CHAPTER 88: CATHETER-ABLATIVE TECHNIQUES

Major advances have been made in the field of interventional cardiac electrophysiology (EP) over the past three decades. Catheter-based ablation enables minimally invasive therapeutic options in the management of various tachyarrhythmias. Ablation is often guided by EP study and mapping to diagnose the arrhythmia and localize the arrhythmogenic substrate that is to be targeted for ablation. Catheter ablation requires expertise and constitutes a major procedural component, in addition to implantation and management of cardiac electronic devices, within the subspecialty of clinical cardiac EP. In this chapter, we discuss (1) general technical considerations for catheter ablation, (2) specifics related to ablation of different arrhythmias, and (3) potential complications of ablation.

EP study and catheter ablation are performed in the clinical EP laboratory, yet prior review of the specific arrhythmia and medical background, especially cardiac function and anatomy, is fundamental. General anesthesia facilitates patient comfort and safety during the procedure, which typically require 4 to 8 hours without significant patient motion. Certain arrhythmias are driven in part by sympathetic/catecholaminergic axes and can be rendered noninducible by anesthetic agents. This can preclude identification of the culprit rhythm, and inhaled anesthetic gases, benzodiazepines, and opioids are commonly avoided, while propofol or ketamine are less suppressive of arrhythmia.

Accessing the Heart

Most EP studies and ablation procedures require percutaneous access to the heart with multiple catheters. These catheters contain multiple electrodes for recording intracardiac electrical signals and in addition are capable of electrical stimulation of the myocardium (Fig. 88–1), and are inserted through sheaths placed in the femoral, jugular, or subclavian veins. Mapping of the relevant electrophysiologic substrate is performed by repositioning and recording of the constellation of electrical signals throughout the relevant sections of the heart. Current catheter technology typically provides a soft, deflectable 1- to 5-mm mapping electrode that can be maneuvered throughout the atria, ventricles, coronary sinus, pulmonary veins, and above and below the atrioventricular (AV) and semi-lunar valves. Left-sided chambers are accessed with a trans-interatrial septal puncture or femoral arterial access for retroaortic mapping of the left ventricle and/or the sinuses of Valsalva. Epicardial mapping is performed through the coronary vein branches of the coronary sinus, or by direct percutaneous access to the pericardial space from the subxiphoid region (Fig. 88–2).¹

Catheter ablation is commonly performed by a single 3.5- to 8-mm electrode ablation catheter via the application of radiofrequency (RF) electrical energy that results in thermal injury to the adjacent myocardium. The procedural risks depend on the location of the arrhythmia in addition to the relevant anatomic and patient considerations. Thrombus formation on catheters and the ablated regions in the left heart chambers can result in systemic embolization and stroke. To mitigate this risk, it is necessary to use systemic anticoagulation (with intravenous heparin) during the procedure.² The use of anticoagulation, however, increases the risk of bleeding, including pericardial effusion and access-site vascular complications.

Catheter Positioning and Imaging Modalities

Echocardiography, cardiac computed tomography (CT), and magnetic resonance imaging (MRI) allow for the appreciation of the cardiac anatomy prior to the ablation procedure. Catheters are positioned during the ablation procedure using fluoroscopy and guided by intracardiac chamber- and contact-specific electrogram recordings (Figs. 88–1 and 88–3). Fluoroscopy is supplemented by other real-time modalities like computerized mapping systems and intracardiac echocardiography (ICE).

Fluoroscopy

Fluoroscopy provides a two-dimensional projection of the cardiac anatomy and catheter orientation, yet is operator dependent, utilizing either a single plane of view or two orthogonal views to create a three-dimensional location of catheters. The right anterior oblique (RAO) and the left anterior oblique (LAO) are common views (Figs. 88–1, 88–2, and 88–4). The RAO is a profile view of the heart. This differentiates the atrial and the ventricular components; however, there is overlap of the left- and right-sided structures. The LAO view is an end-on view from the apex to base with foreshortening of the long axis of the heart. The LAO projection facilitates differentiating the left from the right side chambers, and the septal from the free wall aspect within a chamber. The location of catheters is inferred by relationship to various anatomic references including the cardiac silhouette, vertebral column, diaphragm, fat stripe along the AV groove, implanted lead, and intracardiac catheters. Iodinated contrast injections are used to characterize the anatomy of coronary arteries and veins, pulmonary veins, left atrial appendage, etc.

Intracardiac Echocardiography

Intracardiac echocardiography (ICE) is performed with an 8- or 10-French ultrasound transducer mounted at the tip of a catheter. Linear phased array and radial ICE catheters are available. ICE supplements fluoroscopy by allowing detailed real-time visualization of structures like the interatrial septum, Eustachian ridge, cardiac valves, papillary muscles, false tendons, coronary artery ostia, as well as confirming catheter position, tissue contact, and ablation lesion formation (Fig. 88–5). ICE allows quick assessment for complications like pericardial effusion or formation of thrombus.

Three-Dimensional Mapping Systems

Mapping systems construct a real-time representation of the mapping catheter position in relation to the chamber being mapped. They thereby facilitate less fluoroscopy use, and provide a mechanism to hallmark certain electrical and anatomical features/characteristics. These electroanatomic mapping tools receive electrophysiologic input from a large number of mapped points tagged with three-dimensional spatial localization to create computerized chamber geometries.^3,4 Activation times (in reference to a fiduciary electrical signal), recorded voltage, and other characteristics of local electrograms are depicted with a color-coded display (Figs. 88–6, 88–7, 88–8, 88–9). Mapping systems can also import and integrate the cardiac chamber anatomy from imaging modalities like cardiac CT, MRI, or ICE (Fig. 88–10).⁵

Magnetic field-based systems measure the field strength at the mapping electrode of the magnetic field emanated from a point source to deduce the relative distance. Distance of the mapping electrode from three point sources of time varying magnetic fields of different frequencies is used to triangulate the location in three-dimensional space (Carto 3 System, Biosense-Webster, Diamond Bar, CA).^3,4,6 Electrical impedance-based systems calculate the spatial location by sensing the voltage gradient of three orthogonal low-voltage electrical currents of specific frequencies applied across the patient’s chest (EnSite NavX, St. Jude Medical, St. Paul, MN).³

