber or the coronary sinus resulting in myocardial infarction, perforation, hemopericardium, and cardiac tamponade. Programmed electrical stimulation can result in the induction of life-threatening tachyarrhythmias such as ventricular tachycardia or fibrillation. Catheter manipulation can also result in usually transient but sometimes permanent damage to valvular apparatus or to the conduction of the right or left bundle branches due to mechanical trauma.

RF delivery within cardiac structures carries with it its own set of risks as alluded to previously. Inadvertent ablation of the normal conduction system could result in complete heart block requiring permanent pacing. Perforation of a cardiac chamber or vascular structure can also occur with RF delivery. Collateral damage to coronary circulation could result in myocardial infarction, heart failure, or cardiogenic shock. Phrenic nerve paralysis can occur. Ablation near the pulmonary veins within the left atrium can result in venous stenosis and pulmonary hypertension. Finally, new tachyarrhythmias can arise over the next 1 to 2 months due to what is likely a profound inflammatory process at the site of ablation, as well as from the scars induced by RF ablation.

An 8-year prospective study of 3966 procedures found an overall complication rate of 3.1% for ablative and 1.1% for diagnostic procedures. Complications are more likely to occur in elderly patients and those with systemic disease.³⁵ No deaths were reported in this series and other studies have shown very low mortality rates directly attributable to the electrophysiology study. Body dosimetry studies have shown that the lifetime excess risk per 60 minutes of fluoroscopy exposure is 294 per million cases or 0.03% per patient. The risk is higher for obese patients and the lungs are the most susceptible organs.³⁶

	DIAGNOSTIC ELECTROPHYSIOLOGY TECHNIQUES

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A variety of techniques have been developed to elucidate the origin and mechanism of tachyarrhythmia propagation. These techniques are necessary to reveal targets for ablation. They involve pacing in a specific chamber at particular intervals to initiate a tachyarrhythmia, assess its response to pacing maneuvers, or terminate it.³⁷ Thus some of these techniques involve pacing in sinus rhythm while others are performed during the tachyarrhythmia.

Activation Mapping

Activation mapping is a technique of localizing focal tachycardias and accessory pathways. It involves positioning the mapping/ablation catheter during the tachyarrhythmia in such a way that activation at the catheter electrode tip precedes any other intracardiac activation or corresponding surface P wave or QRS. The earliest site of activation during a focal tachycardia must by definition be the source of the tachycardia.^38,39 The use of electroanatomic mapping systems allows for logging of local activation times in a three-dimensional model.⁴⁰ Earliest activation can then be easily relocated for stable re-entrant rhythms.

Accessory pathways can also be mapped using this technique by tracing the tricuspid and mitral annulus with the ablation catheter. The atrial insertion can be localized by determining the earliest site of retrograde atrial activation during AVRT or in sinus rhythm during ventricular pacing. The ventricular insertion can be localized in patients with preexcitation by determining the site of earliest ventricular activation during sinus rhythm.

Pace Mapping

Pace mapping is performed during sinus rhythm after obtaining a 12-lead surface ECG during tachycardia. By pacing at different sites and comparing the resulting paced ECG to the tachycardia ECG, the disparity can be assessed and the catheter can be repositioned until a perfect 12-lead match is obtained.⁴¹ These sites are then the targets for ablation. This technique is typically used for focal ventricular tachycardias, especially those of right ventricular outflow origin.⁴²

Mapping of local electrogram potentials requires recording an intracardiac signal from the structure targeted for ablation. For instance, to achieve complete heart block, the His bundle is the target and the ablation catheter is positioned such that the distal tip is recording a His bundle potential. Similarly for bundle-branch re-entry, the right bundle potential is used to target the right bundle to achieve right bundle-branch block. Sometimes an accessory pathway potential can be recorded and used to localize a target for ablation.⁴³

Anatomic Mapping

Anatomic mapping is yet another way to localize potential targets for ablation by using fluoroscopy to localize anatomic landmarks for ablation. Catheters placed through the inferior vena cava into the coronary sinus and across the tricuspid valve delineate these structures. In typical atrial flutter that is dependent on the cavotricuspid isthmus, anatomic landmarks are used for the delivery of a line of lesions to prevent conduction across this isthmus. Bidirectional conduction block across this isthmus terminates flutter and prevents its reinitiation.⁴⁴

Entrainment Mapping

Entrainment mapping is a technique of localizing re-entrant circuits for ablation. It involves positioning the catheter in a region thought to be involved in a re-entrant tachycardia. This is confirmed by pacing during the tachycardia slightly faster than the tachycardia rate. If the pacing site is within the circuit, then activation should proceed orthodromically, or in the same direction as the tachycardia, around the circuit resulting in an identical activation pattern. The resultant QRS or P wave should match that of the tachycardia. At the termination of the pacing the activation wavefront proceeds around the circuit. Therefore, if pacing was in the circuit, the first beat should be close to the cycle length of the tachycardia.

