Termination of a long RP supraventricular tachycardia by carotid sinus massage.

Carotid sinus massage is a useful diagnostic and therapeutic maneuver in patients with supraventricular tachycardia. Abrupt tachycardia termination with carotid sinus massage typically indicates a mechanism dependent on the atrioventricular node. Here, we present the case of a 79-year-old patient presenting with a long-RP supraventricular tachycardia terminated with carotid sinus massage that was proven invasively to be due to a focal atrial tachycardia. We discuss mechanistic explanations for this unusual phenomenon and review the literature.

Bundle Branch Re-Entrant Ventricular Tachycardia: Novel Genetic Mechanisms in a Life-Threatening Arrhythmia.

OBJECTIVES: This study sought to investigate for an underlying genetic etiology in cases of apparent idiopathic bundle branch re-entrant ventricular tachycardia (BBRVT). BACKGROUND: BBRVT is a life-threatening arrhythmia occurring secondary to macro-re-entry within the His-Purkinje system. Although classically associated with dilated cardiomyopathy, BBRVT may also occur in the setting of isolated, unexplained conduction system disease. METHODS: Cases of BBRVT with normal biventricular size and function were recruited from 6 North American centers. Enrollment required a clinically documented wide complex tachycardia and BBRVT proven during invasive electrophysiology study. Study participants were screened for mutations within genes associated with cardiac conduction system disease. Pathogenicity of identified mutations was evaluated using in silico phylogenetic and physicochemical analyses and in vitro biophysical studies. RESULTS: Among 6 cases of idiopathic BBRVT, each presented with hemodynamic compromise and 2 suffered cardiac arrests requiring resuscitation. Putative culprit mutations were identified in 3 of 6 cases, including 2 in SCN5A (Ala1905Gly [novel] and c.4719C>T [splice site mutation]) and 1 in LMNA (Leu327Val [novel]). Biophysical analysis of mutant Ala1905Gly Nav1.5 channels in tsA201 cells revealed significantly reduced peak current density and positive shifts in the voltage-dependence of activation, consistent with a loss-of-function. The SCN5A c.4719C>T splice site mutation has previously been reported as disease-causing in 3 cases of Brugada syndrome, whereas the novel LMNA Leu327Val mutation was associated with a classic laminopathy phenotype. Following catheter ablation, BBRVT was noninducible in all cases and none experienced a clinical recurrence during follow-up. CONCLUSIONS: Our investigation into apparent idiopathic BBRVT has identified the first genetic culprits for this life-threatening arrhythmia, providing further insight into its underlying pathophysiology and emphasizing a potential role for genetic testing in this condition. Our findings also highlight BBRVT as a novel genetic etiology of unexplained sudden cardiac death that can be cured with catheter ablation.

Five-year outcome of catheter ablation of persistent atrial fibrillation using termination of atrial fibrillation as a procedural endpoint.

BACKGROUND: This study aimed to determine 5-year efficacy of catheter ablation for persistent atrial fibrillation (AF) using AF termination as a procedural end point. METHODS AND RESULTS: One hundred fifty patients (57±10 years) underwent persistent AF ablation using a stepwise ablation approach (pulmonary vein isolation, electrogram-guided, and linear ablation) with the desired procedural end point being AF termination. Repeat ablation was performed for recurrent AF or atrial tachycardia. AF was terminated by ablation in 120 patients (80%). Arrhythmia-free survival rates after a single procedure were 35.3%±3.9%, 28.0%±3.7%, and 16.8%±3.2% at 1, 2, and 5 years, respectively. Arrhythmia-free survival rates after the last procedure (mean 2.1±1.0 procedures) were 89.7%±2.5%, 79.8%±3.4%, and 62.9%±4.5%, at 1, 2, and 5 years, respectively. During a median follow-up of 58 (interquartile range, 43-73) months after the last ablation procedure, 97 of 150 (64.7%) patients remained in sinus rhythm without antiarrhythmic drugs. Another 14 (9.3%) patients maintained sinus rhythm after reinitiation of antiarrhythmic drugs, and an additional 15 (10.0%) patients regressed to paroxysmal recurrences only. Failure to terminate AF during the index procedure (hazard ratio 3.831; 95% confidence interval, 2.070-7.143; P<0.001), left atrial diameter≥50 mm (hazard ratio 2.083; 95% confidence interval, 1.078-4.016; P=0.03), continuous AF duration≥18 months (hazard ratio 1.984; 95% confidence interval, 1.024-3.846; P<0.04), and structural heart disease (hazard ratio 1.874; 95% confidence interval, 1.037-3.388; P=0.04) predicted arrhythmia recurrence. CONCLUSIONS: In patients with persistent AF, an ablation strategy aiming at AF termination is associated with freedom from arrhythmia recurrence in the majority of patients over a 5-year follow-up period. Procedural AF nontermination and specific baseline factors predict long-term outcome after ablation.

