Identification of 2 Distinct Boundaries Distinguishes Critical From Noncritical Isthmuses in Ablating Atypical Atrial Flutter.

BACKGROUND: Atypical atrial flutters often involve complex circuits. Classic methods of identifying ablation targets, including detailed electroanatomical mapping and entrainment within a well-defined isthmus, may not always be sufficient to allow the critical isthmus to be delineated and ablated, with flutter termination and prevention of reinduction. OBJECTIVES: This study sought a systematic method to classify conduction barriers and isthmuses as critical or noncritical that would improve understanding and ablation success. We also sought a construct unifying single- and dual-loop re-entry. Re-entrant circuits are bounded on 2 sides, although these are not consistently identified. We hypothesized 2 distinct critical boundaries, and a critical isthmus could be consistently defined without requiring entrainment, and ablation connecting these 2 boundaries would terminate tachycardia. METHODS: Activation maps were created electroanatomically. Conduction barriers were classified as noncritical barriers or critical boundaries. Critical boundaries showed sequential activation around the barrier, spanning ≥90% of the cycle length. Noncritical barriers showed nonsequential, parallel, or colliding activation or <90% of the cycle length. Only tissue separating the 2 critical boundaries defined a critical isthmus (CI); all others were considered noncritical. The effect of ablation across a CI was assessed. RESULTS: Complete maps were obtained in 128 cases in 121 patients (28 atypical right atrial, 100 left atrial). In all cases, 2 distinct critical boundaries were identified. Ablation across a CI connecting these critical boundaries terminated tachycardia in 123 of 128 cases (96.1%). Failures were due to inability to achieve block across the isthmus. CONCLUSIONS: Activation mapping of atypical atrial flutter allows consistent identification of 2 critical boundaries. Successful ablation connecting the 2 critical boundaries reliably results in termination of atypical atrial flutter.

Wolff-Parkinson-White, Brugada phenocopy, and flecainide toxicity: All in one patient.

Accessory pathway Wolff-Parkinson-white is sometimes not manifested till later in life, as the conduction properties of AV node become slower, other mechanisms are also possible. Brugada pattern on EKG can be associated with various underlying clinical conditions, such as mechanical compression of RVOT by tumors. It is essential to have high index of suspicion for flecainide toxicity when encountering arrhythmias in patients taking the drug.

Routine Implant of Biventricular Devices Guided by an Electroanatomic Mapping System - Ready for Prime-Time?

Biventricular devices play an important adjunctive role in the treatment of heart failure. However, biventricular device implantation is associated with significant radiation exposure and a high proportion of non-response to cardiac resynchronization therapy (CRT). The use of electroanatomic mapping (EAM) during biventricular device implantation may help overcome these issues. This article will review the literature on the role of EAM in biventricular device implantation.

Electroanatomic mapping of postpacing intervals clarifies the complete active circuit and variants in atrial flutter.

BACKGROUND: Typical atrial flutter is characterized by cavotricuspid isthmus dependence and activation sequentially around the tricuspid annulus (TA), usually counterclockwise. However, analysis of the upper portion of the annulus by postpacing interval after entrainment sometimes suggests it is outside the circuit. Details on the true active circuit are limited, particularly in the upper portions. OBJECTIVE: The purpose of this study was to define the full active circuit in atrial flutter. METHODS: In 26 patients with isthmus-dependent atrial flutter, we created detailed electroanatomic maps of postpacing intervals throughout the entire right atrium. Postpacing intervals within 20 ms of the flutter cycle length were defined as within the circuit. RESULTS: Creating postpacing interval maps allowed characterization of the full active circuit in all patients, and revealed significant variations despite similar counterclockwise or clockwise patterns with activation mapping. In 8, the active circuit was solely around the TA. In 14, an oblique course between the anterior and posterior borders was found, with the upper circuit off the annulus, posterior to the right atrial appendage base. Of these, 8 coursed anterior to the SVC, 5 behind the SVC and 1 bifurcated the SVC. In 4 others, bifurcation of the upper circuit was seen around the right atrial appendage (n = 3), or around the combined right atrial appendage-superior vena cava (n = 1). CONCLUSION: Despite similar activation around the TA, creating electroanatomic postpacing interval maps distinguishes the active flutter circuit from passively activated myocardium. Significant variability exists in the active circuit, with only a minority around the TA. Most commonly, the circuit courses not around a single barrier but obliquely between anterior and posterior borders.