In clinical situations a combination of these mapping techniques is used to localize an arrhythmia for ablation. Usually an anatomic approach is used to find the general region and then more precise mapping is used to specifically localize the focal arrhythmia or re-entrant circuit.

Advanced Mapping Techniques

The success of ablation is very much dependent on localization of arrhythmogenic foci and circuits. The previously mentioned mapping techniques are useful for arrhythmias that originate from specific anatomic locations or have characteristic endocardial electrograms. Conventional fluoroscopy and the use of a single roving mapping catheter have limited success in ablation of complex arrhythmias that may originate from sites without characteristic fluoroscopic landmarks or have variable electrograms as recorded from the catheter tip. Advanced mapping techniques have been developed as adjuncts to conventional methods to improve the efficacy of catheter ablation for arrhythmias that are transient, focal, or hemodynamically unstable and thus require rapid mapping.

The multielectrode "basket" catheter (Constellation, Boston-Scientific, Natick, Mass) is a system with eight splines each with eight electrodes. The splines expand within a cardiac chamber to provide recordings from all 64 electrodes simultaneously to enable reconstruction of activation maps such that a single ectopic beat can be mapped online rapidly. Although these catheters are still fluoroscopically guided, multiple data points are acquired simultaneously, limiting procedure times, especially in patients with hemodynamically unstable arrhythmias.⁴⁵ Low spatial resolution limits this technology to larger macro re-entrant arrhythmias.

An electroanatomic mapping system (CARTO, Biosense, Diamond Bar, Calif) uses a magnetic field to localize the mapping catheter tip in three-dimensional space. Three coils in a locator pad located beneath the patient’s chest generate ultra-low-intensity magnetic fields in the form of a sphere that decays in strength. A sensor in the catheter tip measures the relative strength and hence the distance from each of the coils. This allows for the recording of the spatial and temporal location of the catheter. Electrodes at the catheter tip record local electrograms, and this information is displayed on screen as a three-dimensional map of the local activation times relative to a reference catheter in a color-coded fashion. Data from multiple single mapping points acquired during tachycardia can be reconstructed to show animated sequences of arrhythmia propagation. Voltage maps can be obtained to delineate regions of scar and diseased myocardium.⁴⁶

A similar endocardial mapping system (EnSite NavX, St. Jude Medical, St. Paul, Minn) consists of a catheter with a woven braid of 64 insulated 0.003-mm-diameter wires with 0.025-mm breaks in the insulation that serve as electrodes. A locator signal is generated between the array and a standard mapping catheter to permit nonfluoroscopic localization of the catheter to regions of interest. The position of the roving catheter is acquired over time to construct a three-dimensional map of the endocardial surface. The woven braid also acts to obtain and then reconstruct a virtual electrogram of the chamber of interest. Over 3360 virtual electrograms are simultaneously acquired by this system, allowing high-density maps to be acquired from a single beat. Thus this system is very useful for mapping in unstable or transient, nonsustained arrhythmias.⁴⁷

The largest advantages to these mapping systems are the increase in patient and operator safety through the reduction of fluoroscopy while preserving precise localization of the catheter tip. In addition, recordings of catheter position allow for the repositioning of the catheter to previously mapped sites of interest.

Intracardiac echocardiography (ICE) has extended the principles of intravascular ultrasound (IVUS) for electrophysiologic use.⁴⁸ In contrast to IVUS catheters, ICE catheters use lower-frequency (5.5 to 10 MHz) transducers to extend the imaging range. Newer ICE catheters are steerable and have Doppler capability (Acuson, Mountain View, Calif), allowing for hemodynamic evaluation of intracardiac structures. For electrophysiologic use, ICE catheters are useful for visualization of endocardial structures such as the fossa ovalis and for guiding transseptal catheterization.^49–51 As the recognition of the importance of anatomy in the genesis of arrhythmias has grown, so has the importance of imaging. ICE catheters allow the accurate targeting of anatomic sites such as the crista terminalis and pulmonary vein ostia.⁵² They are useful for imaging diagnostic and ablation catheter positions and visualization of tissue contact for optimal ablation. Through visualization of pericardial effusions, rapid diagnosis of perforation and other complications is feasible.

	CLINICAL APPLICATIONS

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Using the techniques described above, a variety of tachyarrhythmias can be targeted for percutaneous catheter-based ablation, including both atrial and ventricular arrhythmias that are either focal or that utilize re-entrant circuits.

