摘要:

Electrogram in AVNRT.Introduction:The purpose of this study was to determine the predictors of successful ablation versus modification sites of the slow pathway in patients with AV nodal reentrant tachycardia. Complete elimination of slow pathway conduction (“ablation”) is considered to be an appropriate endpoint during radiofrequency (RF) current delivery, whereas the persistence of residual slow pathway conduction with or without single echo beats (“modification”) may be indicative of tachycardia recurrence.Methods and Results:Of 131 patients, 71 consecutive patients were followed for 15.1 ± 7.6 months. After elimination of inducible AV nodal reentrant tachycardia in all patients, residual slow pathway conduction (modification) persisted in 38 patients, whereas complete elimination of slow pathway conduction (ablation) was documented in 33 patients. Including electrophysiologic study after 5 to 7 days and after 3 to 6 months, 6 (8.4%) patients had recurrences: 5 with residual slow pathway conduction after the procedure and 1 with complete elimination of slow pathway conduction (P<0.05). As compared with modulated sites, ablation sites of the slow pathway were characterized as follows: (1) duration of the local atrial electrogram (AEGM) (66.7 ± 10.2 vs 54.1 ± 12.6 msec, P<0.01); (2) interval from the end of the AEGM to onset of His‐bundle deflection (4.4 ± 8.2 vs 16.1 ± 9.3 msec, P<0.01); and (3) number of peaks of the AEGM as an indicator of fractionation (4.1 ± 0.7 vs 3.0 ± 0.8, P<0.01). The rate of junctional tachycardias (103.4 ± 12.1 vs 102.1 ± 16.9 per min), the AV ratio (0.4 ± 0.5 vs 0.5 ± 0.5), the number of RF current deliveries (4.1 ± 4.4 vs 4.5 ± 4.4), the duration of the procedure (124.1 ± 45.3 vs 125.6 ± 42.3 min), and the fluoroscopy time (15.5 ± 10.8 vs 16.6 ± 9.6 min) as well as power and total energy of RF current deliveries and the anatomically calculated catheter position at the successful site were not statistically different. A subset analysis in patients who received only a single RF application showed the same results for both groups. Patients without recurrence (n = 65) were found to have longer duration of the AEGM (61.9 ± 14.6 msec) and a shorter interval from the end of AEGM to the onset of His‐bundle deflection (10.1 ± 12.2 msec) than patients with recurrence (n = 6) (47.5 ± 7.5 msec and 20.8 ± 12.8 msec, respectively).Conclusion:Complete ablation of the slow pathway resulted in a lower recurrence rate. The complete ablation approach is feasible using precisely analyzed local AEGMs to guide RF current in AV nodal reentrant tachy

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00396.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Responses of Transmembrane Potential During a Shock.Introduction:The purpose of this investigation was to study the transmembrane potential changes (δVm) during extracellular electrical field stimulation.Methods and Results:Vmwas recorded in seven guinea pig papillary muscles in a tissue hath by a double‐barrel microelectrode with one barrel in and the other just outside a cell while shocks were given across the bath. The short distance (15 to 30 μm) between the two microelectrode tips and alignment of the tips parallel to the shock electrodes eliminated the shock artifact. Following ten SI stimuli, an S2 shock field created by a 10‐msec square wave was delivered during the action potential plateau or during diastole through shock electrodes 1 cm on either side of the tissue. Four shock strengths creating field strengths of 1.7 ± 0.1, 2.9 ± 0.2, 6.1 ± 0.6. and 8.8 ± 0.9 V/cm were given for the same impalement. Both shock polarities were given at each shock strength. For shocks delivered during the action potential plateau, the magnitudes of the peak δVmcaused by the above four potential gradients were 21.1 ± 8.2, 33.6 ± 13.6, 49.9 ± 24.2, and 52.3 ± 28.0 mV (P<0.05 among the four groups) for the shocks causing depolarization and 37.9 ± 14.2,56.6 ± 16.4,83.1 ± 19.4. and 92.9 ± 29.1 mV (P<0.05 among the four groups) for the shocks causing hyperpolarization. Though δVmincreased as potential gradients increased, the relationship was not linear. The magnitude of hyperpolarization was 1.9 ± 0.5 times that of depolarization when the shock polarity was reversed (P<0.05). As potential gradients increased from 1.7 ± 0.1 to 8.8 ± 0.9 V/cm, the time constant of the membrane response decreased significantly from 3.5 ± 1.8 to 1.6 ± 0.7 msec for depolarizing shocks and from 6.0 ± 3.1 to 3.4 ± 1.9 msec for hyperpolarizing shocks (P<0.01 vs depolarizing shocks). For shocks delivered during diastole, hyperpolarizing shocks induced triphasic changes in Vmduring the shock, i.e., initial hyperpolarization, then depolarization, followed again by hyperpolarization.Conclusion:During the action potential plateau, the membrane response cannot be represented by a classic passive RC membrane model. During diastole, activation upstrokes occur even during hyperpolarization caused by shocks creating potential gradients between