Idiopathic epicardial left ventricular tachycardia originating remote from the sinus of Valsalva: electrophysiological characteristics, catheter ablation, and identification from the 12-lead electrocardiogram.

BACKGROUND: Despite the success of catheter ablation for treatment of idiopathic ventricular tachycardia (VT), occasional patients have been reported in whom VT could not be ablated from the right or left ventricular endocardium or from the aortic sinus of Valsalva (ASOV). METHODS AND RESULTS: In 12 of 138 patients (9%) with idiopathic VT referred for ablation, an epicardial left ventricular site of origin was identified >10 mm from the ASOV. Coronary venous mapping demonstrated epicardial preceding endocardial activation by >10 ms (41+/-7 versus 15+/-11 ms before QRS onset; P<0.001). VT induction was facilitated by catecholamines and terminated by adenosine. Ablation through the coronary veins or via percutaneous transpericardial catheterization was successful in 9 patients; 2 required direct surgical ablation as a result of anatomic constraints. No ECG pattern was specific for epicardial VT. However, slowed initial precordial QRS activation, as quantified by a novel metric, the maximum deflection index, was more useful. A delayed precordial maximum deflection index > or =0.55 identified epicardial VT remote from the ASOV with a sensitivity of 100% and a specificity of 98.7% relative to all other sites of origin (P<0.001). CONCLUSIONS: Although clinically underrecognized, idiopathic VT may originate from the perivascular sites on the left ventricular epicardium. The mechanism is consistent with triggered activity. It is amenable to ablation by transvenous or transpericardial approaches, although technical challenges remain. Recognition of a prolonged precordial maximum deflection index and early use of transvenous epicardial mapping are critical to avoid protracted and unsuccessful ablation elsewhere in the ventricles.

Electroanatomic mapping of the right ventricle in a patient with a giant epsilon wave, ventricular tachycardia, and cardiac sarcoidosis.

A 47-year-old man presented with sustained monomorphic ventricular tachycardia of right ventricular origin. Surface ECG recorded during sinus rhythm showed a bizarre "double QRS" pattern. Biventricular cardiomyopathy was found with predominant right ventricular involvement, due to cardiac sarcoidosis. Electroanatomic mapping was used to characterize the right ventricular substrate abnormalities and to decipher the specific activation abnormalities responsible for the ECG findings.

Influence of age and gender on the mechanism of supraventricular tachycardia.

OBJECTIVES: The objective of this study was to determine the impact of age and gender on the mechanism of paroxysmal supraventricular tachycardia (PSVT). BACKGROUND: Previous studies have indicated that PSVT mechanism may be influenced by age and gender, but contemporary data are limited. METHODS: In 1,754 patients undergoing catheter ablation of 1,856 PSVTs between 1991 and 2003, the mechanism was classified as atrioventricular reentrant tachycardia (AVRT), atrioventricular nodal reentrant tachycardia (AVNRT), or atrial tachycardia (AT). Patients with inappropriate sinus tachycardia, atrial flutter, atrial fibrillation, and age <5 years were excluded. RESULTS: The mean age was 45 +/- 19 years (range 5-96), and the majority were women (62%). Overall, AVNRT was the predominant mechanism (n = 1,042 [56%]), followed by AVRT (n = 500 [27%]) and AT (n = 315 [17%]). There was a strong relationship between age and PSVT mechanism; the proportion of AVRT in both sexes decreased with age, whereas AVNRT and AT increased (PM < .001 by ANOVA). The majority of patients with AVRT were men (273/500 [54.6%]), whereas the majority of patients with AVNRT and AT were women (727/1,042 [70%] and 195/315 [62%], respectively). The distribution of PSVT mechanism was significantly influenced by gender (P < .001). In women, 63% had AVNRT, 20% had AVRT, and 17.0% had AT. In men, 45% had AVNRT, 39% had AVRT, and 17% had AT. AVNRT replaced AVRT as the dominant PSVT mechanism at age 40 in men and at age 10 in women. CONCLUSIONS: The mechanism of PSVT in patients presenting for ablation is significantly influenced by both age and gender.