Atrioventricular Nodal Re-entrant Tachycardia

The most common SVT is AVNRT.⁵³ Of patients with SVT, AVNRT represents up to 60% of cases that present to tertiary centers for electrophysiologic studies. This tachycardia can present at any age, although most patients who present for medical attention are in their 40s and the majority are female.^54,55 Advances in RF catheter ablation of this tachycardia has made it a first-line therapy for those symptomatic patients not wishing to take medications.⁵⁶

This tachycardia has a re-entrant mechanism utilizing two pathways within the AV nodal tissue. The pathways are known as the "slow pathway" and "fast pathway" based on their relative conduction velocities. The anatomic location of these pathways is variable but generally located within the triangle of Koch. The Koch triangle is bounded by the tricuspid annulus and the tendon of Todaro with the coronary sinus at the base. The apex of the triangle is the His bundle at the membranous septum where it passes through the central fibrous body. The anterior third of the triangle contains the compact AV node and the fast pathway, and the middle and posterior portion, near the coronary sinus os, contains the slow pathway (Fig. 58-2).⁵⁷

View larger version (44K): [in this window] [in a new window]   Figure 58-2 (A) Diagrammatic representation of typical atrioventricular nodal re-entrant tachycardia. Surface ECG shows narrow complex tachycardia with no clear P waves. The re-entrant circuit (gray arrows) consists of the posterior slow pathway region acting as the antegrade limb, and the anterior fast pathway region acting as the retrograde limb. The slow pathway target site is located between the coronary sinus os (CS) and the tricuspid valve annulus (TV). IVC = inferior vena cava; RA = right atrium; RV = right ventricle; SVC = superior vena cava. (B) Surface ECG showing precordial leads in AVNRT. This demonstrates that the retrograde P waves are barely discernible in some leads. In V1, it forms a pseudo r' wave (arrow). P waves are also visible in the terminal portions of QRS complexes in V2 and V3 but not in the lateral leads.

In less than 10% of cases, the circuit is reversed. In atypical AVNRT, antegrade conduction occurs over the fast pathway and retrograde conduction occurs over the slow pathway. Thus the ECG of this tachycardia shows inverted P waves in the inferior leads denoting retrograde activation of the atria with short PR segment due to rapid antegrade conduction.⁵⁹

In the early days of catheter ablation therapy, highly symptomatic patients who had failed drug therapy underwent AV junctional ablation utilizing DC shocks with the insertion of a permanent pacemaker. While this greatly improved quality of life, it made patients pacemakerdependent. Initial attempts to selectively eliminate AVNRT while leaving antegrade AV nodal conduction intact were performed with DC energy.⁶⁰ While selective pathway DC shocks were being studied, RF as an energy source was developed and quickly replaced DC shocks as a mode of therapy.

Early procedures utilizing RF energy targeted the fast pathway. While successful in up to 90% of patients, there was still a 5 to 10% incidence of inadvertent complete heart block.⁶¹ In addition, ablation of the fast pathway left the patients with prolonged AV conduction (a long PR interval). In some, this led to symptomatic atrial contraction during ventricular contraction (pseudopacemaker syndrome), especially during sinus tachycardia when they were unable to shorten the AV conduction interval. Subsequently it was determined that the slow pathway could instead be reliably targeted in the posterior triangle of Koch.⁶²

Slow pathway ablation has a high degree of success with a recurrence rate in the range of 2 to 7%, with the complication of complete AV block occurring about 1% (range 0 to 3%) of the time.⁶³ The North American Society of Pacing and Electrophysiology (NASPE) self-reported surveys on 4249 patients who underwent slow pathway ablations had success rates of >96% and complication rates of <1%.^64,65

Pilot trials have demonstrated a similar immediate success rate but a higher recurrence rate in those treated with cryoablation as compared with RF ablation in patients with AVNRT.⁶⁶ This particular pilot trial was underpowered to show increased safety profile with cryoablation, but the European Multicenter Study RF Versus Cryo in AVNRT with 500 anticipated enrollees with 6-month follow-up may be able to provide us with a more definitive answer as to its superiority.

Atrioventricular Re-entrant Tachycardia

The next most common type of SVT is AVRT.⁵³ About 30% of SVTs are due to AVRT. This is a re-entrant tachycardia utilizing the AV node and an accessory pathway (AP). These APs are remnants of conductive tissue from embryonic development that span the normally electrically inert tricuspid and mitral valve annulus and provide an independent path of conduction outside the AV node between the atria and the ventricles. The most common form of AVRT is part of the Wolff-Parkinson-White (WPW) syndrome of ventricular pre(mature)-excitation and symptomatic arrhythmias. The most common APs connect the atrium to the ventricle. Other APs may connect the atria or AV node to the His-Purkinje system. In sinus rhythm, antegrade conduction over the AP results in pre-excitation of the ventricles through conduction by other than the AV node, and is manifested by a short PR segment and slurring of the onset of the QRS, the delta wave. Absence of these findings does not exclude an AP, as the degree of pre-excitation may vary or conduction may only occur in the retrograde direction (~30% of APs).

Patients with WPW typically present with palpitations due to rapid heart rate. This may be the result of AVRT or due to any SVT with resulting rapid AV conduction via the AP. Associated symptoms may be mild such as palpitations and shortness of breath, or as severe as syncope and sudden death.⁶⁷ Sudden death may be due to ventricular fibrillation resulting from the extremely rapid ventricular activation over the AP during atrial fibrillation in some patients.

