Complete AV block developing in a patient with manifest ventricular preexcitation.

This case report describes a 37-year-old man with manifest atriofascicular and fasciculoventricular connections who developed complete atrioventricular block. After resumption of 1:1 atrioventricular conduction, an electrophysiological study was conducted. During sinus rhythm, manifest ventricular preexcitation was observed and the AH and HV intervals were 80 msec and 50 msec, respectively.

Relationship between anatomic location of the crista terminalis and double potentials recorded during atrial flutter: intracardiac echocardiographic analysis.

Introduction: The activation sequence in typical atrial flutter (AFL) around the tricuspid annulus is well described. However, activation of the remainder of the right atrium (RA) is not well defined. Previous studies have shown a linear block at the crista terminalis (CT) during AFL.

HMMC-1: a humanized monoclonal antibody with therapeutic potential against Müllerian duct-related carcinomas.

Purpose: The purpose of this research was to generate a human monoclonal antibody specific to gynecological cancers and to evaluate such an antibody as therapy for gynecological cancers.

Experimental Design: Transchromosomal KM mice were immunized with the human uterine endometrial cancer cell line SNG-S. Hybridomas were constructed between spleen cells from KM mice and mouse myeloma cells.

Comparison of coronary sinus morphology in patients with and without atrioventricular nodal reentrant tachycardia by intracardiac echocardiography.

Introduction: Dual AV nodal physiology is the electrophysiologic substrate for AV nodal reentrant tachycardia (AVNRT), but the anatomic basis for this arrhythmia remains to be elucidated. Atrial flutter (AFL) has been shown to be more frequently inducible in patients with AVNRT.

Methods And Results: A 3.

Brugada-like electrocardiographic pattern unmasked by fever.

Brugada syndrome is characterized by right bundle branch block morphology and ST-segment elevation in the right precordial leads and a propensity to develop ventricular arrhythmias. Mutations in a cardiac sodium channel gene have been linked to this syndrome, and the ionic mechanisms responsible for the electrocardiographic phenotype are temperature-dependent. This case report describes a patient in whom a typical Brugada ECG pattern developed during fever and could be reproduced at normal body temperature by administration of pilsicainide.

Wolff-Parkinson-White syndrome concomitant with asymptomatic Brugada syndrome.

A 29-year-old man was referred for electrophysiological testing and radiofrequency ablation because of repeated episodes of palpitation over 2 years. A 12-lead electrocardiogram during sinus rhythm showed manifest Wolff-Parkinson-White syndrome and during palpitation showed narrow QRS tachycardia at a rate of 213 beats/min. Following successful radiofrequency ablation of the left anterolateral accessory pathway, sustained atrial fibrillation was induced by atrial extrastimulation.

Reproducible induction of atrioventricular nodal reentrant tachycardia with adenosine triphosphate.

A 29-year-old woman was referred for electrophysiological testing and radiofrequency ablation because of repeated episodes of palpitation of a 8-year duration. The 12-lead ECG during palpitations showed narrow QRS tachycardia at a rate of 160 beats/min. Dual AVN physiology according to electrophysiological criteria was not shown by single atrial extrastimulation and the tachycardia could not be induced.

Noninvasive diagnosis of dual AV nodal physiology in patients with AV nodal reentrant tachycardia by adenosine triphosphate test.

Atrioventricular nodal reentrant tachycardia (AVNRT) is a relatively common paroxysmal supraventricular tachycardia. This study investigated whether adenosine-5'-triphosphate (ATP) injection during sinus rhythm might be useful in the noninvasive diagnosis of dual AV nodal pathways. The study group consisted of 9 patients with slow/fast AVNRT and 11 control patients without antegrade dual AV nodal physiology (DAVNP).