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. No change in AH interval during constant atrial pacing was observed by bolus injection of 20 mg of adenosine triphosphate. No changes in the morphology of the delta wave or HV interval were observed by changing the atrial pacing site. This patient developed HV block by atrial extrastimulus (S1S1: 600 msec, S1S2

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. The aim of this study was to evaluate the relationship between the location of the CT and the line of block by intracardiac echocardiography (ICE). METHODS AND RESULTS: Twenty-one patients with typical AFL were included in the study. The ICE imaging catheter (9-French with 9-MHz ultrasound transducer) was advanced to the RA. Under ICE guidance, a 20-pole roving catheter was used to map double potentials (DPs) during AFL, and three-dimensional images of the RA were reconstructed. During counterclockwise (CCW), clockwise (CW) AFL, or both, a line of conduction block manifested by DPs was identified at a septal site adjacent to the CT in 12 patients and in the posteroseptal RA in 9 patients. CONCLUSION: The functional line of block in CCW and CW AFL is localized not at the CT but at the septal edge of the CT or in the posteroseptal RA.

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. Reactivity of the antibody was evaluated by immunohistochemistry of pathological specimens of gynecological cancers. Cytotoxicity of HMMC-1 against SNG-S cells was tested by in vitro cytotoxicity assays. The epitope of HMMC-1 was determined by transfection with a panel of glycosyltransferase cDNAs and by inhibition assays with chemically synthesized oligosaccharides. RESULTS: HMMC-1 is a human IgM monoclonal antibody that reacts positively with mullerian duct-related carcinomas with positive rates of 54.6% against uterine endometrial adenocarcinoma, 76.9% against uterine cervical adenocarcinoma, and 75.0% against epithelial ovarian cancer. HMMC-1 does not react with normal endometrium at proliferative or secretory phases, normal uterine cervix, or normal and malignant tissue from other organs, whereas it reacts weakly with the epithelium of the gall bladder and the collecting duct of the kidney. HMMC-1 exhibits antigen-dependent and complement-mediated cytotoxicity. Upon cotransfection with cDNAs encoding two glycosyltransferases required for fucosylated extended core 1 O-glycan, mammalian cells express HMMC-1 antigen. Finally, binding of HMMC-1 to SNG-S cells is inhibited by synthetic Fucalpha1-->2Galbeta1-->4GlcNAcbeta1-->3Galbeta1-->3GalNAcalpha1-octyl. CONCLUSIONS: These results indicate that HMMC-1 specifically recognizes a novel O-glycan structure. The unique specificity and cytotoxicity of HMMC-1 strongly suggest a therapeutic potential of this antibody.

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 3.2-French, 20-MHz intracardiac ultrasound (ICUS) catheter was introduced into the coronary sinus (CS), and two-dimensional ICUS images were recorded during transducer pullback in 21 patients with AVNRT and 18 control patients. Three-dimensional reconstruction of the CS was created using the TomTec Imaging system. The area of the CS lumen at 15 mm within the CS ostium (os) was not significantly different in patients with and without AVNRT (54.4 +/- 34.7 mm2 vs 39.1 +/- 28.5 mm2). However, the area of the CS os was significantly larger in patients with AVNRT than in those without (112.1 +/- 60.9 mm2 vs 71.7 +/- 44.4 mm2, P < 0.05). Three-dimensional morphology of the CS os revealed flaring in patients with AVNRT, giving it a "windsock" appearance. Sustained AFL was induced in 10 of 21 patients with AVNRT, but in none of 18 control patients (P < 0.005). CONCLUSION: The CS os was significantly wider in patients with AVNRT than in those without. These findings may have important implications for arrhythmia pathogenesis in AVNRT as well as AFL.

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. Cibenzoline (2 mg/kg body weight) was injected to terminate atrial fibrillation. ST-T segment elevation in the right precordial leads was observed following cibenzoline administration. Ventricular fibrillation was reproducibly induced by ventricular extrastimuli (S1: 600 ms, S2: 220 ms, S3: 210 ms).

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. Slow/fast atrioventricular nodal reentrant tachycardia (AVNRT) was induced once by double atrial extrastimuli, but it was not reproducible. However, intravenous bolus injection of adenosine triphosphate (12.5 mg) during sinus rhythm led to reproducible initiation of slow/fast AVNRT.

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). ATP (2.5 to 30 mg, in 2.5-mg increments was injected during sinus rhythm until signs of DAVNP (> or = 50 msec increase or decrease in AH or PR interval in two consecutive beats) or > or = second-degree AV block was observed. DAVNP was diagnosed by ATP test in all 9 patients with slow/fast AVNRT. DAVNP was observed by ATP test in 3 of the 11 control patients. Thus, the test had a sensitivity of 100% and specificity of 73%. ATP test given during sinus rhythm is useful for identifying patients with dual AV nodal pathways who are prone to AVNRT.