Using the techniques described in the preceding, a variety of tachyarrhythmias can be targeted for percutaneous catheter-based ablation, including both atrial and ventricular arrhythmias that are either focal or that use re-entrant circuits.
Atrioventricular Nodal Re-entrant Tachycardia
Of patients with SVT, AVNRT represents up to 60% of cases that present to tertiary centers for electrophysiologic studies. This tachycardia can present at any age, although most patients who present for medical attention are in their forties and the majority are female.56,57 Advances in RF catheter ablation of this tachycardia has made it a first-line therapy for those symptomatic patients not wishing to take medications.58
This tachycardia has a re-entrant mechanism using two pathways within the AV nodal tissue. The pathways are known as the "slow pathway" and "fast pathway" based on their relative conduction velocities. The anatomical location of these pathways is variable but generally located within the triangle of Koch. The Koch triangle is bounded by the tricuspid annulus and the tendon of Todaro with the coronary sinus at the base. The apex of the triangle is the His bundle at the membranous septum where it passes through the central fibrous body. The anterior third of the triangle contains the compact AV node and the fast pathway, and the middle and posterior portion, near the coronary sinus os, contains the slow pathway (Fig. 57-2).59
(A) Diagrammatic representation of typical atrioventricular nodal re-entrant tachycardia. Surface ECG shows narrow complex tachycardia with no clear P waves. The re-entrant circuit (blue arrows) consists of the posterior slow pathway region acting as the antegrade limb, and the anterior fast pathway region acting as the retrograde limb. The slow pathway target site is located between the coronary sinus os (CS) and the tricuspid valve annulus (TV). IVC = inferior vena cava; RA = right atrium; RV = right ventricle; SVC = superior vena cava. (B) Surface ECG showing precordial leads in AVNRT. This demonstrates that the retrograde P waves are barely discernible in some leads. In V1, it forms a pseudo r′ wave (arrow). P waves are also visible in the terminal portions of QRS complexes in V2 and V3 but not in the lateral leads.
In the typical form of AVNRT, antegrade conduction from the atrium to the ventricle occurs over the slow pathway, and the retrograde conduction from the ventricle to the atrium occurs over the fast pathway. Because conduction in the retrograde direction is fast, the atria and ventricle are depolarized almost simultaneously. Thus the electrocardiographic feature of this tachycardia is P waves that are inscribed within the QRS and thus not seen or barely discernible at the termination of the QRS complex.60
In fewer than 10% of cases, the circuit is reversed. In atypical AVNRT, antegrade conduction occurs over the fast pathway and retrograde conduction occurs over the slow pathway. Thus the ECG of this tachycardia shows inverted P waves in the inferior leads denoting retrograde activation of the atria with short PR segment owing to rapid antegrade conduction.61
Slow pathway ablation has a high degree of success with a recurrence rate in the range of 2 to 7%, with the complication of complete AV block occurring about 1% (range 0 to 3%) of the time.62 The North American Society of Pacing and Electrophysiology (NASPE) self-reported surveys on 4249 patients who underwent slow pathway ablations had success rates of greater than 96% and complication rates of less than 1%.63,64
Atrioventricular Re-entrant Tachycardia
About 30% of SVTs are caused by AVRT. This is a re-entrant tachycardia using the AV node and an accessory pathway (AP). These APs are remnants of conductive tissue from embryonic development that span the normally electrically inert tricuspid and mitral valve annulus and provide an independent path of conduction outside the AV node between the atria and the ventricles. The most common form of AVRT is part of the Wolff-Parkinson-White (WPW) syndrome of ventricular pre(mature)-excitation and symptomatic arrhythmias. The most common APs connect the atrium to the ventricle. Other APs may connect the atria or AV node to the His-Purkinje system. In sinus rhythm, antegrade conduction over the AP results in pre-excitation of the ventricles through conduction by other than the AV node, and is manifested by a short PR segment and slurring of the onset of the QRS, the delta wave. Absence of these findings does not exclude an AP, as the degree of pre-excitation may vary or conduction may only occur in the retrograde direction (∼30% of APs).
Patients with WPW typically present with palpitations caused by rapid heart rate. This may be the result of AVRT or any SVT with resulting rapid AV conduction via the AP. Associated symptoms may be mild such as palpitations and shortness of breath, or as severe as syncope and sudden death.65,66 Sudden death may be caused by ventricular fibrillation resulting from the extremely rapid ventricular activation over the AP during atrial fibrillation in some patients.