Inverse relationship between fractionated electrograms and atrial fibrosis in persistent atrial fibrillation: combined magnetic resonance imaging and high-density mapping.

OBJECTIVES: This study sought to evaluate the relationship between fibrosis imaged by delayed-enhancement (DE) magnetic resonance imaging (MRI) and atrial electrograms (Egms) in persistent atrial fibrillation (AF). BACKGROUND: Atrial fractionated Egms are strongly related to slow anisotropic conduction. Their relationship to atrial fibrosis has not yet been investigated. METHODS: Atrial high-resolution MRI of 18 patients with persistent AF (11 long-lasting persistent AF) was registered with mapping geometry (NavX electro-anatomical system (version 8.0, St. Jude Medical, St. Paul, Minnesota)). DE areas were categorized as dense or patchy, depending on their DE content. Left atrial Egms during AF were acquired using a high-density, 20-pole catheter (514 ± 77 sites/map). Fractionation, organization/regularity, local mean cycle length (CL), and voltage were analyzed with regard to DE. RESULTS: Patients with long-lasting persistent versus persistent AF had larger left atrial (LA) surface area (134 ± 38 cm(2) vs. 98 ± 9 cm(2), p = 0.02), a higher amount of atrial DE (70 ± 16 cm(2) vs. 49 ± 10 cm(2), p = 0.01), more complex fractionated atrial Egm (CFAE) extent (54 ± 16 cm(2) vs. 28 ± 15 cm(2), p = 0.02), and a shorter baseline AF CL (147 ± 10 ms vs. 182 ± 14 ms, p = 0.01). Continuous CFAE (CFEmean [NavX algorithm that quantifies Egm fractionation] <80 ms) occupied 38 ± 19% of total LA surface area. Dense DE was detected at the left posterior left atrium. In contrast, the right posterior left atrium contained predominantly patchy DE. Most CFAE (48 ± 14%) occurred at non-DE LA sites, followed by 41 ± 12% CFAE at patchy DE and 11 ± 6% at dense DE regions (p = 0.005 and p = 0.008, respectively); 19 ± 6% CFAE sites occurred at border zones of dense DE. Egms were less fractionated, with longer CL and lower voltage at dense DE versus non-DE regions: CFEmean: 97 ms versus 76 ms, p < 0.0001; local CL: 153 ms versus 143 ms, p < 0.0001; mean voltage: 0.63 mV versus 0.86 mV, p < 0.0001. CONCLUSIONS: Atrial fibrosis as defined by DE MRI is associated with slower and more organized electrical activity but with lower voltage than healthy atrial areas. Ninety percent of continuous CFAE sites occur at non-DE and patchy DE LA sites. These findings are important when choosing the ablation strategy in persistent AF.

Prevalence and types of pitfall in the assessment of mitral isthmus linear conduction block.