Cardiac Mapping

Cardiac mapping is performed with acquisition of data during an arrhythmia and can be achieved in a point-by-point manner or via the use of multielectrode mapping of multiple points simultaneously.⁷ In activation mapping the local activation time (electrogram) can be annotated compared to a fiducial reference point (surface electrocardiogram [ECG] or fixed intracardiac electrode). Compilation of the activation times at all sites within a chamber depicts the spread of the activation wavefront. Focal arrhythmias originate from a point-source and spread in a centrifugal manner, with the earliest site of activation of the myocardium correlating with the successful site of ablation (see Fig. 88–6).⁸ Macroreentrant arrhythmias occur as a result of continuous repetitive activation around a reentry circuit. In this case cardiac activation is occurring at some site throughout the tachycardia cycle without any period of complete quiescence. These reentrant circuits are usually amenable to continuous resetting by pacing at a slightly faster rate than the tachycardia and insights can thereby be gained into mechanism and location of the reentry circuit (entrainment mapping).⁹ Successful treatment of reentry relies on identifying and confirming with entrainment a critical isthmus necessary to maintain the circuit, that is then transected with ablation (see Figs. 88–5 and 88–7).

Substrate mapping can be performed during sinus rhythm or during an arrhythmia (along with activation mapping) to identify diseased myocardial sites. Arrhythmogenic sites may have low-voltage, fractionated or late activated electrograms that are targets for ablation (see Fig. 88–8).¹⁰ Pace mapping is performed by pacing from various sites and comparing the generated surface ECG morphology to the template arrhythmia.⁸ A pace match may identify regions close to the site of origin of a focal arrhythmia or exit site of a reentrant tachycardia.¹¹ Failure to electrically stimulate the tissue in contact depicts presence of electrically inert scar.

Hemodynamic Support

It is optimal to study the mechanism and physiology of the arrhythmia by mapping while the patient is sustained in the pathologic rhythm. Ventricular tachycardias (VTs), especially in patients with structurally diseased hearts, are sometimes hemodynamically unstable despite treatment with vasopressors. This precludes detailed activation and entrainment mapping, with potential failure to appreciate the true arrhythmogenic substrate to ablate successfully. Substrate and pace mapping is important and often may be adequate. However, in some cases, mechanical hemodynamic support (eg, with percutaneous left ventricular assist device) is required to enable mapping and ablation.¹²

Robotic Navigation Systems

Robotic systems are sometimes used to maneuver catheters within the heart. Magnetic navigation systems (Niobe Magnetic Navigation System, Stereotaxis, St. Louis, MO) use large magnets to generate deflecting forces on the magnetized mapping catheter.³ The catheter is robotically manipulated from a computer console. This allows controlled advancement or retractions, and precise rotations in all spatial coordinates. Other systems use regular mechanically deflectable catheters that are controlled with a robotic system that translates operator hand motion to catheter movements (Sensei X Robotic Catheter System, Hansen Medical, Mountain View, CA).

Noninvasive Cardiac Mapping

Major advancements have being made in the bioengineering for activation mapping of cardiac arrhythmias noninvasively to guide ablative therapy. Electric signals are recorded using numerous electrodes (eg, vest with 250 electrodes) from the body surface. High-resolution imaging (noncontrast CT) is used to obtain the atrial or ventricular epicardial geometry and its spatial relationship to the electrodes. Computerized computational analysis then uses this data to reconstruct the regional cardiac electrograms and activation maps (Fig. 88–11).^13,14

Ablation Energy Sources

A variety of techniques have been evaluated for cardiac tissue ablation and include electrical energy in the RF spectrum, cryoenergy, lasers, microwaves, high-intensity focused ultrasound, radiotherapy, and chemical ablation with alcohol, with varying degrees of applicability in current clinical practice.

Radiofrequency Ablation

Initial attempts at catheter ablation of AV node for supraventricular tachycardias (SVTs) were with high-energy direct current (DC) shocks. These were painful and resulted in uncontrolled lesions with risk of life-threatening complications. The advent of RF energy in the ~500 kHz range has permitted more controlled and effective ablation by thermal injury. Reversible loss of myocardial excitability occurs between 43°C and 50°C, and cell death occurs at tissue temperatures above 50°C.¹⁵ The RF current density is highest at the electrode-tissue interface, and a 1- to 2-mm rim of tissue in contact with the electrode is resistively heated (ohmic heating). Passive conductive heating of the surrounding tissue results in a larger lesion (Figs. 88–5 and 88–12).¹⁶

Lesion size is proportional to the RF power delivered to the tissue. However, power delivery is limited by excessive heating at the electrode-tissue interface, which causes formation of coagulum from blood proteins and subsequent char development. Convective cooling of the ablation electrode allows increase in power delivery without coagulum formation. Passive convective cooling increases with regional blood flow, increase in electrode size, and to-and-fro sliding of the electrode with cardiac and respiratory motion. Saline irrigation is often used to actively cool the ablation electrode to allow higher power delivery. In open irrigated catheters, saline is driven through the lumen and cools the electrode as it is forced out of holes at the tip of the catheter. These measures allow increased power delivery without overheating of the ablation electrode; however, excessive heating of the myocardium can lead to tissue vaporization and subsequent injury secondary to steam generation (steam pop).¹⁷

Real-Time Assessment of Ablation

Electrode temperature (measured with a thermistor or thermocouple in the electrode) is used as a surrogate of tissue temperature to ensure adequate heating during ablation. This is, however, not possible with actively cooled catheters. Tissue heating with onset of effective RF delivery results in a 5 to 10 Ω drop in impedance.¹⁸ Loss of excitability of the local myocardium is seen as diminution of the recorded electrogram.¹⁹ Lesion formation is seen in real-time with intracardiac echocardiography,²⁰ and better imaging techniques like MRI thermography have been developed.²¹ Noninducibility of clinical arrhythmia is also an important end point of ablation.