Indications for ablation of APs include patients with symptomatic AVRT or those with atrial tachyarrhythmias with rapid ventricular conduction who fail or do not wish to undergo medical therapy.65 Relative indications for ablations include asymptomatic patients in high-risk professions, those with family history of sudden death, or those mentally distraught over their condition.67
In the typical or orthodromic form of AVRT, antegrade conduction from the atrium to the ventricle occurs over the AV node and retrograde conduction occurs over the AP. In this form of AVRT, the P wave in the tachycardia closely follows the preceding QRS complex with a long PR segment (Fig. 57-3). In the rare antidromic form of AVRT, antegrade conduction occurs over the AP with retrograde conduction over the AV node. This results in eccentric depolarization of the ventricle, producing a wide complex tachycardia with retrograde P waves that can be easily mistaken for ventricular tachycardia with one-to-one ventriculoatrial conduction.
(A) Diagrammatic representation of atrioventricular re-entrant tachycardia. This macro re-entrant circuit (gray arrows) uses the AV node and an accessory pathway (AP), in this case a right lateral pathway. In orthodromic AVRT, antegrade conduction occurs over the AV node and retrograde conduction occurs over the AP. Because of the conduction delay from the His-Purkinje system through the ventricular myocardium to reach the AP, retrograde P waves are discernible after the QRS complexes (arrow). In antidromic AVRT, the re-entrant circuit is reversed and surface ECG shows P waves that closely precede the QRS complexes. CS = coronary sinus; IVC = inferior vena cava; RA = right atrium; RV = right ventricle; SVC = superior vena cava; TV = tricuspid valve. (B) Intracardiac recording of atrioventricular re-entrant tachycardia with termination of eccentric conduction over the accessory pathway during RF ablation. The tracing at 50-mm-per-second speed shows four surface leads (VI, II, I, and aVF) and intracardiac recording from catheters:ablation (ABL); His distal, mid, and proximal; as well as right ventricular apex (RVA). The first three beats of the tracing show evidence of eccentric conduction over an accessory pathway: short PR segment and delta wave. With onset of RF energy (RF On) from the ablation catheter positioned in the region of shortest AV conduction, conduction becomes normal within two beats, with normalization of the PR segment and loss of the delta wave.
The major challenge that remains is the ablation of APs near the normal conduction system and those that are epicardial in location. Ablation of pathways that are anteroseptal and midseptal in location carries a high risk of causing complete heart block. It is hoped that newer ablative energy sources such as cryoablation, although found to be effective, may offer a safer alternative.22,68,69 The 1998 NASPE prospective catheter ablation registry reported on 654 patients with a 94% success rate.64 Success rates are lower (in the range of 84 to 88%) for septal and right free wall pathways. Other pathways have success rates in the range of 90 to 95%.70–72 Mortality rates are less than 1% and nonfatal complications are about 4%.64
Atrial tachycardias depend wholly on atrial tissue for initiation and maintenance of the tachycardia. Ectopic atrial tachycardia, sinoatrial nodal re-entrant tachycardia, inappropriate sinus tachycardia, atrial flutter, and atrial fibrillation can all be considered atrial tachycardias. Focal atrial tachycardias, a less common type of SVT, form about 10% of all SVTs referred for electrophysiologic studies.67 Multifocal atrial tachycardia is caused by multiple foci of abnormal automaticity or triggered activity and is not amenable to curative catheter ablation.73
These arrhythmias are more common in patients with structural heart disease. Indications for ablation include failure or intolerance of medical therapy. Rarely, incessant tachycardias can lead to cardiomyopathy. With ablation and control of heart rate, myocardial dysfunction can be reversed, although there may be a delayed risk of sudden death that necessitates use of a defibrillator.74–76
Surface ECG features of atrial tachycardia include abnormal P-wave morphology or axes that are close to the following QRS complexes. Mapping and ablation of atrial tachycardias can be more difficult, as they can originate from anywhere within the right or left atrium. But there are specific anatomical regions that have a high incidence of foci and serve as primary targets. They include the crista terminalis, atrial appendages, valve annulus, and pulmonary ostia.77
Inappropriate sinus tachycardia and sinoatrial nodal re-entry tachycardias occur more infrequently and experience with catheter ablation of these tachycardias is more limited. Inappropriate sinus tachycardia is also difficult to ablate because of the variability and diffuse location of sinoatrial tissue.78 Catheter ablation should be reserved, and considered as one small part of a multidisciplinary approach, to include cardiovascular, endocrinologic, and psychiatric evaluation and pharmacologic management.79 Catheter ablation may result in complete loss of sinoatrial node function and resulting junctional rhythm, requiring insertion of a pacemaker. Even if the resting heart rate is reduced with nodal modification, symptoms may continue with episodes of tachycardia. Sinoatrial nodal re-entrant tachycardia is targeted for ablation using techniques similar to those used for other atrial tachycardias.