BACKGROUND: To identify and understand clinically encountered pitfalls in the assessment of transmitral conduction block using differential coronary sinus and left atrial appendage pacing techniques in patients with left mitral isthmus linear ablation. METHODS AND RESULTS: All the available assessments of mitral isthmus block were thoroughly reviewed in 271 mitral isthmus ablation procedures undertaken among 236 patients from October 2008 to April 2011. Bidirectional block was established in 186 of 271 (69%) procedures. Careful evaluation of electrograms recorded on the multipolar coronary sinus and ablation catheters was undertaken to identify and understand the characteristics of pitfall, if any. Pitfall was encountered in 55 of 271 (20%) procedures among 51 patients and categorized into 6 types (types 1, 3, 4, and 5 led to spurious diagnosis of block; types 2 and 6 led to erroneous diagnosis of absence of block). There were 14, 10, 17, 2, 15, and 3 (total=61) cases of pitfall types 1 through 6, respectively. Operator recognized 42 of 61 (69%) pitfalls intraprocedurally. Recognition of types 1 and 5 was difficult because of indiscernible electrograms at usual amplifier settings or presence of slow conduction mimicking block. CONCLUSIONS: Every fifth assessment of bidirectional block across mitral isthmus linear lesion using differential coronary sinus and left atrial appendage pacing techniques encounters a pitfall, which can lead to erroneous clinical diagnosis of block or absence of block. Recognition of pitfall during the procedure is feasible and necessitates careful distinction of far-field left atrium from the local coronary sinus electrograms besides appropriate adjustments in catheter position and pacing outputs.

Syncope in Brugada syndrome patients: prevalence, characteristics, and outcome.

BACKGROUND: The report from the 2nd Consensus Committee on BrS suggests that all patients with syncope without a "clear extracardiac cause" should have an implantable cardioverter-defibrillator (ICD). However, a clear extracardiac cause for syncope may be difficult to prove. OBJECTIVE: The purpose of this study was to characterize syncope in patients with Brugada syndrome (BrS). METHODS: All patients diagnosed with BrS at our institution between 1999 and 2010 were enrolled in a prospective registry. Patients with suspected arrhythmic syncope (group 1) were compared to patients with nonarrhythmic syncope (group 2) and to patients with syncope of doubtful origin (group 3). RESULTS: Of 203 patients with BrS, 57 (28%; 44 male, age 46 ± 12 years) experienced at least 1 syncope. Group 1 consisted of 23 patients, all of whom received an ICD. In group 2 (17 patients), 3 received an ICD because of a positive electrophysiologic study. In group 3 (17 patients), 6 received an implantable loop recorder and 6 received an ICD. After mean follow-up of 65 ± 42 months, 14 patients in group 1 remained asymptomatic, 4 had recurrent syncope, and 6 had appropriate ICD therapy. In group 2, 9 patients remained asymptomatic and 7 had recurrent neurocardiogenic syncope. In group 3, 7 remained asymptomatic and 9 had recurrent syncope. One patient from each group died from a noncardiac cause. CONCLUSION: In the present study, syncope occurred in 28% of patients with BrS. The ventricular arrhythmia rate was 5.5% per year in group 1. In 30%, the etiology of the syncope was questionable. No sudden cardiac death occurred in groups 2 and 3.

Diagnostic pacing maneuvers for supraventricular tachycardias: part 2.

The approach to supraventricular tachycardia (SVT) diagnosis can be complex because it involves synthesizing baseline electrophysiologic features, features of the SVT, and the response(s) to pacing maneuvers. In this two-part review, we will mainly explore the latter while recognizing that neither of the former can be ignored, for they provide the context in which diagnostic pacing maneuvers must be correctly chosen and interpreted. Part 1 involved a detailed consideration of ventricular overdrive pacing, since this pacing maneuver provides the diagnosis in the majority of cases. In Part 2, other diagnostic pacing maneuvers that might be helpful when ventricular overdrive pacing is not diagnostic or appropriate, including attempts to reset SVT with single atrial or ventricular beats, para-Hisian pacing, apex versus base pacing, and atrial overdrive pacing, are discussed, as are some specific diagnostic SVT challenges encountered in the electrophysiology lab. There is considerable literature on this topic, and this review is by no means meant to be all-encompassing. Rather, we hope to clearly explain and illustrate the physiology, strengths, and weaknesses of what we consider to be the most important and commonly employed diagnostic pacing maneuvers, that is, those that trainees in cardiac electrophysiology should be well familiar with at a minimum.