Indications for ablation of APs include patients with symptomatic AVRT or those with atrial tachyarrhythmias with rapid ventricular conduction who fail or do not wish to undergo medical therapy. Relative indications for ablations include asymptomatic patients in high-risk professions, those with family history of sudden death, or those mentally distraught over their condition.⁵³

In the typical or orthodromic form of AVRT, antegrade conduction from the atrium to the ventricle occurs over the AV node and retrograde conduction occurs over the AP. In this form of AVRT, the P wave in the tachycardia closely follows the preceding QRS complex with a long PR segment (Fig. 58-3). In the rare antidromic form of AVRT, antegrade conduction occurs over the AP with retrograde conduction over the AV node. This results in eccentric depolarization of the ventricle, producing a wide complex tachycardia with retrograde P waves that can be easily mistaken for ventricular tachycardia with one-to-one ventriculoatrial conduction.

View larger version (26K): [in this window] [in a new window]   Figure 58-3 (A) Diagrammatic representation of atrioventricular re-entrant tachycardia. This macro re-entrant circuit (gray arrows) utilizes the AV node and an accessory pathway (AP), in this case a right lateral pathway. In orthodromic AVRT, antegrade conduction occurs over the AV node and retrograde conduction occurs over the AP. Because of the conduction delay from the His-Purkinje system through the ventricular myocardium to reach the AP, retrograde P waves are discernible after the QRS complexes (arrow). In antidromic AVRT, the re-entrant circuit is reversed and surface ECG shows P waves that closely precede the QRS complexes. CS = coronary sinus; IVC = inferior vena cava; RA = right atrium; RV = right ventricle; SVC = superior vena cava; TV = tricuspid valve. (B) Intracardiac recording of atrioventricular re-entrant tachycardia with termination of eccentric conduction over the accessory pathway during RF ablation. The tracing at 50-mm-per-second speed shows four surface leads (VI, II, I, and a VF) and intracardiac recording from catheters:ablation (ABL); His distal, mid, and proximal; as well as right ventricular apex (RVA). The first three beats of the tracing show evidence of eccentric conduction over an accessory pathway: short PR segment and delta wave. With onset of RF energy (RF On) from the ablation catheter positioned in the region of shortest AV conduction, conduction becomes normal within two beats, with normalization of the PR segment and loss of the delta wave.

The first catheter ablation procedures were performed with DC energy in patients with posteroseptal accessory pathways.⁶⁹ With the development of RF energy for ablation, APs in all locations could be treated.

Ablation of a right-sided AP is performed by accessing the right heart via the femoral vein or occasionally via the antecubital, subclavian, or internal jugular veins. Left-sided APs are ablated via a transseptal approach or via a retrograde approach from the femoral artery. The initial procedures to ablate leftsided accessory pathways were via a retrograde aortic approach. While successful in more than 95% of patients, there was a small risk of aortic valve perforation or dissection of a coronary artery.⁷⁰ Most centers now perform ablation of left-sided accessory pathways via a transseptal approach.

Rarely, left-sided APs can be ablated from within the coronary sinus if they are on the epicardial surface, which is unusual. Due to the more sloping architecture of the tricuspid annulus, it is more difficult to achieve a stable catheter position for right-sided pathways. While the use of long curved vascular sheaths may be helpful, the success rates for right free wall APs may be lower than for other locations.

The major challenge that remains is the ablation of APs near the normal conduction system and those that are epicardial in location. Ablation of pathways that are anteroseptal and midseptal in location carries a high risk of causing complete heart block. It is hoped that newer ablative energy sources such as cryoablation, although found to be effective, may offer a safer alternative.¹⁵ Recently, elimination of epicardial accessory pathways via a pericardial approach has been attempted.⁷¹

Unusual accessory pathways include atriofascicular (Mahaim) pathways. These show decremental conduction and the atrial insertion is typically located in the right free wall. These can often be successfully ablated via an endocardial catheter approach.⁷² The 1998 NASPE prospective catheter ablation registry reported on 654 patients with a 94% success rate.⁶⁵ Success rates are lower (in the range of 84 to 88%) for septal and right free wall pathways. Other pathways have success rates in the range of 90 to 95%.^43,73,74

Complications associated with ablation of accessory pathways include those associated with any ablation procedure. A specific complication associated with transseptal catheterization may be persistent intra-atrial shunt. Although acute shunt may be present in up to 50% of patients, longterm sequelae and persistence beyond 3 weeks are rare.^75,76 Mortality rates are less than 1% and nonfatal complications are about 4%.⁶⁵

Atrial Tachycardia

Atrial tachycardias depend wholly on atrial tissue for initiation and maintenance of the tachycardia. Ectopic atrial tachycardia, sinoatrial nodal re-entrant tachycardia, inappropriate sinus tachycardia, atrial flutter, and atrial fibrillation can all be considered atrial tachycardias. Focal atrial tachycardias, a less common type of SVT, form about 10% of all SVTs referred for electrophysiologic studies.⁵³ Multifocal atrial tachycardia is due to multiple foci of abnormal automaticity or triggered activity and is not amenable to catheter ablation.⁷⁷

Patients with atrial tachycardia present with palpitations and associated symptoms may include chest discomfort, shortness of breath, and dizziness. Symptoms most often are benign and not life-threatening. These arrhythmias are more common in patients with structural heart disease. Indications for ablation include failure or intolerance of medical therapy. Rarely, incessant tachycardias can lead to cardiomyopathy. With ablation and control of heart rate, myocardial dysfunction can be reversed, although there may be a delayed risk of sudden death that necessitates use of a defibrillator.^78–80

Surface ECG features of atrial tachycardia include abnormal P-wave morphology or axes that are close to the following QRS complexes. Mapping and ablation of atrial tachycardias can be more difficult, as they can originate from anywhere within the right or left atrium. But there are specific anatomic regions that have a high incidence of foci and serve as primary targets. They include the crista terminalis, atrial appendages, valve annulus, and pulmonary ostia.⁸¹ Intracardiac echocardiography has been used to localize these anatomic regions of interest.^82,83 Mapping can be facilitated by techniques previously mentioned and reviewed here.

Activation mapping by means of a roving mapping catheter is used to localize a region of earliest activation. Successful targets for ablation usually have intracardiac activation 30 ms or more prior to any surface P wave. Sometimes two catheters are used to triangulate a target by moving one catheter at a time toward sites of earlier activation. A caveat to this mapping technique is that an early right atrial activation site may in fact originate from the left atrium, as the posterior septum of the right atrium overlies the left atrium.⁸⁴ Other techniques that have aided focal ablation are the use of noncontact and electroanatomic mapping systems.^85,86 These newer mapping catheters have increased the success rate of ablation of focal tachycardias, especially in patients with altered atrial anatomy such as those with congenital anomalies and post–atrial surgery.^87–89

Inappropriate sinus tachycardia and sinoatrial nodal re-entry tachycardias occur more infrequently and experience with catheter ablation of these tachycardias is more limited. Inappropriate sinus tachycardia is also difficult to ablate due to the variability and diffuse location of sinoatrial tissue.⁹⁰ Medical therapy is the preferred method of therapy and catheter ablation is attempted only after drug failure. Catheter ablation may result in complete loss of sinoatrial node function and resulting junctional rhythm, requiring insertion of a pacemaker. Even if the resting heart rate is reduced with nodal modification, symptoms may continue with episodes of tachycardia. Sinoatrial nodal re-entrant tachycardia is targeted for ablation using techniques similar to those used for other atrial tachycardias.

Success with ablation of atrial tachycardia is quite variable depending on the location of the arrhythmogenic foci and the experience of the operator. The 1998 NASPE survey showed a success rate of 80% for right-sided versus 72% for left-sided versus 52% for septal foci in 216 cases of atrial tachycardia ablation.⁶⁵ Another large review examined the frequency of arrhythmias as a predictor of success. In 105 patients, the overall initial success rate was 77%, and 10% had recurrence over a 33-month follow-up period. There was an 88% success rate for the paroxysmal form versus 71% for permanent and 41% for repetitive forms of atrial tachycardia.⁹¹

Atrial Flutter

Atrial flutter is a type of atrial tachycardia that utilizes a macro re-entrant circuit contained within the atria. A variety of natural and surgical barriers to conduction can create a re-entrant circuit within the atria. Typical atrial flutter is due to a right atrial circuit, bound anteriorly by the tricuspid valve (TV) annulus. Posteriorly, it is confined by the superior vena cava, crista terminalis, inferior vena cava (IVC), eustachian ridge, and coronary sinus (CS)⁹² (Fig. 58-4).

View larger version (28K): [in this window] [in a new window]   Figure 58-4 Diagrammatic representation of typical or counter-clockwise right atrial flutter. Surface ECG shows large inverted P waves in the inferior leads. Lead III above shows 2:1 AV conduction with "sawtooth" flutter waves. The re-entrant circuit (gray arrows) is confined to the right atrium by the tricuspid valve annulus (TV) and barriers to conduction within the right atrium. These include the superior vena cava (SVC), crista terminalis (CT), inferior vena cava (IVC), eustachian ridge (ER), and coronary sinus (CS). The isthmus between the IVC and TV is the preferred target for ablation.

