摘要:

Identifying the Tachycardia‐Related Coronary Artery.Introduction:Transcatheter chemical ablation is a new treatment option for patients with ventricular tachycardia. Availability of a safe, simple, and sensitive method to identify the ventricular tachycardia‐related artery is required for successful intracoronary chemical ablation for ventricular tachycardia. The purpose of this study was to compare bolus intracoronary iced saline injection to bolus intracoronary antiarrhythmic drug injection as methods for identifying the ventricular tachycardia‐related coronary artery.Methods and Results:Patient selection was limited to eight individuals with recurrent sustained monomorphic ventricular tachycardia, coronary artery disease, remote myocardial infarction, and in whom programmed stimulation could reproducihiy induce the clinical arrhythmia. An infusion catheter was positioned in the putative ventricular tachycardia‐related artery and ventricular tachycardia was provoked hy programmed stimulation. In four patients the putative ventricular tachycardia‐related artery was a patent infarct‐related vessel and in the other four patients was a vessel supplying collateral flow to an occluded infarct‐related artery. The effects of selective intracoronary iced saline bolus injection (10 mL), and then of selective intracoronary bolus antiarrhythmic drug injection (2.5 mg lidocaine in one patient, procainamide 1.0–9.0 mg in seven patients) were observed. Bolus intracoronary iced saline injection did not alter ventricular tachycardia in any patient. Bolus intracoronary antiarrhythmic drug injection, however, led to ventricular tachycardia cycle length prolongation in two patients and arrhythmia termination in four patients. In two of these individuals, infusion of ethanol into the tachycardia‐related vessel previously identified by intracoronary drug injection resulted in ablation of the ventricular tachycardia.Conclusions:In the present study, selective intracoronary antiarrhythmic drug injection appeared to be more effective than intracoronary iced saline for identifying the ventricular Uchycardia‐related coronary artery, (J Cardiovasc Electrophysiol, Vol. 3, pp

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00967.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

β‐Adrenergic Receptor Activation and Intracellular Ca2+.Introduction:β‐Adrenergic receptor agonists have been shown to increase the voltage‐dependent Ca2+current in cardiac myocytes. Additionally, adrenergic receptor activation has been shown to increase intracellular Ca2+, to increase systolic Ca2+transients and to enhance Ca2+uptake into the sarcoplasmic reticulum, thereby accelerating relaxation. The present study was designed first to characterize the influences of β‐adrenergic receptor activation on intracellular Ca2+activity as well as membrane potential in ventricular myocytes characterized as normal based on rigorous morphologic and electrophysiologic criteria. The second objective was to assess whether the increase in intracellular Ca2+activity elicited by β‐adrenergic receptor activation could elicit afterdepolarizations and triggered activity.Methods and Results:Intracellular Ca2+and whole‐cell voltage recordings were measured in cells in which indo‐1 free acid was delivered intracellularly through the recording pipette. Isoproterenol produced complex Ca2+transients underlying both early and delayed afterdepolarizations during pacing as well as aftertransients underlying triggered action potentials and delayed afterdepolarizations in the absence of pacing. The coupling interval of Ca2+iaftertransients was frequency dependent and followed that of the delayed afterdepolarizations. Ca2+iafter transient amplitudes, however, exhibited a biphasic response with frequency revealing that factors other than pacing frequency alone contribute to control of the amplitude of the aftertransients. Inhibition of sarcoplasmic reticular release of Ca2+by ryanodine abolished Ca2+iaftertransients and afterdepolarizations otherwise elicited by isoproterenol.Conclusion:These data demonstrate that normal cells stimulated by β‐adrenergic agonists exhibit marked changes in intracellular Ca2+homeostasis that may serve as the substrate for abnormal ion fluxes that ultimately contribute to electrophysiologic derangements underlying arrhythmogenesis in the intact heart. (J Cardiovasc Electrophysiol, Vol. 3, pp