Disparate activation of the coronary sinus and inferior left atrium during atrial tachycardia after persistent atrial fibrillation ablation: prevalence, pitfalls, and impact on mapping.

INTRODUCTION: Persistent atrial fibrillation (AF) ablation may lead to partial disconnection of the coronary sinus (CS). As a result, disparate activation sequences of the local CS versus contiguous left atrium (LA) may be observed during atrial tachycardia (AT). We aimed to evaluate the prevalence of this phenomenon and its impact on activation mapping. METHODS: AT occurring after persistent AF ablation were investigated in 74 consecutive patients. Partial CS disconnection during AT was suspected when double potentials with disparate activation sequences were observed on the CS catheter. Endocardial mapping facing CS bipoles was performed to differentiate LA far-field from local CS potentials. RESULTS: A total of 149 ATs were observed. Disparate LA-CS activations were apparent in 20 ATs after magnifying the recording scale (13%). The most common pattern (90%) was distal to proximal endocardial LA activation against proximal to distal CS activation, the latter involving the whole CS or its distal part. Perimitral macroreentry was more common when disparate LA-CS activations were observed (67% vs 29%; P = 0.002). Partial CS disconnection also resulted in "pseudo" mitral isthmus (MI) block during LA appendage pacing in 20% of patients as local CS activation was proximal to distal despite distal to proximal activation of the contiguous LA. CONCLUSION: Careful analysis of CS recordings during AT following persistent AF ablation often reveals disparate patterns of activation. Recognizing when endocardial LA activation occurs in the opposite direction to the more obvious local CS signals is critical to avoid misleading interpretations during mapping of AT and evaluation of MI block.

Functional nature of electrogram fractionation demonstrated by left atrial high-density mapping.

BACKGROUND: Complex fractionated atrial electrograms (CFAE) are targets of atrial fibrillation (AF) ablation. Serial high-density maps were evaluated to understand the impact of activation direction and rate on electrogram (EGM) fractionation. METHODS AND RESULTS: Eighteen patients (9 persistent) underwent high-density, 3-dimensional, left-atrial mapping (>400 points/map) during AF, sinus (SR), and CS-paced (CSp) rhythms. In SR and CSp, fractionation was defined as an EGM with ≥4 deflections, although, in AF, CFE-mean <80 ms was considered as continuous CFAE. The anatomic distribution of CFAE sites was assessed, quantified, and correlated between rhythms. Mechanisms underlying fractionation were investigated by analysis of voltage, activation, and propagation maps. A minority of continuous CFAE sites displayed EGM fractionation in SR (15+/-4%) and CSp (12+/-8%). EGM fractionation did not match between SR and CSp at 70+/-10% sites. Activation maps in SR and CSp showed that wave collision (71%) and regional slow conduction (24%) caused EGM fractionation. EGM voltage during AF (0.59+/-0.58 mV) was lower than during SR and CSp (>1.0 mV) at all sites. During AF, the EGM voltage was higher at continuous CFAE sites than at non-CFAE sites (0.53 mV (Q1, Q3: 0.33 to 0.83) versus 0.30 mV (Q1, Q3: 0.18 to 0.515), P<0.00001). Global LA voltage in AF was lower in patients with persistent AF versus patients with paroxysmal AF (0.6+/-0.59 mV versus 1.12+/-1.32 mV, P<0.01). CONCLUSIONS: The distribution of fractionated EGMs is highly variable, depending on direction and rate of activation (SR versus CSp versus AF). Fractionation in SR and CSp rhythms mostly resulted from wave collision. All sites with continuous fractionation in AF displayed normal voltage in SR, suggesting absence of structural scar. Thus, many fractionated EGMs are functional in nature, and their sites dynamic.