A macro re-entrant circuit can be cured by lesions that transect the circuit between two anatomic barriers. In the case of isthmus-dependent flutter, the target for ablation is the isthmus between the IVC and TV. This is a relatively narrow target and easily reachable by ablation catheters introduced from the IVC. Success rates for ablation of this form of atrial flutter are high. Initial success rates are up to 90% with recurrence rates of 10 to 15%.^94,95 Given these results, ablation has become the first line of therapy for recurrent isthmus-dependent atrial flutter.⁵³ In addition, studies have shown that the incidence of atrial fibrillation is markedly reduced in patients with atrial flutter treated with ablation as compared to medications.⁹⁶

In some patients with atrial fibrillation, treatment with class IC antiarrhythmics or amiodarone results in the development of typical atrial flutter. A hybrid approach using ablation of the IVC-TV isthmus and continued use of the antiarrhythmic medication has been shown to be highly successful in reducing the incidence of atrial fibrillation.⁹⁷

While the right atrial circuit described above is the most common, a variety of other circuits in the right and left atrium are possible. These are more common in patients with underlying heart disease. Although initially thought not to be amenable to ablative therapy, mapping and ablation of these arrhythmias are now routinely performed. However, the success rate is somewhat lower than that for typical isthmus-dependent atrial flutter. An electroanatomic map of a patient with left atrial flutter can be seen in Fig. 58-5. Ablation in the isthmus between these scars resulted in termination of the flutter.

View larger version (97K): [in this window] [in a new window]   Figure 58-5 An electroanatomic map of a patient with left atrial flutter is shown in the right anterior oblique projection. Two large areas of scar can be seen in gray. Gradation in color shows activation sequence, with lighter being the earliest and darker being late in relation to a reference catheter, in this case positioned in the coronary sinus. The circulating wavefronts describe a figure-eight pattern around these two areas of scar but are confined by the narrow region (isthmus) between them. Ablation in the isthmus resulted in termination of the flutter.

Incisional scars from prior cardiac surgery can be the substrate for re-entrant atrial arrhythmias.^87–89 The most common is an atypical atrial flutter related to a lateral right atrial incision. Mapping demonstrates a circuit circling the incision. Ablation from the end of the incision to either the superior vena cava or more commonly the inferior vena cava is often curative.⁹⁸

It had been thought that there was conduction block between the donor and recipient atria in patients who have undergone heart transplantation. Recent reports have demonstrated re-entrant arrhythmias due to donor-recipient atrial conduction. Mapping the connection between the atria can successfully ablate these arrhythmias.^99–101 Atrial arrhythmias have also been reported in a number of patients who have undergone the surgical Maze procedure for atrial fibrillation. These treatment failures are most often due to re-entrant circuits involving gaps in the Maze lesion or through alternative pathways such as the musculature surrounding the coronary sinus.¹⁰² These arrhythmias can now be successfully mapped and ablated. Mapping systems are useful in improving success of these ablations. The principle of interrupting these circuits by placing lesions to connect conduction barriers remains the same.¹⁰³

Atrial Fibrillation

Atrial fibrillation is another difficult-to-treat atrial tachycardia with variable targets for ablation. Atrial fibrillation is often symptomatic for patients due to irregular and/or rapid ventricular rates. Patients can also be completely asymptomatic and present with stroke or be diagnosed on routine examination. Medical therapy for atrial fibrillation is of limited efficacy and pharmacologic control of atrial fibrillation may be associated with increased mortality in large trials.^104–106 In addition, sustained rapid ventricular rates can lead to a tachycardia-related cardiomyopathy.⁸⁰ When medical therapy aimed at maintaining sinus rhythm or blocking AV nodal conduction to slow ventricular response fails, ablation can be considered.⁵³

In the past, AV nodal or His ablation, with placement of a permanent pacemaker, was considered in patients with difficult-to-control ventricular rates and symptomatic palpitations. The advantages of the approach are the relative ease and speed of the procedure. The downside is that it renders the patient pacemaker-dependent. Success rates of this procedure are nearly 100%.^53,107 Complications of this procedure include the same complications as those seen in other ablation procedures. A unique complication associated with creation of complete heart block is bradycardia-related ventricular tachycardia (torsades de pointes).¹⁰⁸ The incidence of this complication is reduced with high-rate atrial pacing at 80 to 90 bpm for up to a month following ablation. In highly symptomatic patients, this approach to the treatment of atrial fibrillation has been associated with improvement in quality of life and left ventricular function, and with a reduction in hospitalizations.¹⁰⁹ With up to 3 years of follow-up, no long-term sequelae have been noted.¹¹⁰ Patients with congestive heart failure and atrial fibrillation may particularly benefit from this approach, and in some cases restoration of function will return as tachycardia slows; but in many cases it may be more beneficial to proceed directly with implantation of a cardiac resynchronization device.^111,112

Surgical experience with the Maze procedure to create lines of conduction block in the atrium has led the way for catheter-based ablation procedures to treat atrial fibrillation. Studies have attempted to replicate the success of the surgical procedure using a catheter-based approach. Atrial fibrillation consists of multiple re-entrant circuits within the atrium; around the vena cava, pulmonary veins, and appendages; and around areas of functional block.¹¹³ Creation of multiple lines of block between these nonconducting structures may prevent propagation of arrhythmic circuits.

A variety of catheter techniques have been employed including a "point-by-point" approach, a "drag" approach, and a multielectrode approach. Right atrial lesions alone were shown to be ineffective.¹¹⁴ Attempts at left atrial or biatrial lesions have met with limited success due to the prolonged procedure times, high risk of complications, and limited efficacy.^115,116 There is also concern about reduced mechanical function of the atria following extensive ablation. This limits the hemodynamic benefit of the restored sinus rhythm. As understanding of the mechanism of atrial fibrillation has evolved, attempts to block propagation of atrial fibrillatory circuits have been abandoned in favor of attempted ablation of the fibrillatory triggers.

Data suggest that atrial fibrillation may in some cases be triggered by an organized SVT. About 12% of patients with AVNRT or AVRT will develop symptomatic atrial fibrillation in 1 year of follow-up.¹¹⁷ Thus ablation of the initiating trigger arrhythmia may prevent atrial fibrillation. In a series of patients undergoing a left-sided catheter Maze procedure, it was discovered that rapidly firing premature atrial contractions arising from the musculature of the pulmonary veins were triggering atrial fibrillation.¹¹⁸ Ablation of these foci eliminated atrial fibrillation in some patients. This procedure has evolved to empiric electrical isolation of the pulmonary veins. One approach is the complete encircling of the pulmonary veins (i.e., wide area circumferential ablation).¹¹⁹ Another approach is segmental isolation of each vein by mapping the location of the connecting fibers.¹²⁰ The encircling and nonencircling procedures have shown to be equally efficacious in 6-month follow-up. The advantage to the nonencircling method, whereby the focus is on pulmonary vein exit block, is the ability to avoid a posterior wall line. The placement of posterior wall lines is thought to be responsible for the finding of atrioesophageal fistula postoperatively. Electroanatomic mapping and intracardiac echocardiography have been employed to facilitate ablation.¹²¹ Data on the long-term efficacy and complications of this procedure are limited and it is still considered to be a procedure in evolution. In one series of 251 patients, the short-term success over 10.4 months of follow-up was 80%. There was an 85% success rate in those with paroxysmal and 68% success in those with permanent atrial fibrillation. There was a continued need for antiarrhythmic medications in some patients.¹²²

A major complication of ablation within the pulmonary veins was focal pulmonary vein stenosis. In 102 patients undergoing pulmonary vein focal ablation, 39% with right upper vein ablation and 23% with left vein ablation developed focal pulmonary vein stenosis by transesophageal echocardiography 3 days after the procedure.¹²³ In this series, only three patients experienced symptoms of dyspnea on exertion and only one had a mild increase in pulmonary pressure. Although most cases are asymptomatic, severe cases have been reported that progress to pulmonary hypertension and lung transplant. Changes to prevent this complication include limiting ablation to the vein ostia, limiting power, and using ultrasound imaging during ablation. Since its recognition as a possible adverse event, the occurrence postprocedurally should now be considered rare.

In some patients, triggering foci arise from outside the pulmonary veins. Reported sites have included the superior vena cava, ligament of Marshall, crista terminalis, posterior wall of the left atrium, tricuspid/mitral valve annulus, and limbus of the fossa ovalis. Pulmonary vein isolation failures in some cases may be due to the triggers from these alternative sites. In patients with persistent and/or chronic atrial fibrillation, there may be a combination of triggers and substrate responsible. Successful ablation may require elimination of triggers combined with modification of substrate.²² The future of ablation for atrial fibrillation has been driving the future for electrophysiology.

Ventricular Tachycardia

Ablation techniques can also target ventricular tachycardia (VT). Over 90% of life-threatening ventricular arrhythmias originate from myocardium with structural abnormalities. Regions of scarred or aneurysmal myocardium create channels for re-entrant circuits. Initial successes with resection of ventricular arrhythmogenic foci and re-entrant circuits surgically have led to advancements in catheter-based ablation techniques. Beginning with DC ablation, techniques have advanced with the use of RF ablation catheters and electroanatomic mapping systems. Despite these advances, ablation for VT in patients with coronary artery disease has a secondary role. Given the life-threatening potential of VT in patients with structural heart disease, even a single recurrence can be disastrous. Therefore implantable cardiac defibrillators have become the primary therapy. Indications for ablation in this population are failure of antiarrhythmic medication to suppress symptomatic, sustained monomorphic VT, or more often frequent shocks from an implanted defibrillator despite optimal medical therapy.

There are several factors limiting the role of catheter ablation of ischemic VT. The hemodynamic instability of patients with coronary artery disease and depressed left ventricular function limits mapping during the tachycardia. A patient may have multiple re-entrant circuits, not all of which are clinically significant. The VT re-entrant circuits involve scarred myocardium or can be epicardial in locations that may be out of reach for RF energy to penetrate. Finally, short-term success may be eclipsed by development of new VTs with further myocardial injury.

Success of ischemic VT ablation is variable due to the heterogeneity of the population. Reported studies have shown efficacy in the range of 60 to 90% using the criteria of reduced defibrillator shocks and decreased need for antiarrhythmic medications. The recurrence rate is as high as 40%. Recently, success has been reported with an approach employing "substrate mapping." This technique defines the potential arrhythmic substrate using electroanatomic voltage maps. Ablation is targeted to eliminate potential re-entrant circuits. Complications are in the range of 2%, with concern for perforation and cardiac tamponade due to the thin, scarred ventricles that are the substrates for ablation and thromboembolic events in those undergoing extensive ablation.^124–126 One reason for failure of ischemic VT ablation is the deep or epicardial location of circuits. Catheter ablation has been directed at these epicardial circuits using a pericardial approach with some success.¹²⁷

In patients with dilated cardiomyopathy and His-Purkinje system disease, sustained monomorphic VT can occur due to a macro re-entrant circuit using the bundle branches. Patients typically present with syncope or sudden death or can present with palpitations. The most common circuit is down the right bundle branch and up the left bundle branch resulting in a wide complex tachycardia with a left bundle-branch block pattern. Treatment involves ablation of one of the fascicles involved in the re-entrant circuit. The right bundle is most commonly targeted to interrupt the reentrant circuit. Long-term success is good for prevention of recurrent bundle branch re-entry. Due to intrinsic conduction disease, patients may develop heart block. Patients may also develop other VTs due to other structural abnormalities, requiring further ablation, antiarrhythmic therapy, or defibrillator implantation.^128,129

Other cardiac disorders can be associated with VT and are potential candidates for catheter ablation. These include right ventricular dysplasia,¹³⁰ infiltrative disorders (sarcoid), and tumors. As in patients with atrial arrhythmias due to surgical incisions, patients with prior ventricular surgery can develop incision-related VT. This has occurred most often in patients who have undergone repair of congenital abnormalities such as tetralogy of Fallot.

Ventricular tachycardia that presents in patients with no structural heart disease is termed idiopathic and represents up to 10% of all VTs that present to tertiary referral centers. Patients may be asymptomatic or present with palpitations, dizziness, or syncope. Idiopathic VT may be focal or a micro–re-entrant circuit utilizing the Purkinje fibers.

Focal VT can originate from either the right or left ventricle. Right ventricular tachycardia typically originates from the outflow tract, on the septal or free wall sites. It has typical left bundle-branch morphology with leftward, inferior axis. This occurs more often in women than men, and patients typically present in their 30s to 50s. Idiopathic left ventricular tachycardia typically originates from the left posterior fascicle. It has a right bundle-branch morphology with rightward, superior axis, and may be verapamil sensitive. It occurs more often in men. These VTs are localized by activation or pace mapping. Ablation is facilitated by the lack of other cardiac pathology and the presence of only one VT. Success rates for idiopathic VT are in the range of 70 to 90% with recurrence rates in the range of 15%. Complication rates are consistent with those of other ablative procedures.^131,132

Cost-Effectiveness

Several studies have shown the cost-effectiveness of catheter ablation compared to medical therapy and surgical ablation. Catheter ablation has lower procedural costs than surgical ablation and reduces the need for further medical care and emergency department visits in comparison to drug therapy. Studies from both the United States and from Australia have shown both cost savings and improvement in quality of life for those undergoing catheter-based ablation compared to medical management.^133–135

	FUTURE DIRECTIONS

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After the advent of steerable catheters, newer imaging techniques have been the most useful in directing the positioning of catheters to specific areas of interest within the heart. The techniques of nonfluoroscopic mapping discussed above have extended the efficacy of catheter-based ablation. Newer imaging techniques are in development that will continue to push the field of electrophysiology. The Niobe system (Steroetaxis, Inc., St. Louis, Mo) is a magnetic navigation system that uses two externally located magnets to create a steerable field that can be used to affect the magnetically active catheter tip. For advancing and retracting, the unit can be completely controlled remotely through a small motor. The entire system can be controlled from a shielded room by joystick and touch-screen monitors to allow for catheter manipulation through hands-free robotic catheter control. The ability to perform an entire ablative procedure with the primary operator behind a glass in a lead-lined room may be the next step in development of electrophysiologic treatment. One novel technology in development is the use of magnetic resonance imaging that would allow high-resolution three-dimensional mapping of the heart and localization of catheters in three-dimensional space in real time without radiation.¹³⁶ Magnetic resonance imaging would also allow for the visualization of any tissue injury due to attempted ablation in real time.

	CONCLUSION

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The past 35 years have seen the development of intracardiac recording, programmed stimulation, and catheter ablation. The field of interventional electrophysiology is relatively young. Over the past two decades, great advances have been seen in the interventional management of atrial and VTs. Where the surgeons have gone with their scalpels, electrophysiologists have followed with their catheters. Transvenous RF ablation, once the standard of care for the treatment of many arrhythmias, may be phased out in preference of alternative energy sources. These procedures have been proven to be safe and efficacious. Improved treatments for arrhythmias such as atrial fibrillation and VT will come with further understanding of the mechanisms underlying these arrhythmias. Future advances in catheter design, energy delivery, and imaging techniques will continue to advance the field of electrophysiology.