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00968.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Electrogenic Sodium/Potassium Pump in Ventricular Myocytes.Introduction:The membrane current generated by the sodium/potassium pump was measured in ventricular myocytes isolated from guinea pig hearts.Methods and Results:Cells were impaled with microelectrodes to minimize dialysis of the intracellular milieu and thus maintain normal physiological conditions. To selectively record pump current, it was necessary to suppress potassium currents with external barium and to buffer intracellular calcium with a calcium chelator. Exposure to potassium‐free solution was used to inhibit the sodium/potassium (Na/K) pump and load the cell with intracellular sodium (Nai). When the pump was subsequently reactivated by replacing extracellular potassium, there was a sharp increase of a transient outward membrane current, which declined back to control with a time constant of 50.7 ±12.9 seconds (mean ± SD, n = 11). The increase of outward membrane current became larger after longer periods of potassium removal and was abolished by the pump inhibitor strophanthidin. These features show that the transient outward current was generated by the Na/K pump. The pump current of quiescent myocytes was assessed by two different methods. First, it was evaluated directly by measuring the loss of outward pump current upon exposure to a maximal blocking dose of strophanthidin. The loss of outward current was 20.3 ± 5.5 pA (n = 11), which is equivalent to a pump current density of 0.164 /μA/cm2. The second method was to estimate passive Na influx into quiescent myocytes, by measuring the charge extruded by the pump after a period of potassium removal. The charge extruded during recovery reflects the magnitude of Naiaccumulation during potassium removal. Passive Na influx was found to be 4.58 ± 2.4 pmol/cm2per second. If passive Na influx is normally balanced fully by Na extrusion on the Na/K pump, this will result in an average pump current of 18.0 pA (equivalent to a pump current density of 0.147 μA/cm2). Thus, although the two methods for estimating the pump current of quiescent myocytes were different, their results agreed well. A pump current of 20 pA will contribute only about 0.4 mV to the resting potential of ventricular myocytes. This conclusion was confirmed experimentally by showing that pump inhibition depolarized the resting potential of myocytes by only 0.45 ± 0.05mV(n = 10).Conclusion:An important finding of this study is that the electrogenic Na/K pump makes a much lower contribution to the resting potential of ventricular muscle than was previously supposed. (J Cardiovasc Electrophysiol, Vol. 3, pp. 225–238,

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00969.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Mechanism of Reentry's Instability.Introduction:The purpose of this investigation was to study the mechanisms responsible for instability and termination of functionally determined reentry.Methods and Results:The activation sequence was recorded using multielectrode mapping technique in preparations isolated from rabbit right ventricle. In nine preparations, functional inhomogeneity was created on the epicardial surface. For this purpose, two parts of a preparation divided by a thin rubber barrier were superfused by different solutions: normal Tyrode's solution and Tyrode's solution containing quinidine (5–10 mg/L). As a result, there was a difference of refractory period of 45 ± 12 msec (n = 6). Premature stimulation of sites situated in the normally superfused region led to the appearance of unstable reentrant circuits at the border of inhomogeneity (32 cases) in seven of the nine preparations. In most cases (24 of 32) reentrant circuits shifted along the border of inhomogeneity. Reentrant circuits with clockwise and counterclockwise rotations had opposite directions of shift. Because of the shift, reentrant circuits moved to the border of the preparation where they were extinguished.Conclusion:Our results suggest that inhomogeneity in refractoriness that gives rise to initiation of reentrant circuits also causes their termination. (J Cardiovasc Electrophysiol, Vol. 3, pp. 255–265, June

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00971.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Amiodarone Therapy. Amiodarone is a unique compound, with actions of all four antiarrhythmic drug classes. It has been used effectively to treat a broad range of ventricular and supraventricular arrhythmias. As a result of amiodarone's enormous volume of distribution and slow disposition kinetics, gradual accumulation occurs during maintenance dosing, and the drug's clinical action can be produced more rapidly with the use of an early loading period. Similarly, plasma concentrations and effects of amiodarone decrease slowly after drug discontinuation. There is a clinical impression that amiodarone is superior over other agents for a wide variety of arrhythmias, but this remains unproven. Because of uncertainty regarding amiodarone's efficacy compared to alternative therapies, and amiodarone's important potential for causing cardiac, pulmonary, hepatic, central nervous system, ocular, thyroid, and cutaneous adverse effects, amiodarone's precise role in antiarrhythmic therapy remains to be established. (J Cardiovasc Electrophysiol, Vol. 3, pp. 266–280, June 199

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00972.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Torsades de Pointes. Torsades de pointes are typically characterized by an ECG pattern of polymorphous but organized electrical activity of ventricular origin that occurs in the setting of a long QT interval, long‐coupled bigeminy, and has specific precipitating causes and therapeutic responses. Torsades de pointes can result from congenital (adrenergic dependent) and acquired (pause dependent) factors and may have similar cardiac substrates with different precipitating events. (J Cardiovasc Electrophysiol, Vol. 3, pp. 281–292, June 1

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00973.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Books reviewed in this article:Contemporary Management of Ventricular Arrhythmias. Cardiovascular Clinics Series.Edited by Arnold J. Greenspon and Harvey L. Waxman, F.A. Davis Company, Philadelphia, 1992, 368 pages, $75.00.

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00974.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY