Robotics for catheter ablation of cardiac arrhythmias: Current technologies and practical approaches.

Robotic technology has emerged as an important tool to facilitate catheter ablation of arrhythmias. Robotic cardiac electrophysiology technology includes remote magnetic navigation and manual robotic navigation. Robotics can confer advantages with respect to ease of catheter manipulation in anatomically challenging spaces, minimization of fluoroscopic exposure to both patients and operators, and reduction in operator fatigue. This review provides a comprehensive summary of robotic electrophysiology technology, its practical applications and its safety and efficacy for targeting cardiac arrhythmias.

Effects of focal impulse and rotor modulation-guided ablation on atrial arrhythmia termination and inducibility: Impact on outcomes after treatment of persistent atrial fibrillation.

INTRODUCTION: The role of focal impulse and rotor modulation (FIRM)-guided ablation for the treatment of atrial fibrillation (AF) remains unclear. Previous studies on the FIRM-guided ablation outcomes have been limited by a focus on AF termination as an endpoint and by patient population heterogeneity. We sought to determine differences in rates of AF termination, inducibility, and recurrence in patients with persistent AF undergoing first-time ablation with a FIRM-guided approach compared with patients undergoing conventional ablation. METHODS AND RESULTS: Eight-five consecutive patients (38 FIRM, 47 conventional) with persistent AF undergoing first-time ablation were retrospectively analyzed. There were no significant differences in the rates of AF termination in the FIRM group compared to the conventional group (26% vs 15%; P = .15). Rates of inducible AF after ablation were 37% in the FIRM group and 30% in the conventional group (P = .32). Over a median follow-up of 2.4 years, the rates of freedom from AF were similar between the FIRM and conventional groups (1-year freedom from AF 65% vs 50%, respectively; P = .18). Procedural termination of AF with either FIRM ablation or conventional ablation was not associated with any significant reduction in AF recurrence. CONCLUSION: A FIRM-guided approach was not associated with a significant difference in freedom from AF when compared to conventional ablation. Termination of AF with ablation was not associated with increased freedom from AF. While AF termination using substrate-based ablation may have mechanistic implications for understanding AF rotor physiology, its impact on clinical outcomes remains unclear.

Comparison of robotic magnetic navigation-guided and manual catheter ablation of ventricular arrhythmias arising from the papillary muscles.

Aims: Due to the complex anatomy of the left ventricular (LV) and right ventricular (RV) papillary muscles (PMs), PM ventricular arrhythmias (VAs) can be challenging to target with ablation. We sought to compare the outcomes of robotic magnetic navigation-guided (RMN) ablation and manual ablation of VAs arising from the LV and RV PMs. Methods and results: We evaluated 35 consecutive patients (mean age 65 ± 12 years, 69% male) who underwent catheter ablation of 38 VAs originating from the LV and RV PMs as confirmed by intracardiac echocardiography. Catheter ablation was initially performed using RMN-guidance in 24 (69%) patients and manual guidance in 11 (31%) patients. Demographic and procedural data were recorded and compared between the two groups. The VA sites of origin were mapped to 20 (53%) anterolateral LV PMs, 14 (37%) posteromedial LV PMs, and 4 (11%) RV PMs Acute successful ablation was achieved for 20 (74%) VAs using RMN-guided ablation and 8 (73%) VAs using manual ablation (P = 1.000). Fluoroscopy times were significantly lower among patients undergoing RMN ablation compared to patients undergoing manual ablation [median 7.3, interquartile range (IQR) 3.9-18 vs. 24 (16-44) min; P = 0.005]. Retrograde transaortic approach was used in 1 (4%) RMN patients and 5 (46%) manual patients (P = 0.005). No procedural complications were seen in study patients. Conclusion: Use of an RMN-guided approach to target PM VAs results in comparable success rates seen with manual ablation but with lower fluoroscopy times and decreased use of transaortic retrograde access.

Left atrial thrombus and dense spontaneous echocardiographic contrast in patients on continuous direct oral anticoagulant therapy undergoing catheter ablation of atrial fibrillation: Comparison of dabigatran, rivaroxaban, and apixaban.