Success with ablation of atrial tachycardia is quite variable depending on the location of the arrhythmogenic foci and the experience of the operator. The 1998 NASPE survey showed a success rate of 80% for right-sided versus 72% for left-sided versus 52% for septal foci in 216 cases of atrial tachycardia ablation.64 Another large review examined the frequency of arrhythmias as a predictor of success. In 105 patients, the overall initial success rate was 77%, and 10% had recurrence over a 33-month follow-up period. There was an 88% success rate for the paroxysmal form versus 71% for permanent and 41% for repetitive forms of atrial tachycardia.80
Atrial flutter is a type of atrial tachycardia that uses a macro re-entrant circuit contained within the atria. A variety of natural and surgical barriers to conduction can create a re-entrant circuit within the atria. Typical atrial flutter is owing to a right atrial circuit, bound anteriorly by the tricuspid valve (TV) annulus. Posteriorly, it is confined by the superior vena cava, crista terminalis, inferior vena cava (IVC), eustachian ridge, and coronary sinus (CS)81 (Fig. 57-4).
Diagrammatic representation of typical or counterclockwise right atrial flutter. Surface ECG shows large inverted P waves in the inferior leads. Lead III above shows 2:1 AV conduction with "sawtooth" flutter waves. The re-entrant circuit (gray arrows) is confined to the right atrium by the tricuspid valve annulus (TV) and barriers to conduction within the right atrium. These include the superior vena cava (SVC), crista terminalis (CT), inferior vena cava (IVC), eustachian ridge (ER), and coronary sinus (CS). The isthmus between the IVC and TV is the preferred target for ablation.
In the typical and more common form of atrial flutter, the circuit transverses the right atrium in a counterclockwise manner in the frontal plane. Because the anatomy of the right atrium is elongated in a caudad-cephalad direction, a typical atrial flutter spends large portions of circuit activation going either directly away, or directly toward the inferior leads; therefore, in leads II, III and a VF, the P waves are negative and have a sawtooth appearance. In V1, the P wave is usually upright and in V6 it is inverted. Clockwise flutter uses the same circuit but in a reversed manner. The ECG also shows a reversed pattern. In the inferior leads the P waves are upright, with inverted P waves in V1 and upright in V6. This surface ECG morphology is suggestive of the circuit but needs intracardiac confirmation.82 These two forms of atrial flutter have been termed isthmus dependent because of the use of the IVC-tricuspid annular isthmus.
A macro re-entrant circuit can be cured by lesions that transect the circuit between two anatomical barriers. In the case of isthmus-dependent flutter, the target for ablation is the isthmus between the IVC and TV. Success rates for ablation of this form of atrial flutter are high. Given high success rates, ablation has become the first line of therapy for recurrent isthmus-dependent atrial flutter. Despite successful treatment of flutter, nearly one-quarter of patients developed de novo atrial fibrillation during chronic follow-up.83
Although the right atrial circuit described in the preceding is the most common, a variety of other circuits in the right and left atria are possible. These are more common in patients with underlying heart disease, or in those having previously undergone pulmonary vein ablation or surgical management of atrial arrhythmia.55,84–86 Although initially thought not to be amenable to ablative therapy, mapping and ablation of these arrhythmias are now routinely performed. However, the success rate is somewhat lower than that for typical isthmus-dependent atrial flutter. An electroanatomical map of a patient with left atrial flutter can be seen in Fig. 57-5. Ablation in the isthmus between these scars resulted in termination of the flutter.
An electroanatomic map of a patient with left atrial flutter is shown in the right anterior oblique projection. Two large areas of scar can be seen in gray. Gradation in color shows activation sequence, with lighter being the earliest and darker being late in relation to a reference catheter, in this case positioned in the coronary sinus. The circulating wavefronts describe a figure-eight pattern around these two areas of scar but are confined by the narrow region (isthmus) between them. Ablation in the isthmus resulted in termination of the flutter.
Surgical Scar–Related Atrial Arrhythmias
As mentioned, incisional scars from prior cardiac surgery can be the substrate for re-entrant atrial arrhythmias.87–89 The most common is an atypical atrial flutter related to a lateral right atrial incision. Mapping demonstrates a circuit circling the incision. Ablation from the end of the incision to either the superior vena cava or more commonly the inferior vena cava is often curative.90
It had been thought that there was conduction block between the donor and recipient atria in patients who have undergone heart transplantation. Recent reports have demonstrated re-entrant arrhythmias owing to donor–recipient atrial conduction. Mapping the connection between the atria can successfully ablate these arrhythmias.91–93 Atrial arrhythmias have also been reported in a number of patients who have undergone the surgical Maze procedure for atrial fibrillation. These treatment failures are most often caused by re-entrant circuits involving gaps in the Maze lesion or through alternative pathways such as the musculature surrounding the coronary sinus.94 These arrhythmias can now be successfully mapped and ablated. Mapping systems are useful in improving success of these ablations. The principle of interrupting these circuits by placing lesions to connect conduction barriers remains the same.95
Atrial fibrillation is another difficult-to-treat atrial tachycardia with variable targets for ablation. Atrial fibrillation is often symptomatic for patients owing to irregular and/or rapid ventricular rates. Patients can also be completely asymptomatic and present with stroke, dilated cardiomyopathy, or be diagnosed on routine examination. Medical therapy for atrial fibrillation is of limited efficacy and pharmacologic control of atrial fibrillation may be associated with increased mortality in large trials.96–99 In addition, sustained rapid ventricular rates can lead to a tachycardia-related cardiomyopathy.76,80 When medical therapy is aimed at maintaining sinus rhythm or blocking AV nodal conduction to slow ventricular response fails, ablation can be considered.100,101
In the past, AV nodal or His ablation, with placement of a permanent pacemaker, was considered in patients with difficult-to-control ventricular rates and symptomatic palpitations. The advantages of the approach are the relative ease and speed of the procedure. The downside is that it renders the patient pacemaker-dependent. Success rates of this procedure are nearly 100%.102 Complications of this procedure include the same complications as those seen in other ablation procedures. In highly symptomatic patients, this approach to the treatment of atrial fibrillation has been associated with improvement in quality of life and left ventricular function, and with a reduction in hospitalizations.103 Patients with congestive heart failure and atrial fibrillation may particularly benefit from this approach, and in some cases restoration of function will return as tachycardia slows, but in many cases it may be more beneficial to proceed directly with implantation of a cardiac resynchronization device, even in the setting of only minimally symptomatic ventricular dysfunction.104–106
Surgical experience with the Maze procedure to create lines of conduction block in the atrium has led the way for catheter-based ablation procedures to treat atrial fibrillation. Studies have attempted to replicate the success of the surgical procedure using a catheter-based approach. Atrial fibrillation consists of multiple re-entrant circuits within the atrium; around the vena cava, pulmonary veins, and appendages; and around areas of functional block.107 Creation of multiple lines of block between these nonconducting structures may prevent propagation of arrhythmic circuits.
Attempts at catheter-based left atrial or biatrial lesions for purpose of replicating the Maze have met with limited success because of the prolonged procedure times, high risk of complications, and limited efficacy.108,109 As understanding of the mechanism of atrial fibrillation has evolved, attempts to block propagation of atrial fibrillatory circuits have been abandoned in favor of attempted ablation of the fibrillatory triggers.
In a series of patients undergoing a left-sided catheter Maze procedure, it was discovered that rapidly firing premature atrial contractions arising from the musculature of the pulmonary veins were triggering atrial fibrillation.110 Ablation of these foci eliminated atrial fibrillation in some patients. This procedure has evolved to empiric electrical isolation of the pulmonary veins. One approach is the complete encircling of the pulmonary veins (ie, wide area circumferential ablation).111 Another approach is segmental isolation of each vein by mapping the location of the connecting fibers.112 The encircling and nonencircling procedures have shown to be equally efficacious in 6-month follow-up. The advantage to the nonencircling method, whereby the focus is on pulmonary vein exit block, is the ability to avoid a posterior wall line. The placement of posterior wall lines is thought to be responsible for the finding of atrioesophageal fistula postoperatively.
Data on the long-term efficacy and complications of this procedure are limited and it is still considered to be a procedure in evolution. In one series of 251 patients, the short-term success was 80%. There was an 85% success rate in those with paroxysmal and 68% success in those with permanent atrial fibrillation. There was a continued need for antiarrhythmic medications in some patients.113 In a study of those with paroxysmal atrial fibrillation, randomized therapy comparing medical management to catheter ablation has shown significant results. The A4 trial showed at 1-year, 23% of those randomized to antiarrhythmic drug therapy, and 89% of those randomized to ablation had no recurrence of atrial fibrillation.114 A recent meta-analysis of PV isolation for paroxysmal atrial fibrillation versus medical management found that at 1 year, ablation was associated with a 16-fold rate of freedom from atrial fibrillation (odds ratio, 15.78; 95% CI, 10.07 to 24.73) and with decreased hospitalization for cardiovascular causes (rate ratio, 0.15; 95% CI, 0.10 to 0.23).115
Although the procedure itself has been demonstrated to be effective, the method for optimizing outcomes is still in evolution. This is in part because of the mechanistic shift that goes from predominant PV triggers in those with paroxysmal atrial fibrillation, to a diseased atrium, manifest by complex fractionated atrial electrograms (CFAE) in those with persistent atrial fibrillation.29 In randomized trials, the addition of targeting of CFAE, to a conventional PV antral isolation did not result in increased freedom from recurrent arrhythmia.116,117 In a three-arm study, patients with paroxysmal atrial fibrillation were randomized to PV isolation, substrate modification targeting CFAE, or a combination of the two. At 1-year follow-up, freedom from AF/atrial tachyarrhythmia was documented in 89% of patients in the PV antral isolation group, 91% in the PV antral isolation plus CFAE group, and 23% in the group undergoing CFAE modification alone.118 In a study comparing the efficacy of adding linear lesions to PV antral isolation, a group was able to demonstrate increased maintenance of sinus rhythm in those with atrial fibrillation, although the results were much more apparent in those with persistent atrial fibrillation at baseline.119 Those with a more permanent form of atrial fibrillation have been demonstrated to have either atrial scarring or structural disease in 65%.120 Despite prior failure of antiarrhythmic therapy, long-term restoration of sinus rhythm could be seen in up to 94% of those patients after two procedures and while on antiarrhythmic drugs having undergone targeting of CFAE and PV antral isolation, whereby PV antral isolation alone had success in only 83% (p < .001).120 The role of antral or ostial isolation appears to favor antral isolation, both for reduction in pulmonary vein stenosis, and for efficacy. In one randomized trial of single procedure without drug therapy, the freedom from AF was 49% in those with single vein lasso-guided isolation, compared with 67% in those undergoing antral isolation of ipsilateral vein groupings (p ≤ 0.05).121
In a retrospective study comparing PV antral isolation versus AV node ablation and pacemaker implantation, the definitive rate control strategy was a shorter procedure and with fewer complications, and although there was higher rate of continued, albeit asymptomatic, atrial fibrillation, the procedure may be advocated for the older patient, or those with comorbidities, which may limit the procedural safety.114
One major complication of ablation within the pulmonary veins was focal pulmonary vein stenosis. In 102 patients undergoing pulmonary vein focal ablation, 39% with right upper vein ablation and 23% with left vein ablation developed focal pulmonary vein stenosis by transesophageal echocardiography 3 days after the procedure.122 In this series, only three patients experienced symptoms of dyspnea on exertion and only one had a mild increase in pulmonary pressure. Although most cases are asymptomatic, severe cases have been reported that progress to pulmonary hypertension and lung transplant. Changes to prevent this complication include limiting ablation within the vein ostia, limiting power, and using ultrasound imaging during ablation.123 Since its recognition as a possible adverse event, the occurrence postprocedurally should now be considered rare.
Ablation techniques can also target ventricular tachycardia (VT). Greater than 90% of life-threatening ventricular arrhythmias originate from myocardium with structural abnormalities. Regions of scarred or aneurysmal myocardium create channels for re-entrant circuits. Initial successes with resection of ventricular arrhythmogenic foci and re-entrant circuits surgically have led to advancements in catheter-based ablation techniques. Given the life-threatening potential of VT in patients with structural heart disease, even a single recurrence can be disastrous. Therefore, implantable cardiac defibrillators have become the primary therapy. Indications for ablation in this population are failure of antiarrhythmic medication to suppress symptomatic, sustained monomorphic VT, or more often frequent shocks from an implanted defibrillator despite optimal medical therapy.
Success of ischemic VT ablation is variable because of the heterogeneity of the population. Reported studies have shown efficacy in the range of 60 to 90% using the criteria of reduced defibrillator shocks and decreased need for antiarrhythmic medications. The recurrence rate is as high as 40%. Recently, success has been reported with an approach employing "substrate mapping." This technique defines the potential arrhythmic substrate using electroanatomical voltage maps. Ablation is targeted to eliminate potential re-entrant circuits. Complications are in the range of 2%, with concern for perforation and cardiac tamponade owing to the thin, scarred ventricles that are the substrates for ablation and thromboembolic events in those undergoing extensive ablation.124–128
In patients with dilated cardiomyopathy and His-Purkinje system disease, sustained monomorphic VT can occur because of a macro re-entrant circuit using the bundle branches. Patients typically present with syncope or sudden death or can present with palpitations. The most common circuit is down the right bundle branch and up the left bundle branch resulting in a wide complex tachycardia with a left bundle-branch block pattern. Treatment involves ablation of one of the fascicles involved in the re-entrant circuit. The right bundle is most commonly targeted to interrupt the re-entrant circuit. Long-term success is good for prevention of recurrent bundle branch re-entry. Because of intrinsic conduction disease, patients may develop heart block. Patients may also develop other VTs because of other structural abnormalities, requiring further ablation, antiarrhythmic therapy, or defibrillator implantation.129,130
Other cardiac disorders can be associated with VT and are potential candidates for catheter ablation. These include right ventricular dysplasia,131 infiltrative disorders (sarcoid),132,133 and tumors. As in patients with atrial arrhythmias caused by surgical incisions, patients with prior ventricular surgery can develop incision-related VT. This has occurred most often in patients who have undergone repair of congenital abnormalities such as tetralogy of Fallot,134 but has also been seen in patients after corrective valve surgery.135
Ventricular tachycardia that presents in patients with no structural heart disease is termed idiopathic and represents up to 10% of all VTs that present to tertiary referral centers. Patients may be asymptomatic or present with palpitations, dizziness, or syncope. Idiopathic VT may be focal or a micro–re-entrant circuit using the Purkinje fibers.
Right ventricular tachycardia typically originates from the outflow tract. It has typical left bundle-branch QRS morphology with leftward, inferior axis. This occurs more often in women than men, and patients typically present in their thirties to fifties. Idiopathic left ventricular tachycardia typically originates from the left posterior fascicle. It has a right bundle-branch morphology with rightward, superior axis, and may be verapamil sensitive. It occurs more often in men. These VTs are localized by activation or pace mapping. Ablation is facilitated by the lack of other cardiac pathology and the presence of only one VT. Success rates for idiopathic VT are in the range of 70 to 90% with recurrence rates in the range of 15%. Complication rates are consistent with those of other ablative procedures.136,137
Several studies have shown the cost-effectiveness of catheter ablation compared with medical therapy and surgical ablation. Catheter ablation has lower procedural costs than surgical ablation and reduces the need for further medical care and emergency department visits in comparison to drug therapy. Studies from the United States, Canada, the United Kingdom, and from Australia have shown both cost savings and improvement in quality of life for those undergoing catheter-based ablation compared to medical management.138–142
Of particular concern, is cost-effectiveness of catheter ablation for the treatment of atrial fibrillation. In a United States model looking at catheter ablation versus antiarrhythmic drugs for paroxysmal atrial fibrillation, although incremental cost-effectiveness for ablation was demonstrated to be only marginally favorable at $51,431 per quality adjusted life year over 5 years, there was no adjustment for known favorable effect on heart failure admissions, a not insignificant additional savings.143 In a Canadian model, although results demonstrated cost savings with antiarrhythmic drug therapy from 2 months to 1 year, the sustained benefit of ablation quickly led to demonstrable cost-savings within 2 years from time of ablation, and anticipated sustained benefit.138 One particular United Kingdom assessment found that for treatment of paroxysmal atrial fibrillation, catheter ablation had economic benefit compared to antiarrhythmic drug therapy alone with or without serial cardioversion.144 Of particular note was cost savings for catheter ablation in combination with antiarrhythmic drug therapy compared to drug therapy alone, in large part driven by reduction in healthcare utilization rather than the mere cost of the drug itself.