Contact Force

Titrating the applied force with a force-sensing catheter has been shown to be associated with improved ablation efficacy.^22,23,24 Further greater force is counterproductive because it limits convective cooling and power delivery because of catheter wedging in the tissue, and increases risk of steam pop and myocardial perforation.^23,24

Bipolar Radiofrequency Ablation

Conventional RF ablation is delivered between an ablation electrode and a large grounding patch placed on the patient’s skin. In this configuration, ablation of substrate deep within the thick ventricular myocardium may not be possible. Transmural ablation can be performed with bipolar delivery of RF current between electrodes on either side of the target tissue.²² On the other hand, a continuous ablation line can be delivered with phased bipolar RF between respective electrode pairs on a linear or circular multi-electrode ablation array.²⁵

Needle Radiofrequency Ablation

A novel needle-tip electrode is under development for accurate mapping and ablation of deep ventricular myocardial arrhythmogenic substrate. The needle is inserted within the myocardium and delivers RF with saline irrigation allowing for extension of the ablation lesion.²⁶

Cryothermal Ablation

Cryoablation results in well-defined homogenous lesions preserving the ultrastructural integrity of the tissue (see Fig. 88–12). The mechanism of tissue injury includes freezing, thawing, inflammation, and fibrosis.^27,28 Commercially available cryocatheters use nitrous oxide as the refrigerant and achieve temperatures in the –80°C range. Cryoablation lesions take longer to deliver than RF and may be less durable.

Advantages of Cryoablation

Cryoablation results in adhesion of the catheter to the target tissue during the freeze. This is advantageous in regions with poor catheter stability and in vicinity of critical structures like the AV node. Additionally, an initial period of reversible injury during the freeze provides an opportunity to assess safety and efficacy.²⁷ Cryoablation has a lower risk of thromboembolism, cardiac perforation, and coronary arterial injury compared to RF.^27,29 A cryoballoon-based ablation at the pulmonary vein ostium can electrically isolate the entire vein with a single freeze, and has been shown to be equivalent in terms of efficacy and safety to RF ablation for paroxysmal atrial fibrillation (AF).^27,30

Alcohol Ablation

Chemical ablation of the myocardium is achieved by selective injection of ethanol or phenol in a coronary vessel that is proximally occluded with a balloon. Alcohol septal ablation via a ventricular-septal perforator artery is used to alleviate outflow obstruction in patients with hypertrophic cardiomyopathy. Similar ablation can be performed for deep septal substrate of VT.³¹ This is limited by the availability of a suitable coronary arterial branch and difficulty in controlling the size of myocardial infarction. Alcohol ablation is also feasible to ablate the vein of Marshall for AF.³²

Laser Ablation

A phase-coherent monochromatic high-intensity light beam in the visible, ultraviolet, or infrared frequency range is used to focus energy for thermally mediated ablation.³³ Carbon dioxide and argon lasers cause superficial lesions as a result of high energy absorption in water and myocardium, while Nd:YAG lasers result in deeper lesions because of higher scattering.²⁸ A variable inflatable balloon with an optical endoscope to visualize the adjacent tissue and a laser for point-to-point ablation have been used for durable electrical isolation of pulmonary veins.³⁴

Microwave Ablation

Electromagnetic radiation in the microwave frequency range (300 MHz-300 GHz) causes dielectric heating by oscillation of polarized water molecules in the target tissue.^28,33 Adjacent tissue is heated by indirect conductive heating. Microwaves travel farther with less energy absorption in tissues with little water like fat, and have greater absorption in tissue with a high water content like myocardium. Ablation can be performed without direct tissue contact, across an intervening layer of adipose tissue, and results in deeper lesions compared to RF ablation. Microwave ablation is not available for commercial use.^35,36

Noninvasive Radiation Therapy

Stereotactic body radiotherapy using x-rays and gamma spectrum radiation has been used for treatment of cancers. This modality is now being explored as a noninvasive technique for cardiac ablation. In vivo animal experiments have shown feasibility and safety for AV node ablation, right atrial flutter ablation, and pulmonary vein isolation (PVI) with stereotactic body radiotherapy.^38,39 There have been case reports of successful noninvasive ablation of malignant VT in humans.^40,41

With x-rays and gamma radiation, DNA damage in active cancer cells is incurred largely indirectly through formation of hydroxyl ions, which interfere with cellular function and replication.⁴² Direct ionizing effects of ionized particles like protons and alpha particles with high-energy absorption in tissue may be more effective for myocardial ablation. Heavy charged carbon-12 ions may allow for cardiac ablation with high precision without any exit dose.⁴³

Supraventricular Tachycardias

The prevalence of SVT in the general population is ~2.25 per 1000 persons.⁴⁴ Paroxysms of SVTs, often with 1:1 AV relationship, can occur in the pediatric population and healthy adults in absence of overt structural heart disease. These include atrioventricular nodal reentry tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and focal atrial tachycardia (AT). Symptoms are often paroxysmal and include palpitations, chest pain, lightheadedness, and rarely syncope. Symptoms of SVT overlap with and are attributed to panic and anxiety disorders in a majority of patients. Macroreentrant AT (atrial flutter) tends to occur in older patients and those with structural heart disease, and often presents as a persistent arrhythmia that conducts 2:1 to the ventricles. Some incessant SVTs like AVRT using a decrementally conducting accessory pathway, incessant focal ATs, and persistent atrial flutter may present with tachycardia-mediated cardiomyopathy. EP study and catheter ablation is a suitable first-line option for management of SVT, though medical management with drugs can also be offered.⁴⁵ Overall risk of major complications with ablation is less than 1% to 3% depending on the specific SVT diagnosis.