Mitral isthmus ablation with and without temporary spot occlusion of the coronary sinus: a randomized clinical comparison of acute outcomes.

OBJECTIVE: To evaluate the safety and outcomes of mitral isthmus (MI) linear ablation with temporary spot occlusion of the coronary sinus (CS). BACKGROUND: CS blood flow cools local tissue precluding transmurality and bidirectional block across MI lesion. METHODS: In a randomized, controlled trial (CS-occlusion = 20, Control = 22), MI ablation was performed during continuous CS pacing to monitor the moment of block. CS was occluded at the ablation site using 1 cm spherical balloon, Swan-Ganz catheter with angiographic confirmation. Ablation was started at posterior mitral annulus and continued up to left inferior pulmonary vein (LIPV) ostium using an irrigated-tip catheter. If block was achieved, balloon was deflated and linear block confirmed. If not, additional ablation was performed epicardially (power ≤25 W). Ablation was abandoned after ∼30 minutes, if block was not achieved. RESULTS: CS occlusion (mean duration -27 ± 9 minutes) was achieved in all cases. Complete MI block was achieved in 13/20 (65%) and 15/22 (68%) patients in the CS-occlusion and control arms, respectively, P = 0.76. Block was achieved with significantly small number (0.5 ± 0.8 vs 1.9 ± 1.1, P = 0.0008) and duration (1.2 ± 1.7 vs 4.2 ± 3.5 minutes, P = 0.009) of epicardial radiofrequency (RF) applications and significantly lower amount of epicardial energy (1.3 ± 2.4 vs 6.3 ± 5.7 kJ, P = 0.006) in the CS-occlusion versus control arm, respectively. There was no difference in total RF (22 ± 9 vs 23 ± 11 minutes, P = 0.76), procedural (36 ± 16 vs 39 ± 20 minutes, P = 0.57), and fluoroscopic (13 ± 7 vs 15 ± 10 minutes, P = 0.46) durations for MI ablation between the 2 arms. Clinically uneventful CS dissection occurred in 1 patient CONCLUSIONS: Temporary spot occlusion of CS is safe and significantly reduces the requirement of epicardial ablation to achieve MI block. It does not improve overall procedural success rate and procedural duration. Tissue cooling by CS blood flow is just one of the several challenges in MI ablation.

Instantaneous electrophysiological changes characterizing achievement of mitral isthmus linear block.

BACKGROUND: Achievement of complete conduction block across left mitral isthmus (MI) is a challenging endpoint of linear lesion, and recognizing the precise moment of block is important during ongoing ablation. The objective of this study is to evaluate the changes in P wave morphology and local MI potential at the moment of block during ongoing radiofrequency (RF) application. METHODS AND RESULTS: We evaluated 69 patients (procedures) in whom successful MI linear conduction block was achieved during coronary sinus (CS) pacing. P wave morphology and/or local MI potential could be evaluated in 64 (93%) and 69 (100%) procedures, respectively. The achievement of MI block was associated with substantial instantaneous changes in 57/69 (82.6%) procedures. P wave morphology changed in 44 (64%) procedures with the change restricted to lateral leads in 39 (57%). Abrupt prolongation of local conduction delay from 106 ± 24 ms to 167 ± 39 ms (P < 0.0001) was observed on proximal bipole of ablation catheter in 34/69 (49.3%) procedures during ongoing RF application. In addition, prolongation of conduction delay was associated with significant change in the electrogram amplitude and polarity in 11 and 19 procedures, respectively. The substantial change in P wave morphology was not observed in any patients without achievement of complete block. CONCLUSIONS: The achievement of conduction block across MI line is associated with recognizable changes in the local MI electrograms and the P wave morphology especially in the lateral leads. These instantaneous critical changes may assist catheter ablation and indicate the requirement for prolonged RF application, if necessary.