BACKGROUND: Left atrial thrombus (LAT) and dense spontaneous echocardiographic contrast (SEC) detected by transesophageal echocardiography (TEE) in patients on continuous direct oral anticoagulants (DOAC) therapy before catheter ablation of atrial fibrillation (AF) or atrial flutter (AFL) have been described. OBJECTIVE: We sought to compare rates of TEE-detected LAT and dense SEC among patients taking different DOACs. METHODS: We evaluated 609 consecutive patients from 3 tertiary hospitals (median age 65 years; interquartile range 58-71 years; 436 (72%) men) who were on ≥4 weeks of continuous DOAC therapy (dabigatran, n = 166 [27%]; rivaroxaban, n = 257 [42%]; or apixaban, n = 186 [31%]) undergoing TEE before catheter ablation of AF/AFL. Demographic, clinical, and TEE data were collected for each patient. RESULTS: Despite ≥4 weeks of continuous DOAC therapy, 17 patients (2.8%) had LAT and 15 patients (2.5%) had dense SEC detected by TEE. The rates of LAT were 3.0%, 3.5%, and 1.6% for patients on dabigatran, rivaroxaban, and apixaban, respectively (P = .482). The rates of dense SEC were 1.2%, 3.5%, and 2.2% for patients on dabigatran, rivaroxaban, and apixaban, respectively (P = .299). Congestive heart failure (odds ratio 4.4; 95% confidence interval 1.6-12; P = .003) and moderate/severe left atrial enlargement (odds ratio 3.1; 95% confidence interval 1.1-8.6; P = .026) were independent predictors of LAT. CONCLUSION: In this study, ∼3% of patients on continuous DOAC therapy had LAT detected before catheter ablation of AF/AFL. Specific DOAC therapy did not significantly affect the rates of LAT detection.

Utility of Pre-Induction Ventriculoatrial Response to Adenosine in the Diagnosis of Orthodromic Reciprocating Tachycardia.

OBJECTIVES: This study sought to evaluate the utility of ventriculoatrial (VA) conduction patterns in response to adenosine in predicting inducibility of orthodromic reciprocating tachycardia (ORT). BACKGROUND: Adenosine is known to consistently block atrioventricular (AV) nodal conduction. We hypothesized that persistent VA conduction despite administration of adenosine would have a high predictive value for identifying the presence of a retrograde accessory pathway (AP) and associated ORT. METHODS: A total of 168 patients undergoing electrophysiological study for supraventricular tachycardia (SVT) had assessment of VA conduction during ventricular pacing and adenosine administration. Standard pacing maneuvers were then used for induction and diagnosis of the SVT mechanism. RESULTS: Absence of VA block to adenosine (doses up to 24 mg) had 88% sensitivity and 91% specificity for identifying ORT (positive predictive value 76%, negative predictive value 96%). Four patients with adenosine-induced VA block and inducible ORT had decremental APs. Adenosine caused VA block in 6 patients with eccentric VA activation due to atypical AV nodal conduction, and concentric VA conduction persisted in all 12 patients with a septal AP. Adenosine unmasked free-wall APs in 10 patients by blocking AV nodal conduction, shifting VA activation from concentric to eccentric. CONCLUSIONS: The response of VA conduction to adenosine is a highly sensitive and specific method for detecting retrograde AP conduction and inducible ORT. Adenosine-induced VA block rules out inducible ORT due to a nondecremental AP. In cases of VA fusion, adenosine-induced block of AV nodal conduction can delineate the location of the AP atrial insertion site.

Differentiation of papillary muscle from fascicular and mitral annular ventricular arrhythmias in patients with and without structural heart disease.

BACKGROUND: Idiopathic left ventricular arrhythmias (VAs) and those caused by structural heart disease can originate from the papillary muscles, fascicles, and mitral annulus. Differentiation of these arrhythmias can be challenging because they present with a right bundle branch block morphology by electrocardiography. We sought to identify clinical, electrocardiographic, and electrophysiological features that distinguish these left VAs in patients with and without structural heart disease. METHOD AND RESULTS: Patients undergoing catheter ablation for papillary muscle, fascicular, or mitral annular VAs were studied. Demographic data and electrocardiographic and electrophysiological findings were analyzed. Fifty-two VAs in 51 patients (32 [63%] male; mean age 61±15 years) with papillary muscle (n=18), fascicular (n=15), and mitral annular (n=19) origins were studied. Patients with papillary muscle VAs were older and had higher prevalence of left ventricular dysfunction (67% versus 13% of fascicular VA patients [P=0.009]) and coronary artery disease (78% versus 37% of mitral annular VA patients [P=0.036]). Papillary muscle VAs were distinguished electrocardiographically from fascicular VAs by longer QRS durations and lower prevalence of r

Mechanisms and clinical significance of adenosine-induced dormant accessory pathway conduction after catheter ablation.

