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.

Neurologic complications of catheter ablation/defibrillators/pacemakers.

Approaches to the management of patients with cardiac arrhythmias have significantly evolved over the last decade, with advancement in catheter ablation and device implantation techniques. As the techniques and tools evolve, so does our understanding of the possible complications from these procedures. The focus of this chapter is discussion of the neurologic complications involved with catheter ablation, pacemaker and defibrillation implantation, with the focus on timely diagnosis, and management strategies.

Prospective study of cardiac sarcoid mimicking arrhythmogenic right ventricular dysplasia.

INTRODUCTION: Case studies indicate that cardiac sarcoid may mimic the clinical presentation of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C); however, the incidence and clinical predictors to diagnose cardiac sarcoid in patients who meet International Task Force criteria for ARVD/C are unknown. METHODS AND RESULTS: Patients referred for evaluation of left bundle branch block (LBBB)-type ventricular arrhythmia and suspected ARVD/C were prospectively evaluated by a standardized protocol including right ventricle (RV) cineangiography-guided myocardial biopsy. Sixteen patients had definite ARVD/C and four had probable ARVD/C. Three patients were found to have noncaseating granulomas on biopsy consistent with sarcoid. Age, systemic symptoms, findings on chest X-ray or magnetic resonance imaging (MRI), type of ventricular arrhythmia, RV function, ECG abnormalities, and the presence or duration of late potentials did not discriminate between sarcoid and ARVD/C. Left ventricular dysfunction (ejection fraction <50%) was present in 3/3 patients with cardiac sarcoid, but only 2/17 remaining patients with definite or probable ARVD/C (P = 0.01). CONCLUSIONS: In this prospective study of consecutive patients with suspected ARVD/C evaluated by a standard protocol including biopsy, the incidence of cardiac sarcoid was surprisingly high (15%). Clinical features, with the exception of left ventricular dysfunction and histological findings, did not discriminate between the two entities.

Posterior myocardial infarction: unique diagnosis to an elusive problem.

The clinical presentation of posterior myocardial infarction is not easy. The diagnosis is often missed due to lack of ST-segment elevation in standard 12-lead electrocardiogram. The diagnosis is made by seeing ST-segment elevation in the posterior leads V7, V8, and V9, which are typically placed in the left posterior axillary line, left midscapular line, and halfway between the mid scapular and left paraspinal line, respectively. The investigators describe a case of posterior myocardial infarction where additional posterior leads were placed in the left paraspinal line, right paraspinal line, and right midscapular line, displaying more prominent current of injury than seen with traditional posterior lead placement. This may lead to a more robust identification of posterior myocardial infarction that, in turn, may allow for adequate treatment and triage.