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.
A. Ablation of a left-sided accessory pathway in a patient with Wolff-Parkinson-White syndrome. Shown is a left anterior oblique fluoroscopic image depicting catheter position for transablation of a left-sided accessory pathway by a transeptal approach. A decapolar catheter is seen in the coronary sinus (CS). The ablation catheter (Ablation) is passed through a sheath, which crosses the fossa ovalis into the left atrium for mapping along the tricuspid valve annulus. B. Five surface electrocardiographic leads and two intracardiac leads depicting ablation of a left lateral accessory pathway during atrial pacing. The right atrium is being paced (pacing stimuli indicated by S). Pacing stimuli initially conduct from the atrium to the ventricles over the atrioventricular (AV) node and an accessory pathway producing a pattern of ventricular preexcitation with a wide QRS with a slurred initial delta wave as indicated by the left-hand schematic at the bottom of the figure. The pathway blocks within seconds of the application of radiofrequency energy with sudden narrowing of the QRS complex (Pathway blocks) indicating that conduction to the ventricles is occurring only over the normal conduction system of AV node and His bundle (right-hand schematic at the bottom of the figure). RA, right atrium.
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 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
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
Left atrial ablation for atrial fibrillation. A. Left lateral view of cardiac dissection demonstrating two important targets for arrhythmia therapy—the left atrial appendage (LAA) and the pulmonary veins. Shown is a catheter placed in the left superior pulmonary vein (LSPV). Myocardium of the pulmonary vein is an important location for triggers initiating paroxysms of atrial fibrillation. Ablation techniques involve electrical isolation of the pulmonary veins by ablating the left atrial tissue adjacent to the pulmonary vein ostia. The LAA is not a common ablation target because this structure is a common source for cerebral thromboembolism. B. Present ablation techniques to electrically isolate the pulmonary veins. The catheter is advanced to the left atrium via transseptal puncture. Large-area circumferential lesions are placed around the ostia of the left- and right-sided pulmonary veins. This procedure may be combined with linear ablation to prevent atrial flutters and possible targeted ablation of abnormal myocardium and the retroatrial ganglia. C. Catheters may be placed into the pulmonary vein, including circumferential mapping catheter depicted in this figure placed in the LSPV. Electrical signals retrieved from these catheters are characteristic of abnormalities associated with atrial fibrillation substrate. After circular left atrial ablation, these signals should no longer be seen. LA, left atrium; LIPV, left inferior pulmonary vein; LV, left ventricle.
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
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
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.
Three examples to demonstrate the complex regional anatomy of the outflow tracts: Top Panel. Angiography is being performed through a catheter engaging the left main coronary artery with a wire advanced into the left anterior descending (LAD) artery. Note the close proximity of catheters advanced to map outflow tract ventricular ectopy from different cardiac chambers. (E, epicardial space; G, great cardiac vein [GCV]; R, right ventricular outflow tract [RVOT]). This patient had a high burden of premature ventricular complexes (PVCs) resulting in left ventricular systolic cardiomyopathy. PVCs were mapped to close proximity of the LAD. After mapping the left ventricular outflow tract (LVOT) and left coronary cusp (LCC) in addition to the aforementioned sites, radiofrequency ablation was performed in the distal GCV, epicardial region, and the LCC with successful elimination of PVCs without injury or need for intervention on the LAD. Middle Panel. Anatomic chamber geometry to show the correlative anatomy of the outflow tracts generated with three-dimensional mapping using intracardiac ultrasound and mapping catheters. PVC focus was mapped and ablated at the commissure between RCC and LCC (maroon spheres). Bottom Panel. Color-coded three-dimensional activation map of outflow tract ectopy with earliest site at the anterior interventricular vein (AIV)-great cardiac vein (GCV) junction (red) with subsequent activation in the endocardial LVOT/anterior mitral annular region and RVOT. Ablation lesions (maroon spheres) were delivered at the earliest site (cluster 1) and consolidation lesions on corresponding endocardial site at anterior mitral annulus (cluster 2) to sandwich the mid-myocardial arrhythmia focus. Left hand panel shows the surface ECG leads of the mapped premature ventricular beat with presystolic bipolar (cyan) and unipolar (orange) electrogram noted at the earliest site. LAO, left anterior oblique; LM, left main coronary artery; LV, left ventricle; NCC, noncoronary cusp; PA, pulmonary artery; RAO, right anterior oblique; RCC, right coronary cusp.
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