BACKGROUND: Adenosine can unmask dormant pulmonary vein conduction after isolation. The role of adenosine in uncovering dormant accessory pathway (AP) conduction after AP ablation is unknown. METHODS AND RESULTS: We evaluated 109 consecutive patients (age, 41 ± 28 years; 62 [57%] men) who were administered adenosine after successful AP ablation. Dormant AP conduction was defined as adenosine-induced recurrent AP conduction, as demonstrated by recurrent preexcitation or change in retrograde ventriculoatrial activation patterns. Dormant AP conduction was identified in 13 (12%) patients. Adenosine led to transient retrograde AP conduction in 6 patients and transient anterograde AP conduction in 8 patients. In all these cases, adenosine-induced AP conduction occurred during the bradycardia phase of adenosine effect and resulted in dormant AP conduction times shorter than atrioventricular nodal conduction times before adenosine administration. On the basis of analysis of timing of occurrence of dormant AP conduction, the mechanism of adenosine-induced AP conduction was determined to be caused by AP excitability recovery in ≥ 12 (92%) cases. The presence of dormant AP conduction was a significant predictor of chronic recurrent AP conduction requiring repeat ablation (odds ratio, 8.54; 95% confidence interval, 1.09-66.9; P=0.041). CONCLUSIONS: Adenosine can unmask dormant AP conduction after catheter ablation. Direct effects of adenosine on the AP, possibly via AP membrane potential hyperpolarization, are the dominant mechanism of adenosine-induced AP conduction after ablation. Dormant AP conduction is associated with higher rates of recurrent AP conduction requiring repeat ablation.

Ubiquitous myocardial extensions into the pulmonary artery demonstrated by integrated intracardiac echocardiography and electroanatomic mapping: changing the paradigm of idiopathic right ventricular outflow tract arrhythmias.

BACKGROUND: Idiopathic ventricular arrhythmias of left bundle branch block inferior axis morphology are usually localized to the right ventricular outflow tract (RVOT), presumably below the pulmonic valve (PV). However, the PV location is usually not confirmed by direct visualization. METHODS AND RESULTS: Intracardiac echocardiography was used to visualize and tag the PV annulus, which was then integrated with 3-dimensional voltage maps of the RVOT. Distances were measured from the furthest extent of myocardial signal (bipolar voltage ≥1.5 mV) to the PV annulus. This was performed in 24 control patients and 24 prospective patients with RVOT arrhythmias. Myocardial signal beyond the PV was found in 92% of controls and 88% of RVOT arrhythmia patients (P=1.000). Average myocardial extension was further on the septal side than on the free wall side for control patients (5.6 mm; interquartile range [IQR], 3.6-7.7, versus 1.7 mm; IQR (-)0.1 to (+)4.0; P=0.002) and RVOT arrhythmia patients (5.7 mm; IQR, 2.7-7.7, versus 1.4 mm; IQR, (-)0.8 to (+)4.8; P=0.004). Eleven (46%) RVOT arrhythmia foci were localized beyond the valve in the pulmonary artery (median 8.2 mm above PV; IQR, 6.6-10.3 mm); these locations were confirmed as supravalvular by direct intracardiac echocardiography visualization. CONCLUSIONS: Myocardial voltage extension into the pulmonary artery in humans is ubiquitous and can be demonstrated in vivo using 3-dimensional integrated intracardiac echocardiography to localize the PV. These extensions frequently serve as origins of presumed RVOT arrhythmias; intracardiac echocardiography localization of the PV allows reclassification of these as pulmonary arterial arrhythmias.

Unifying mechanism of sustained idiopathic atrial and ventricular annular tachycardia.

BACKGROUND: Based on the current understanding of cardiac conduction system development and the observation that arrhythmogenic foci can originate in areas near the atrioventricular annuli, we hypothesized that focal annular tachycardias, whether atrial or ventricular, share a common mechanism. We, therefore, prospectively evaluated this hypothesis in patients with sustained atrial and ventricular tachycardia originating from the peri-tricuspid and mitral annuli. METHODS AND RESULTS: Forty-nine consecutive patients with sustained, focal annular tachycardia comprised the study group. All underwent electrophysiological evaluation and the mode of tachycardia initiation, termination, sensitivity to catecholamine infusion, and response to adenosine/verapamil were evaluated. Electroanatomical activation maps identified the sites of arrhythmia origin. Tachycardias could be initiated or terminated or both with programmed stimulation in 46 of 46 patients and most (70%) were catecholamine facilitated. Of the 9 patients with sustained annular ventricular tachycardia, 3 were localized to the tricuspid annulus, and 6 to the mitral annulus. All the 9 ventricular tachycardias (100%) terminated with adenosine, 2 of 2 terminated with verapamil, and 2 of 2 terminated with Valsalva. Of the 40 patients with annular atrial tachycardia, 4 tachycardias were localized to the mitral annulus and 37 to the tricuspid annulus (including 9 para-Hisian), and all were adenosine sensitive. CONCLUSIONS: Peri-annular atrial and ventricular tissue correspond to a region enriched with arrhythmogenic foci, which may reflect a common developmental origin. Furthermore, the sensitivity of these tachycardias to adenosine provides evidence for a shared arrhythmia mechanism, consistent with intracellular calcium overload and triggered activity.

Adenosine-induced pulmonary vein ectopy as a predictor of recurrent atrial fibrillation after pulmonary vein isolation.

BACKGROUND: Adenosine can unmask dormant pulmonary vein (PV) conduction after PV isolation. Adenosine can also induce ectopy in electrically silent PVs after isolation, possibly via activation of autonomic triggers. We sought to identify the implications of adenosine-induced PV ectopy for atrial fibrillation (AF) recurrence after PV isolation. METHODS AND RESULTS: A total of 152 patients (age, 60±11 years; 63% paroxysmal AF) undergoing PV isolation for AF were studied. After each PV was isolated, adenosine was administered and the presence of adenosine-induced PV reconnection and PV ectopy were recorded. Dormant conduction was targeted with additional ablation. Adenosine-induced PV ectopy was seen in 45 (30%) patients, and dormant conduction was seen in 44 (29%) patients. After a median follow-up of 374 days, 48 (32%) patients had recurrent AF after a single ablation procedure. Rates of freedom from AF among patients with adenosine-induced PV ectopy were significantly lower than patients without adenosine-induced PV ectopy (63% versus 76% at 1 year; log rank, 0.014). Rates of freedom from AF among patients with dormant conduction were also lower than patients without dormant conduction (64% versus 76% at 1 year; log rank, 0.062). With multivariate analysis, adenosine-induced PV ectopy was found to be the only independent predictor of AF after PV isolation (hazard ratio, 1.90; 95% confidence interval, 1.06-3.40; P=0.032). CONCLUSIONS: Adenosine-induced PV ectopy is a predictor of recurrent AF after PV isolation and may be a marker of increased susceptibility to autonomic triggers of AF.

Method for differentiating left superior pulmonary vein exit conduction from pseudo-exit conduction.

BACKGROUND: Electrical isolation of pulmonary vein (PV) conduction from the left atrium (LA) is the cornerstone of successful atrial fibrillation (AF) ablation. Exit block is confirmed by the absence of LA capture during pacing from a circular mapping catheter positioned in the PV; however, far-field capture of the left atrial appendage (LAA) (pseudo-pulmonary vein exit conduction) can occur. In this study, we evaluated a methodology for identifying pseudo-exit conduction. METHODS AND RESULTS: A total of 135 consecutive AF patients undergoing PV isolation were studied. After circumferential ablation established PV entrance block, circumferential pacing (10 mA at 2.0 msec) was performed to assess exit block. In 16 (11.9%) patients, pacing the anterior poles of the left superior PV (LSPV) captured the LA. To differentiate true PV exit conduction from pseudo-exit conduction, the ablation catheter was positioned within the LAA during PV pacing. LAA activation preceding PV capture was consistent with far-field capture and this was confirmed by demonstrating local capture and exit block with decreasing pacing output. Using this approach, 14 patients (10.4%) were identified with pseudo-exit conduction. CONCLUSIONS: Due to the close proximity between the LSPV and LAA, pseudo-exit conduction is not uncommon and may lead to the erroneous conclusion that the LSPV is not isolated. Using this method to differentiate pseudo-exit conduction from true exit conduction should prevent unnecessary ablation after achievement of complete PV isolation.

