Thomas Korte

Atrial Reentrant Tachycardia After Surgery for Congenital Heart Disease Endocardial Mapping and Radiofrequency Catheter Ablation Using a Novel, Noncontact Mapping System

BackgroundThe purpose of the present study was to determine the role of a novel, noncontact mapping system for assessing a variety of atrial reentrant tachycardias (ART) in patients after the surgical correction of congenital heart disease. Methods and ResultsIn 14 patients, an electrophysiological study using the Ensite 3000 system was performed to assess ARTs resistant to medical treatment. Sixteen different forms of ART were inducible in the 14 patients studied. The reentrant circuit of all ARTs could be characterized and localized with respect to anatomic landmarks such as atriotomy scars, intraatrial patches/baffles, and cardiac structures. In 15 of the 16 ARTs (in 13 of the 14 patients), a target area of the reentrant circuit for radiofrequency current application (ie, an area of conduction between 2 anatomical obstacles such as surgical barriers and cardiac structures of electrical isolation) could be localized within the systemic venous atrium. Nine patients exhibited macroreentry, and 4 showed microreentry. In 12 patients, ART could be terminated by creating linear radiofrequency current lesions (75°C, 180 to 390 s). Completeness of linear lesions after radiofrequency current delivery was proven by analyzing color-coded isopotential maps of atrial activation while applying atrial pacing techniques. The mean duration of the procedures was 286 minutes (range, 130 to 435 minutes); fluoroscopy time ranged from 7 to 33.8 minutes (mean, 17.4 minutes). ConclusionsIn patients with ART after the surgical correction of congenital heart disease, the use of the noncontact mapping system allows for characterization of the tachycardia and guidance for effective radiofrequency current delivery.

Increased open probability of single cardiac L-type calcium channels in patients with chronic atrial fibrillation. role of phosphatase 2A.

Background: The L-type calcium channel (LCC) plays a crucial role in the electrical remodeling of atrial fibrillation (AF). AF is associated with reduction of L-type calcium current density, due to a transcriptional downregulation of the pore forming alpha1c-subunit of LCC. However, it is unclear, whether this current reduction is related to a decrease in channel number or to alterations in channel function. Hence, we performed a single LCC analysis to assess channel gating and function in human AF. Methods and results: We used the cell-attached patch-clamp technique in isolated atrial human cardiomyocytes of 25 patients with sinus rhythm (SR) and 15 patients with chronic AF. Protein expression of the pore-forming α1c-subunit of LCC was reduced by 40% in AF. Single channel peak average current was 1.7-fold higher in AF than in SR, due to a 3.1-fold higher open probability of LCC. Since phosphatase 2A (PP2A) is known to preferentially reduce LCC open probability via channel dephosphorylation, we assessed whether PP2A expression or activity is reduced in AF. Okadaic acid, an inhibitor of phosphatases, increased channel open probability in SR, but not in AF. However, Western blot analysis of atrial homogenates of the same patient population revealed unchanged expression of PP2A. Conclusions: Human AF is characterized by increased single LCC activity, due to an increase of channel open probability. The blunted effect of PP2A on LCC as shown by single channel analysis may be related to a reduction of cytosolic PP2A activity or impaired local interaction between PP2A and LCC in AF.

Chronic experiences with a single lead dual chamber implantable cardioverter defibrillator system.

Monitoring of atrial rhythm in patients implanted with ICDs may improve accuracy in identifying supraventricular arrhythmias and, therefore, prevent inappropriate therapies. Since difficulties were found in dual chamber ICDs with separate leads, a new designed single lead dual chamber ICD system was tested. Twenty‐five patients implanted with a Deikos A+ (single coil defibrillation lead with two atrial sensing rings combined with a dual chamber ICD with a high amplifying atrial channel) were tested. Atrial and ventricular signals were analyzed during sinus rhythm (SR) and sinus tachycardias (STs), atrial flutter and AF, and VT or VF. Follow‐ups were performed after 1, 3, 6, 9, and 12 months after implantation. Analysis of EGM amplitudes of stored episodes revealed that atrial signals during atrial flutter (2.1 ± 0.51 mV) were comparable to those of ST (2.2 ± 0.5 mV). Atrial amplitudes during AF were significantly lower (0.81 ± 0.5 mV, P < 0.01). During VF atrial “sinus“ signals (2 ± 0.8 mV) were stable. Ventricular parameters did not differ from a standard ICD lead; defibrillation threshold was 11.4 ± 4.5 J (16 patients). During intraoperative and prehospital discharge measurements, 97.1% of SR‐P waves and 99.2% of atrial flutter waves were detected correctly. In AF 91.11% of atrial signals were detected. Analysis of 505 stored episodes showed that 96.8% of ST and 100% of atrial flutter and 100% of AF episodes have been classified correctly and no underdetection of VT/VF was found. The first experiences with the new VDD‐ICD system show an increase of the specificity to detect ventricular tachycardias to a level comparable to dual chamber ICDs with two leads. The reliability of this system has to be proven in a prospective randomized study. (PACE 2003; 26:1937–1943)

Arrhythmia Susceptibility in Mice after Therapy with β-Catenin-Transduced Hematopoietic Progenitor Cells after Myocardial Ischemia/Reperfusion

Background: Hematopoietic progenitor cells (HPCs) can improve cardiac function after myocardial infarction. However, occurrence of arrhythmias is a potential limitation of cell therapy. In this study, we investigated the cardiac electrophysiological properties of ex vivo expanded HPCs, generated by β-catenin gene transfer, after transcoronary delivery in a murine model of ischemia/reperfusion (I/R) injury. Methods and Results: To assess arrhythmia inducibility of ex vivo expanded HPCs, mice were subjected to I/R and assigned to sham operation (n = 8), I/R (n = 21) and HPC (n = 15) treatment. Six weeks later, mice were subjected to long-term electrocardiogram recording and in vivo transvenous electrophysiological study. After I/R, mice showed a significant prolongation of conduction and repolarization compared with sham-operated mice. There was a marked increase in ventricular ectopic activity in infarcted mice as compared with sham-operated mice. Cardiac electrophysiological parameters and ventricular ectopic activity were not altered in mice treated with HPCs in comparison with control I/R mice. Conclusion: Transcoronary delivery of genetically ex vivoexpanded HPCs did not alter the electrophysiological properties in mice after I/R. Therefore, ex vivo β-catenin-mediated HPC expansion may represent an attractive therapeutic option for cell transplantation treatment of myocardial infarction without electrophysiological side effects.