Atrioventricular Nodal Reentrant Tachycardia

AVNRT is the most common regular paroxysmal SVT in adults and has a female preponderance. AVNRT is a reentrant tachycardia involving the AV node, the adjacent atrial tissue, and two distinct atrionodal connections (see Fig. 88–4). EP study often shows evidence of dual atrionodal pathways for conduction from atrium through the AV node to the His bundle, with a discontinuity in conduction times during atrial extra-stimulus testing.⁴⁶ AVNRT may be inducible with programmed atrial stimulation at baseline, or more commonly with administration of catecholaminergic drugs like isoproterenol. Typically, there is 1:1 relationship of V to A, with A being activated retrogradely through the “fast pathway” synchronously or immediately following the QRS (RP interval < 90 ms). In atypical forms of AVNRT, atrial activation occurs retrogradely through the “slow pathway” with a longer ventriculoatrial (VA) interval (long RP tachycardia). The diagnosis of AVNRT is confirmed by pacing maneuvers during tachycardia.⁴⁷

As a result of inability of current techniques to record activation of the AV node, and the decremental conduction properties of the AV nodal tissue, use of entrainment maneuvers to define the tachycardia circuit is challenging. However, participation of any atrionodal connection can be inferred with resetting the tachycardia with late-coupled extra-stimuli from that site,⁴⁸ or terminating/resetting the tachycardia without global atrial capture, for example, with subthreshold stimulation or cryomapping.^49,50 Regardless, such maneuvers are largely unnecessary; and ablation is often performed solely anatomically, guided by local electrogram characteristics. This is possible because AVNRT tends to be dependent on conduction through an anatomically distinct “slow pathway.” This right inferior atrionodal connection is ablated in the inferoseptal region along the isthmus between the septal tricuspid leaflet and the coronary sinus ostium without undue risk of injury to the compact AV node and the essential AV conduction system (see Fig. 88–4).⁵¹

AVNRT ablation is acutely successful in more than 95% cases and has a 5% recurrence rate.^45,52 The major risk is inadvertent damage to the compact AV node producing heart block that requires permanent pacemaker implantation (~1%).^45,52 Cryoablation has a lower risk of heart block, but also has lower long-term efficacy.^27,50 Slow pathway ablation in the inferoseptal region may result in elevation of sinus heart rates for up to 6 months, possibly related to ablation of adjacent autonomic nerve fibers.⁵³

Accessory Pathway–Mediated Tachycardia

An extra–AV-nodal (accessory) AV pathway/connection that conducts antegradely from atrium to ventricle causes partial ventricular depolarization during sinus rhythm before normal ventricular activation through the His-Purkinje system catches up (ventricular preexcitation).⁵⁴ This is characterized by a short PR interval and a slurred onset of the QRS complex (delta wave). The presence of ventricular preexcitation on ECG along with paroxysmal tachypalpitations is called Wolff-Parkinson-White (WPW) syndrome. Antegrade conduction over an accessory pathway poses a potential risk of a very rapid ventricular response to AF that can cause ventricular fibrillation (VF) and sudden death.⁵⁵ Some accessory pathways have no antegrade conduction and only conduct from ventricle to atrium. These are termed “concealed” because preexcitation is absent during sinus rhythm, but AVRT can still occur.

AVRT is the second most common paroxysmal SVT after AVNRT, and tends to present at an earlier age with the prevalence being highest in adolescents.⁴⁵ The usual tachycardia circuit involves antegrade conduction over the AV node, producing a narrow QRS (or typical right or left bundle branch aberrancy) and retrograde conduction, from ventricle to atrium, over the accessory pathway (orthodromic reentry tachycardia). Sometimes reentry can proceed in the opposite direction with the entire ventricular activation occurring from the accessory pathway (completely preexcited) and retrograde conduction to the atrium over the AV node (antidromic reentry tachycardia). AVRT is usually inducible with programmed stimulation, and the mechanism is confirmed with additional pacing maneuvers.⁴⁷

Accessory AV pathways occur anywhere along the tricuspid or the mitral annulus. The majority traverse the mitral annulus and are accessed by a transseptal approach through the fossa ovalis to the left atrium or retrogradely by inserting the catheter from the femoral artery across the aortic valve to the left ventricle (Fig. 88–13).⁵⁶ Many septal and all right free wall pathways are accessible by a standard venous approach to the right heart. The target of ablation is the accessory pathway potential, yet this can be difficult to identify, and the onset of the earliest myocardial activation produced by conduction through the accessory pathway can also be considered.⁵⁷ Most accessory pathways are thin strands of myocardial tissue traversing the fibrous AV annulus, which are vulnerable to being inhibited temporarily with mechanical injury during catheter manipulation.⁵⁴ In absence of recurrent conduction, the region of a “catheter bump” may be a suitable site for ablation.

Approximately 25% of patients with overt WPW syndrome have pathways that place them at risk of VF if AF occurs. Catheter ablation is the preferred treatment for AVRT, especially if preexcitation is present on baseline ECG (WPW syndrome) and for preexcited AF.⁴⁵ The management of asymptomatic patients who are found to have preexcitation on ECG is more controversial. Even though the odds of incident symptomatic tachyarrhythmia are high, the risk of sudden death is estimated to be 1 in 1000 per year.^55,58 Exercise testing or EP study may be helpful in risk stratification, and individualized consideration of the risks and benefits of ablation is warranted. Overall acute success in ablation of accessory pathway is 93%, with an 8% risk of recurrent conduction.^45,59 AV block can occur with attempted ablation of pathways that are located close to the AV node.

Focal Atrial Tachycardia

Focal AT represents approximately 10% of SVTs referred for ablation. AT may be paroxysmal, occur in repetitive bursts, or may be incessant. It may respond to β-blockers, calcium channel blockers, and membrane-active antiarrhythmic drugs. Catheter ablation is an alternative to pharmacologic therapy.⁴⁵ AT foci tend to occur in specific anatomic locations, including the crista terminalis, tricuspid or mitral annulus, coronary sinus, atrial appendages, and the pulmonary veins. Foci in the left atrium often have a P wave that is negative in leads I and aVL, and positive in lead V₁; whereas those from the right atrium tend to have a negative terminal component in V₁. AT originating from the septum has narrow P waves whereas foci in the free walls have wider P waves, on account of simultaneous or sequential activation of the two atria.^45,60 The wide range of possible locations requires accurate mapping to identify the earliest site of activation to target ablation (see Fig. 88–6). Paroxysmal AT can, however, be difficult to induce in the EP lab, especially when sedation or anesthesia is used. Ablation is successful in more than 80% of patients with reported recurrence rate after successful ablation from 4% to 27%.⁴⁵

Ectopic ATs arising from the peri-AV nodal region, verapamil- or adenosine-sensitive septal ATs, as well as junctional ectopic tachycardia (JET) have a higher risk of AV block with ablation. The noncoronary aortic sinus of Valsalva is an adjunctive region for mapping and ablation of these tachycardias (and anteroseptal accessory pathways) because of its anatomic apposition with the anteroseptum.⁶¹

Inappropriate Sinus Tachycardia

Inappropriate sinus tachycardia (IST) is an uncommon disorder characterized by sinus tachycardia out of proportion to physiologic demand. IST is often associated with fatigue and palpitations that respond poorly to pharmacologic therapy.⁶² Catheter ablation is feasible to target sinus node tissue along the crista terminalis. The septal portion of the crista has the most rapid automaticity and is initially targeted, often reducing the sinus rate.⁶³ Ablation can be difficult because of the epicardial location of the sinus node and epicardial ablation can be considered. The long-term success is limited, with frequent recurrences and persistent symptoms despite rate control in some patients.⁶³ Complications include superior vena cava obstruction, phrenic nerve paralysis, and sinus node dysfunction.^62,63 The role of ablation for IST is controversial and is infrequently recommended—even as a measure of last resort, with nonablative therapy being the accepted approach of choice.

Macroreentrant Atrial Tachycardias or Atrial Flutter

The most common form of sustained macroreentrant AT (typical atrial flutter) consists of electrical reentry around the tricuspid valve. The circuit traverses the myocardium between the inferior vena cava and the tricuspid valve, and is also labeled as cavotricuspid isthmus flutter. This arrhythmia frequently presents with regular 2:1 AV conduction. The ECG pattern is highly characteristic and the P wave is negative with a “saw tooth” morphology in the inferior leads, positive in V₁, and negative in V₆—correlating with a counterclockwise activation around the tricuspid annulus viewed in the LAO projection. Activation in the opposite direction (clockwise flutter) gives rise to positive flutter waves in the inferior leads, but this is not a distinctive and consistent pattern.

Atrial flutter is a marker for atrial disease; a third of patients will subsequently develop AF, though the risk of AF continues to increase with extended follow-up.^45,64 Antiarrhythmic drug therapy may suppress AF, but lead to sustained atrial flutter. Ablation of the atrial flutter with continuation of antiarrhythmic medications to prevent AF can be useful to maintain sinus rhythm. Contiguous ablation lesions placed across the cavotricuspid isthmus to create a line of conduction block abolish the typical flutter with a success rate of 97% (see Figs. 88–5 and 88–7).^45,65

Atypical atrial flutters (non–isthmus-dependent) are often caused by reentry around atrial scars from prior heart surgery, such as congenital heart disease repair, mitral valve surgery, surgical atrial maze, or after catheter ablation for AF. Inferring the circuit of atypical atrial flutters from ECGs can be extremely challenging.⁶⁶ Detailed activation and entrainment mapping and a thoughtful strategy to transect a critical limb of the circuit between two anatomic boundaries (or regions of scar/ablation) with linear ablation eliminates the circuit. Success rates of 80% to 85% are reported, and late recurrences are more frequent than for ablation of typical atrial flutter.⁶⁷

Atrial Fibrillation

Atrioventricular Node Ablation for Rate Control

Catheter ablation of the AV node to create complete heart block with implantation of a permanent pacemaker is an option for controlling the heart rate in patients with AF and difficult-to-control ventricular rates.⁶⁸ This is typically a low-risk, relatively quick procedure with high efficacy. The heart rate is controlled without medications and the ventricular rate is regularized. This leads to improvements in quality of life, exercise tolerance, and ejection fraction.⁶⁹

Several potential disadvantages require careful consideration before using this strategy. The atria usually continue to fibrillate, so patients remain at risk for thromboembolic complications. The abrupt restoration of a slower rate with ventricular pacing has been associated with occasional cases of sudden death possibly caused by polymorphic VT (torsades de pointes). This risk appears to be largely mitigated by setting the pacemaker lower rate to 90 bpm for the first several weeks and then gradually reducing the rate over time.⁷⁰ Further, chronic right ventricular apical pacing has important adverse hemodynamic consequences in some patients. Patients with poor left ventricular function and mitral regurgitation are at greatest risk for aggravation of heart failure with right ventricular pacing, and biventricular pacemaker for cardiac resynchronization therapy may be warranted.⁶⁹

AV node ablation is usually considered for patients who already have a pacemaker inserted, are elderly, or those who cannot tolerate either rate-control medications or antiarrhythmic drug therapy. The procedure is less attractive for younger patients because of dependency on permanent pacing for decades with need for multiple generator changes, risk of pacing lead complications, and the potential for deleterious consequences of chronic right ventricular pacing.

Atrial Ablation to Maintain Sinus Rhythm

Maintenance of sinus rhythm is indicated to manage symptoms related to AF.⁷¹ Sinus rhythm may have hemodynamic benefits, especially in patients with diastolic dysfunction, as ventricular filling is improved with slower heart rates and restoration of atrial mechanical function.

Initiation of paroxysmal AF in humans by rapid firing of triggers in myocardial sleeves in the pulmonary veins was demonstrated in 1998, and the feasibility of preventing AF by ablating these foci was described.⁷² It was soon recognized that focal triggers for AF could also occur in the atria outside the pulmonary veins, and RF ablation within the pulmonary veins was accompanied by a significant risk of pulmonary vein stenosis. This led to ablation approaches that encircle and electrically isolate the entire broader antral regions of the pulmonary veins (see Figs. 88–10 and 88–14).^73,74,75 Techniques have evolved to address both triggers that initiate AF, as well as the atrial substrate that allows perpetuation of the arrhythmia.⁷⁵ PVI is effective for many patients with paroxysmal AF, but more extensive atrial ablation is often required for persistent AF, though the optimal technique has not been confirmed in a randomized trial.⁷⁶

Post-AF ablation AT and AF are common, but typically dissipate spontaneously over a period of several weeks as ablation lesions heal and the atrium remodels. Antiarrhythmic medications may be continued for 1 to 3 months after ablation. It is also not uncommon for some patients to need a second procedure to ablate recurrent ATs. These arrhythmias may be caused by recovery of conduction across ablation lines or may arise from areas that were not ablated at the first procedure.

Ablation success varies with the type of AF and severity of underlying heart disease. Young patients with paroxysmal AF and without structural heart disease have the best outcome; more than 70% to 80% have sinus rhythm after the initial healing phase after ablation.⁷⁷ Success rates are lower for patients with persistent or long-standing (> 1 year) persistent AF. A worldwide survey on outcomes of catheter ablation of AF suggests clinical benefit in about 80% of patients after an average 1.3 procedures per patient, with about 70% of patients not requiring antiarrhythmic drug therapy at a mean follow-up of 18 months.^75,78

Oral anticoagulation is recommended for at least 2 to 3 months following AF ablation, and subsequent anticoagulation should not be dictated by apparent procedural success, but rather by the clinical assessment of the individual patient’s stroke risk. The overall complication rate with AF ablation is approximately 5%, major complications around 2%, and in-hospital mortality less than 0.5%.^78,79 Myocardial perforation with tamponade occurs in 1% to 2% of procedures and can usually be managed by reversing anticoagulation and performing pericardiocentesis, although emergency surgery may be required. The intensive anticoagulation during the procedure and extensive ablation required are likely factors that increase this risk compared with other ablation procedures. Stroke or a transient ischemic attack occurs in 0.5% to 1% of patients. Severe pulmonary vein stenosis was reported in 2% to 6% of patients and may present months after the procedure with dyspnea, pneumonia, or pulmonary infiltrate, or may be asymptomatic.⁸⁰ Pulmonary vein stenosis appears to have become less frequent with the avoidance of ablating inside the pulmonary vein ostia. Rare, but usually fatal, atrial-esophageal fistulae, presenting days to a few weeks after the procedure with endocarditis, septic emboli, or gastrointestinal bleeding, have been reported (estimated ~0.1%).^75,80,109

The feasibility of catheter ablation for maintaining sinus rhythm and improving symptoms in patients with AF has been well demonstrated. Data are largely from relatively young patients treated at experienced centers and followed-up for less than 3 years. The procedure is mainly reserved for symptomatic patients in whom the potential benefit is believed to justify the risks. Technologic advances and ongoing studies should continue to improve patient selection and outcomes.

Beyond Pulmonary Vein Isolation

PVI alone as the first procedure has good results for paroxysmal AF. However, outcomes in persistent AF have been suboptimal. Additional ablation targets have been sought for AF recurrence after PVI and for ablation of persistent AF. Extrapulmonary vein triggers of AF can be mapped with testing on high-dose isoproterenol in the EP lab and targeted for ablation. These include the superior vena cava, vein of Marshall, coronary sinus, left atrial appendage, and other sites of focal AT.⁷⁵ Techniques to identify and ablate regions of presumed anchoring of rotors that sustain persistent AF are being evaluated, though clinical utility needs to be validated.⁸¹ The role of cardiac autonomic nervous system in the pathogenesis of AF is well documented, and endocardial ablation at sites of epicardial cardiac ganglia has been demonstrated to improve outcomes.⁸² Ablation of atrial regions with fibrosis as determined by MRI imaging has been proposed to eliminate the substrate that sustains AF.⁸³ These additional targets of ablation—autonomic ganglia, rotors, areas of fibrosis—are often localized to the pulmonary vein antra and the posterior left atrial wall, and empiric linear ablations to isolate the entire left atrial posterior wall in addition to wide area pulmonary vein antral isolation can be performed. Extrapolating from the surgical maze literature of compartmentalizing the atria to prevent AF, catheter-based maze with empiric linear ablations can be performed. However, empiric linear ablations can be proarrhythmic and lead to atypical atrial flutters if there are gaps in ablation lines. There is also evidence that extensive atrial ablation can affect interatrial conduction, atrioventricular synchrony, and atrial mechanical function.⁸⁴

AF more commonly develops in the context of systemic inflammation and metabolic derangements related to sedentary lifestyle, unhealthy eating habits, obesity, sleep apnea, metabolic syndrome, hypertension, and increased left atrial pressures. Therefore, ablation therapy for AF should be considered in context of such underlying aggravating factors; and aggressive lifestyle modification, weight reduction, and treatment of sleep apnea and hypertension markedly improve outcomes.⁸⁵

Cryoballoon Ablation

A cryoballoon catheter has been specially designed for the ostial pulmonary vein and antral ablation to occlude and freeze the pulmonary vein ostium with a single freeze. The cryoballoon has a 70% success in preventing recurrent AF over 12 months in patients with paroxysmal AF, comparable to RF ablation.^86,87 Injury to the right phrenic nerve (coursing adjacent to right superior pulmonary vein) was the most frequently observed complication, reported in ~6%.^27,86 Monitoring of the diaphragmatic compound motor action potential (CMAP) using electrodes on the torso while electrically stimulating the phrenic nerve can be used to detect and avoid impending hemidiaphragmatic paralysis during cryoballoon ablation of right-sided pulmonary veins.^88,89

Ventricular Tachycardias

Premature Ventricular Complexes

Premature ventricular complexes (PVCs) can arise from any ventricular tissue, yet the outflow tracts and adjacent epicardial regions, papillary muscles, tricuspid and mitral valve annuli, and the fascicular conduction system are more common as sources of this form of arrhythmia.⁸ Frequent PVCs can cause symptoms of palpitations, dyspnea, chest pain, lightheadedness, and anxiety. A very high burden of PVCs, typically more than 10,000 or 20,000 per 24 hours, can depress the left ventricular systolic function in a subset of patients. Analogous to tachycardia-mediated cardiomyopathy, suppression of PVCs can result in resolution of ventricular dysfunction.^8,90 PVC suppression may also be indicated when a consistent PVC triggers sustained VF or VT and results in syncope or implanted cardioverter-defibrillator (ICD) shocks.^8,91

PVCs occasionally respond to β-blockers or calcium channel blockers, and antiarrhythmic drugs like flecainide, sotalol, or amiodarone may be effective. When one or two PVC morphologies predominate, PVC ablation can be performed when drug therapy is ineffective, not tolerated, or not desired.^8,92 Most commonly, PVCs arise from the right ventricular outflow tract (RVOT), and have a left bundle branch block (LBBB) configuration in lead V₁ with an inferiorly directed axis and tall positive QRS complexes in leads II, III, and aVF. PVCs may be suppressed with anesthesia, but are sometimes inducible with isoproterenol or rapid ventricular pacing resulting in calcium loading of cells and triggering of PVCs.⁹³ Activation mapping is critical to identify the earliest site of activation, and often a prepotential at the earliest site is the target of ablation. As a result of the complex anatomy of the outflow tracts, multiple sites like the RVOT, left ventricular outflow tract (LVOT), supravalvar myocardium in the aortic sinuses of Valsalva, and the epicardial region accessible through the great cardiac and the anterior interventricular veins may need to be mapped. Intracardiac echocardiography is useful to visualize intracavitary structures like papillary muscles, moderator band, and false tendons to facilitate mapping of PVCs originating from these respective sites.⁸

Outflow Tract Ventricular Tachycardia

The most common region in the heart responsible for PVCs and VT in the absence of structural heart disease is the RVOT. Tachycardia may be sustained or present with repetitive bursts of nonsustained VT, and has an inferiorly directed QRS axis on ECG. The mechanism of idiopathic outflow tract VT is thought to be cyclic AMP-triggered automaticity.⁹³ Outflow tract VT is often exercise induced and may respond to vagal maneuvers, intravenous adenosine, β-blockers, or calcium channel blockers. Catheter ablation is an alternative to drug therapy, or can be performed when drugs fail to suppress VT.^8,92

Ablation is performed at the area of earliest ventricular activation during the VT. Occasionally, the focus originates from the LVOT, along the mitral annulus, or in sleeves of ventricular myocardium that extend above the aortic or pulmonic valves (Fig. 88–15). Catheter ablation successfully eliminates tachycardia in more than 80% of patients. An inability to induce the arrhythmia in the EP laboratory can prevent mapping and is a major cause of failed ablation.

Fascicular Ventricular Tachycardia

Idiopathic fascicular VT occurs typically related to micro-reentry in or near the fascicles of the left bundle,⁹⁴ though focal origin of fascicular PVCs and VT can also occur. Idiopathic fascicular VT has a right bundle branch block (RBBB) configuration in lead V₁ and usually a superiorly directed axis on ECG. Fascicular VT has a male preponderance and typically occurs during the young adulthood years. It is often provoked with exertion and responds to verapamil or adenosine. The sites of early fascicular activation or diastolic activation located along the left ventricular septum are targets for ablation. Difficulty in inducing the VT during the ablation procedure and the risk of “catheter bump” suppressing the arrhythmia can limit mapping. Ablation may be successful in more than 80% of cases. There is a small risk of left fascicular block or even AV block if ablation is performed too proximally in the conduction system.

Ventricular Tachycardia in Structurally Diseased Hearts

In patients with structural heart disease, VT is most commonly caused by reentry through areas of myocardial scar. These scars are associated with areas of conduction block with intervening regions of slowly conducting diseased myocardium that can support reentrant circuits. VT can usually be induced with programmed stimulation. Most often, the scar is a late sequela of prior myocardial infarction, and VT in this setting is associated with a risk of death that generally warrants an ICD to prevent sudden cardiac death. Although many VTs are nonsustained or terminated by antitachycardia pacing before significant symptoms develop, some patients experience lightheadedness or syncope, or sustain painful shocks for VT termination. Further, ICD shocks are associated with an increased risk of death despite effective termination of the VT.⁹⁵ Catheter ablation is an important alternative to antiarrhythmic drug therapy for preventing or reducing the frequency of VT episodes, and ablation can be lifesaving if VT becomes incessant.⁹²

Any ventricular scar can lead to development of reentry and VT. Myocardial infarction is the most common cause, but arrhythmogenic cardiomyopathy, cardiac sarcoidosis, Chagas disease, hypertrophic cardiomyopathies, and idiopathic dilated cardiomyopathies are all associated with scar-related VT. Ventricular scars from prior cardiac surgery such as tetralogy of Fallot repair can also cause VT.

Premature ectopic beats can induce VT that is typically regular and monomorphic. The morphology of the QRS helps to localize the exit site from the scar region to the healthy ventricular myocardium. VTs with a LBBB configuration in V₁ on ECG often map to the right ventricle or interventricular septum. Those with a RBBB configuration originate from the left ventricle.

Most patients with scar-related VT possess several potential reentry circuits, creating VTs with different QRS morphologies and cycle lengths. These are often terminated promptly by ICDs, such that the QRS morphologies are unknown. In addition, VT often produces hypotension and is not tolerated to allow extensive mapping during VT. Substrate mapping approaches that facilitate identification of potential reentry circuits while mapping during sinus rhythm allow effective ablation of many of these VTs. Potential areas of scar can be identified on imaging as regions with hypokinesis, akinesis, or dyskinesis, or directly imaged with myocardial perfusion techniques, or late gadolinium enhancement on MRI. During the ablation procedure, areas of scar are identified as regions with very low voltage electrograms and inability to electrically capture with local stimulation.^92,96 Plotting the electrogram amplitude in three-dimensional anatomic maps identifies regions of very low voltage that coincide with myocardial disease and scar (see Figs. 88–8 and 88–9). Fragmented, delayed electrograms, and pace mapping help identify regions of abnormal conduction and potential exit sites.¹¹ Ablation then targets conducting channels through the scar region or the exit sites in the border region of the scar.¹⁰ When VT is hemodynamically tolerated, additional mapping can be performed during VT to target the specific clinical VT.

Ablation of scar-related VT is more difficult than ablation for SVT and has lower success rates. Even so, over two-thirds of patients experience clinical benefit from a marked reduction in frequency of VT episodes. With improvements in ablation methods and techniques, freedom from VT recurrence at 1-year follow–up has improved to 70%, yet frequently the underlying cardiomyopathic process progresses, leading to the development of other VT.⁹⁷ Procedural mortality is approximately 3%, though the most common cause of death is uncontrollable VT from a failed procedure. Stroke, perforation with tamponade, femoral hematomas, and heart block can also occur.⁵⁹

The presence of culprit substrate deep to the endocardium, or in the subepicardium, is a major reason for failure of endocardial ablation approaches. Epicardial VTs can be approached by a subxiphoid percutaneous puncture into the pericardial space for mapping and ablation (see Fig. 88–2).¹ Pericardial scarring from prior surgery, epicardial adipose tissue, and the presence of epicardial coronary arteries limit applicability of this approach in some patients.

Bundle Branch Reentry Ventricular Tachycardia

Approximately 6% of patients with VT associated with structural heart disease are found to have reentry involving the bundle branches as the mechanism for at least one of their inducible VTs.⁹⁸ These patients often have a left intraventricular conduction delay or a pattern of LBBB during sinus rhythm and coexistent advanced ventricular dysfunction. A diseased Purkinje system supports a reentry circuit revolving up one bundle branch and down the contralateral bundle branch. Catheter ablation of the right bundle branch interrupts the reentry circuit and is curative.⁹⁹

Polymorphic Ventricular Tachycardia and Ventricular Fibrillation

Polymorphic VT and VF are generally not thought of as arrhythmias amenable to ablation. However, some patients with repetitive episodes of idiopathic VF, or VF associated with recent myocardial infarction or hereditary ion channel diseases, have episodes of arrhythmia triggered by ventricular ectopy from identifiable foci in the Purkinje system or RVOT that can be targeted for ablation.^100,101 Ablation in these circumstances can be lifesaving. Recently, ablation of the RVOT free wall to modify the substrate and susceptibility for VF in patients with Brugada syndrome has been described.¹⁰²

Patients with malignant ventricular arrhythmias refractory to medical therapy or ablation can be considered for sympathetic denervation surgery.¹⁰³ Typically performed via a thorascopic approach by the thoracic surgeon, the technical details of cardiac denervation are beyond the scope of this chapter. Results of cardiac denervation are particularly encouraging in certain subsets of patients—with the most consistent salutary, anti-fibrillatory results in patients with genetic channelopathies.¹⁰⁴

Cardiac Perforation and Pericardial Tamponade

Any catheter-based intervention in the heart has risk of perforation with pericardial effusion and tamponade, especially in the atria and right ventricle. AF ablation may have a 3% risk of effusion.^78,79 Although intracardiac echocardiography is invaluable in the early recognition, tamponade can be fatal unless emergent pericardiocentesis is accomplished, whereas a minority may still require open thoracotomy to stabilize bleeding.

Thromboembolism and Stroke

Coagulum is formed during thermally mediated ablation by direct heating of blood near the electrode-endocardial interface causing denaturation of proteins, especially in absence of active electrode cooling with saline irrigation.¹⁰⁵ Coagulum formation may limit delivery of ablation energy. It is a nidus for further thrombogenesis and embolic complications, especially stroke, when ablating in left heart chambers. Limiting RF ablation power, open irrigation, and therapeutic heparin anticoagulation are important to reduce risk. In addition to clinical strokes, a high rate of silent cerebral ischemia is seen with MRI.¹⁰⁶ Additionally, the injured and inflamed endocardial surface can result in thromboembolic complications even weeks after ablation, and two to three months of systemic anticoagulation may be warranted after extensive ablation in left heart chambers.

Collateral Damage

Collateral injury to extracardiac structures occurs when lesion depth exceeds myocardial wall thickness. Depending on the ablation target, damage to the phrenic nerve, coronary arteries, esophagus, lung parenchyma, or aorta can occur. It is critical to understand the anatomical relationships of cardiac and extracardiac structures in vicinity of the ablation target. High-output pacing near anterior aspect of right superior pulmonary vein and along the right atrial free wall can detect the course of the right phrenic nerve by diaphragmatic stimulation, and diaphragmatic stimulation can be monitored with phrenic nerve pacing from the superior vena cava above the level of potential injury during ablation.^88,107,108 Coronary arteriography is useful to ensure ablation is not delivered in close proximity, especially during epicardial ablation or ablation in the epicardial coronary veins.

Atrioesophageal fistula is a rare (~0.1%), but highly fatal, complication of AF ablation usually presenting a few weeks after ablation.¹⁰⁹ The mechanism of injury probably includes damage of the esophageal vasculature, inflammatory response with esophageal ulceration, and progressive erosion from the esophagus into the pericardium and eventually the atrium. Caution is needed when ablation is performed on the posterior left atrial wall, with limiting the power and duration of RF delivery, and avoiding ablation of atrial tissue in direct apposition to the esophagus. Monitoring luminal esophageal temperature near the ablation site is useful but does not guarantee safety.

Atrioventricular Block

Ablation in proximity to the AV node, fast pathway, and the His bundle in the mid and anterior septal region has risk of complete heart block. AV block can occur during ablation for AVNRT, septal ATs, mid and anteroseptal accessory pathways, junctional tachycardia, and para-Hisian or septal PVCs or VT. Injury to the essential AV conduction system can occur from the right heart chambers, aortic root, left ventricle, and left atrium. As there is no distinct electrogram signature for the AV node, safety relies on understanding the critical anatomic relationships of the conduction system, and close monitoring or AV conduction during ablation. Early recognition of rapid junctional beats is crucial, and cryoablation may be considered when risk of irreversible AV block with RF ablation is high.

Access Site Complications

Multiple venous cannulations and arterial access can result in vascular complications including venous thrombosis, arteriovenous fistula, pseudoaneurysm, hematoma, and retroperitoneal bleeding.

Catheter ablation is rapidly evolving and currently offers a more effective alternative to antiarrhythmic drug therapy for most tachyarrhythmias. Appropriate patient selection depends on an individualized assessment of risks and benefits. Ablation procedures have revolutionized the approach to the management of patients with tachycardias and have evolved to the point where ablation is a reasonable first-line therapy for symptomatic patients with accessory pathways, AVNRT, ATs, atrial flutter, PVCs, idiopathic VTs, and paroxysmal AF. Catheter ablation is an option for symptomatic persistent AF, but is still an evolving procedure that requires careful assessment of risks and benefits. Ablation for VT and VF can be lifesaving in those with recurrent ICD shocks.

We would like to thank Dr. Usha Tedrow and Dr. William Stevenson, who contributed to the previous version of this chapter in the 13th edition.