A novel criterion for conduction block after catheter ablation of right atrial tachycardia after mitral valve surgery.

BACKGROUND: One operative approach to the mitral valve, the superior transseptal incision, is proarrhythmic because of extensive atriotomies. The objective of this study is to describe complex atrial tachycardias (ATs) that occur after this approach and propose methods to verify lines of block as an end point for catheter ablation. METHODS AND RESULTS: Of the 69 patients who had electrophysiological studies for AT after mitral valve surgery, 20 patients had prior superior transseptal incisions. Of these, 14 had complex ATs involving the lateral right atrium (RA). There were 9 dual-loop, 4 single-loop, and 1 focal tachycardias. Lateral wall ablation was performed either by creating a linear lesion from the lateral atriotomy to the inferior vena cava, superior vena cava, or tricuspid annulus or by ablating focally in the lateral RA. After a single ablation procedure, conduction block in the lateral wall was verified in 10 of 14 patients using 1 of 2 distinct patterns of block. One pattern consisted of late activation in an anterolateral corridor of the RA, and a second pattern consisted of wide-spaced double potentials. Recurrent conduction through the lateral wall lesions was associated with intraprocedural and late recurrences of ATs. CONCLUSIONS: The optimal end point for ablating ATs after mitral valve surgery with the superior transseptal approach is to establish lines of block that can be recognized by characteristic patterns of activation in the lateral RA. A novel criterion for lateral conduction block after catheter ablation is identification of a late-activated corridor in the anterolateral RA.

Differentiating pacemaker-mediated tachycardia from tachycardia due to atrial tracking: utility of V-A-A-V versus V-A-V response after postventricular atrial refractory period extension.

BACKGROUND: Dual-chamber pacemaker systems can lead to two forms of pacemaker-facilitated tachycardia: pacemaker-mediated tachycardia (PMT) and tracking of sinus or atrial tachycardia. Current pacemaker algorithms cannot always differentiate between these two tachycardias. OBJECTIVE: The purpose of this study was to investigate a novel algorithm for distinguishing the two mechanisms of pacemaker-facilitated tachycardia, which is based on the specific termination response to postventricular atrial refractory period (PVARP) extension. METHODS: We prospectively tested our algorithm using the Medtronic Virtual Interactive patient (VIP) II simulator (version 1.53) and a Medtronic Adapta ADDR01 dual-chamber pacemaker. RESULTS: Thirty-five scenarios that triggered "PMT detection" by the device were evaluated. All 12 scenarios of atrial tachycardias with intact AV conduction terminated with a Vp-Ar-Vs (V-A-V) response as a result of PVARP extension. Of the 11 scenarios of atrial tachycardia with complete heart block, all terminated with a Vp-Ar-As-Vp response. All four episodes of PMT with intact AV conduction terminated with a Vp-Ar-As-Vs (V-A-A-Vs) response. Of the eight episodes of PMT with complete heart block, all terminated with a Vp-Ar-As-Vp response. CONCLUSION: In the presence of intact AV conduction, the V-A-V response to PVARP extension is specific to atrial (or sinus) tachycardia, whereas the V-A-A-Vs response is specific to PMT. Recognizing the difference between the two forms of pacemaker-facilitated tachycardias has important implications for pacemaker programming.

Predictive value of microvolt T-wave alternans in patients with left ventricular dysfunction.

OBJECTIVES: The purpose of this study was to prospectively evaluate the utility of microvolt T-wave alternans (TWA) in predicting arrhythmia-free survival and total mortality in patients with left ventricular (LV) dysfunction. BACKGROUND: Microvolt TWA has been proposed as a useful tool in identifying patients unlikely to benefit from prophylaxis with implantable cardioverter-defibrillator (ICD) prophylaxis. METHODS: We evaluated 286 patients with an LV ejection fraction