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00397.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00398.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Thermometry and Radiofrequency Catheter Ablation.Introduction: Temperature monitoring has been proposed as a control for lesion occurrence and dimension during radiofrequency transcatheter ablation. Effective temperature measurement depends on thermistor positioning relative to the heated cardiac tissue and the convective cooling effects of the circulation. But the accuracy of a single tip thermistor as a measure of peak electrode‐tissue interface temperature is unknown.Methods and Results:A standard 8‐French, 4‐mm electrode catheter with 5 thermistors (1 tip thermistor, 4 radial thermistors) was used to deliver radiofrequency energy in vitro to 3 porcine right ventricles and in vivo to 7 mongrel dogs. In vitro, the catheter orientation was varied. In vivo the catheter was positioned under fluoroscopy at a variety of atrial, tricuspid annular, and ventricular sites, with no attempt to adjust catheter orientation. In both cases varied discrete power levels were used so that a wide temperature range was attained. Lesions created in vivo with a standard, single thermistor tipped electrode were compared to those of a catheter with a thermistor extending 1 mm from the tip. Power was varied and tip thermistor temperatures recorded. All lesions were examined pathologically. Comparisons of radial thermistor temperature to tip thermistor temperature for 3 catheter orientations in vitro resulted in tip thermistor underestimation of peak electrode‐tissue interface temperature by a median of 0.5°C in 35% of the perpendicular orientations, 1.9°C in 82% of the 45 orientations, and 5°C in 83% of the parallel orientations. During in vivo trials, the tip thermistor underestimated the peak electrode‐tissue interface temperature during 2 of 51 lesions by 1.2°C and 7.6°C. There was a sudden rise in electrical impedance in 17 of 51 radiofrequency energy deliveries. Only one case was observed where the peak electrode‐tissue interface temperature was below 95°C. The normal to extended tip thermistor configurations analysis showed similar relationships between lesion size and temperature.Conclusions:Accuracy of a single tip thermistor was found to be dependent upon catheterlissue orientation. With routine catheter positioning in vivo, the tip thermistor was a good indicator of peak electrode‐tissue interface temperature. Thus with power regulation to avoid temperatures greater than 90°C, a single flush‐mounted tip thermistor is probably adequate for temperature monitoring of lesion formation and avoida

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00399.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Abolished Early Afterdepolarization by Nicorandil. We describe a 17‐year‐old boy with idiopathic long QT syndrome and repeated syncopal episodes. Early afterdepolarization (EAD) in the monophasic action potential (MAP) was demonstrated in the posterior septum of the left ventricle. Injection of the potassium channel opener nicorandil decreased KAD and shortened MAP duration. The syncopal episodes due to ventricular fibrillation disappeared after administration of the potassium channel ope

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00400.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00401.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Reentrant Activity in Cardiac Tissue. This review article summarizes theoretical insights into the principles and mechanisms associated with reentrant activity in cardiac tissue. A mathematical ring model is used in computer simulations to investigate, at the cellular level, mechanistic aspects of initiation, perpetuation, and termination of reentry. Taking advantage of the ability to compute membrane processes in this model, we relate dynamic properties of the reentrant action potential (e.g., beat‐to‐beat alternans) to the underlying kinetics of membrane ionic channels. Effects on reentry of inhomogeneities in refractoriness, excitability, cellular coupling at gap junctions, and fiber cross‐section are also st

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00402.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00403.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Molecular Basis of Cardiac CI−Channels. Recent electrophysiologic studies have provided evidence suggesting that as many as six different CI−conductances can be identified in the sarcolemma of cardiac myocytes isolated from various animal species and areas of the heart. These include CI−conductances activated by stimulation of protein kinase A, protein kinase C, extracellular ATP, intracellular Ca2+, membrane stretch, and a basally active CI−conductance. Many basic biophysical and pharmacologic properties of these channels are presently unknown, and the only molecular information presently available suggests that the cAMP‐activated CI−conductance is due to cardiac expression of an isoform of the cystic fibrosis transmembrane conductance regulator (CFTR) CI−channel normally found in epithelial cells. We used the polymerase chain reaction (PCR) to amplify four distinct regions corresponding to the cardiac CFTR gene product from several cardiac tissues to determine if the molecular distribution of CFTR matches the distribution of cAMP‐dependent CI−channels in native myocytes. Amplification of regions corresponding to the first nucleotide binding domain (NBD1), transmembrane segments (TS) VII‐XII, and the regulatory (R) domain showed a precise correlation to tissues that electrophysiologically exhibit sarcolemmal cAMP‐dependent CI−channels, whereas region TS I‐VI exhibited a distribution independent of the presence of cAMP‐dependent CI−channels. Since the TS I‐VI region of the CFTR gene product is believed to comprise the pore region of the channel, we propose that one explanation for the anomalous expression of this region of CFTR in cardiac tissues that do not exhibit cAMP‐dependent CI−currents but do exhibit other types of macroscopic CI−currents may be sequence homology in a molecularly conserved pore region common to d

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00404.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY