摘要:

Nonlinear Analysis of AF in Man.Introduction:We applied methods from the theory of nonlinear dynamics to characterize unipolar epicardial right atrial electrograms of electrically induced atrial fibrillation (AF) in man.Methods and Results: Electrograms were selected from a high‐density mapping study, which confirmed the existence of at least 3 different types of induced AF (types I, II, and III) in patients undergoing open chest surgery. We analyzed sets of 5 electrograms (4 sec, sampling frequency 1 kHz, resolution 8 bits) in 9 patients (AF type I, n = 3; type II, n = 3; type III, n = 3). The Grassberger‐Procaccia method was applied to estimate the correlation dimension and correlation entropy from the electrograms. In 2 patients (AF type I) some electrograms (2 of 5 and 3 of 5, respectively) showed scaling at normalized distances ranging from 0.2 to 0.5 in phase space. Correlation dimension D ranged from 1.8 to 3.2 and correlation entropy K from 2.2 to 3.8 nats/sec. The patients were ranked according to increasing coarse‐grained correlation dimension Dcg(range 3.7 to 7.9) and coarse‐grained correlation entropy Kcg(range 5.6 to 18.6 nats/sec). The method of surrogate data was applied to detect nonlinearity in the electrograms. Using the correlation integral as test statistic, it could be excluded that electrograms of type I AF have been generated by linear stochastic dynamics. Episodes of sinus rhythm (Dranging from 1.0 to 5.1 andKfrom 2.0 to 8.6 nats/sec) and induced atrial flutter (Dranging from 2.7 to 4.2 andKfrom 2.2 to 4.2 nats/sec) in 2 different patients showed features of low‐dimensional chaos.Conclusion:Nonlinear analysis discriminated between electrograms during electrically induced AF in humans. The results are consistent with a classification of AF into 3 types based on the spatiotemporal complexity of right atrial activation

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00416.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.tb00417.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Electrophysiologic Effects of Terodiline.Introduction:Terodiline hydrochloride, widely prescribed for urinary incontinence, has been reported to cause bradycardia and torsades de pointes.Methods and Results:In this study, we characterized the electrophysiologic effects of terodiline in dog cardiac tissues in vivo and in isolated canine cardiac Purkinje fibers. Terodiline (1 to 10 μM) resulted in dose‐dependent reduction of action potential amplitude and maximal upstroke velocity (Vmax). The threshold for these effects was ∼ 2 μM (0.6 mg/L), and the changes were cycle‐length dependent. Terodiline (≥ 2 μM) also depressed the action potential plateau but did not significantly alter action potential duration at concentrations ≤ 10 μM. In vivo studies demonstrated that high doses of terodiline (3 mg/kg) lengthened AH and HV intervals, slowed spontaneous sinus rate, prolonged ventricular refractoriness, and inhibited vagally induced slowing of the sinus node. Sympathetic effects on spontaneous sinus rate were unchanged. In both isolated canine Purkinje fibers and anesthetized dogs, terodiline did not evoke afterdepolarizations, repetitive firing, or ventricular tachyarrhythmias under normal or hypokalemic conditions.Conclusion: Our findings suggest that terodiline (≤ 1 to 2 μM) leads to blockade of sodium and calcium channels as well as muscarinic receptors in canine

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00418.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Na‐Ca Exchange Tail Currents and CaiTransientIntroduction:in mammalian cardiac myocytes, a rise of intracellular calcium (Cai) is well known to activate Ca extrusion via forward Na‐Ca exchange, which generates an inward membrane current. This can be observed as an inward “tail” current (INa‐Ca) when the membrane is repolarized after a depolarization‐activated rise of Cai. If, during a voltage step, the membrane is repolarized at the time of the peak of the Ca, transient, the size of the INa‐Catail might he expected to reflect the magnitude of the Caitransient. Therefore, it might be possible to estimate the amplitude and voltage dependence of the Caitransient without, for instance, using fluorescent indicators that can interfere with Cairegulation. The first aim of this study was to use INa‐Catails to investigate the voltage dependence of the Caitransient in whole cell patch clamped rabbit ventricular myocytes dialyzed with a “normal” level of internal Na. The second aim was to investigate how the voltage dependence of the INa‐Catails varied with changes to the dialyzing Na concentration. The third aim was to test the correlation of voltage dependence of INa‐Catails with the voltage dependence of the Caitransient obtained using a fluorescent Ca indicator.Methods and Results:Experiments were performed at 35° to 37°C using whole cell patch clamp, and the holding potential was set at ‐40 mV. Depolarization elicited a Caitransient that peaked in 40 to 50 msec. We reasoned, therefore, that membrane repolarization after 50 msec would cause the raised level of Caito activate an inward current on forward Na‐Ca exchange. The amplitude of INa‐Cameasured shortly (10 msec) after repolarization should reflect the peak amplitude of the Caitransient elicited by the depolarization. In cells dialyzed with 10 mM Na‐containing solution and depolarized for 50 msec to differing test potentials, the INa‐Catail on repolarization increased progressively after pulses to between −40 and +20 mV. The INa‐Catail was maximal after a +20‐mV pulse and showed no decline after depolarizations to more positive potentials, up to +100 mV (P>0.1; n = 8). This implies that the Caitransient has a similar amplitude for depolarizing pulses between +20 and +100 mV. When Na‐free solution dialyzed the cell, the voltage dependence of the INa‐Catail became bell‐shaped, with a maximum at +20 mV (n = 4). Voltage dependence of the INa‐Catail was little affected by raising dialyzing Na from 10 to 20 mM (n = 4); but the amplitude of the INa‐Catail increased. Inhibition of the Na‐K pump with strophanthidin in cells dialyzed with 10 mM Na had qualitatively similar effects to increasing dialyzing Na. In Fura‐2 loaded cells dialyzed with 10 mM Na, the Caitransient exhibited a similar voltage dependence to the 1Na‐Catail (n = 6).Conclusion:The results of this study suggest that in cells dialyzed with 10 mM Na, the voltage dependence of the Caitransient is different from the L‐type Ca current, since this current declines at potentials>+20 mV. The results obtained using Fura‐2 suggest that the INa‐Catail current measurement tracked the Caisufficiently well to reflect the voltage dependence of the Caitransient. The data also confirm that the voltage dependence of the Caitransient in rabbi

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00419.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Adrenergic Effects on VF.Introduction:We hypothesized that drugs which alter ventricular refractoriness or excitability produce quantifiable changes in ventricular fibrillation.Methods and Results:We used a 528‐channel mapping system to quantify the effects of the beta‐antagonist, propranolol, and the beta‐agonist, isoproterenol, on activation patterns in ventricular fibrillation. A plaque of 506 (22 × 23) electrodes spaced 1.12 mm apart and covering about 5% of the ventricular epicardium was sewn to the anterior right ventricle in 18 pigs (30 kg). Propranolol (0.25 to 0.4 mg/kg) increased the refractory period at a right ventricular epicardial site while isoproterenol (3 to 5 μg/min) shortened it. Ventricular fibrillation was induced by programmed stimulation, and unipolar electrograms were recorded from the 506 plaque electrodes for 2 seconds beginning 1, 15, and 30 seconds after the onset of fibrillation. Active epicardial recording sites were identified from the first derivative of the unipolar potentials (dV/dt) detected at each electrode. Then, neighboring active sites were grouped into activation fronts by computer analysis. In six pigs the effect of repeated inductions of ventricular fibrillation was assessed by comparing ventricular fibrillation after saline with a preceding control episode of fibrillation. Each activation front excited 40%± 46% of the mapped region before blocking. No changes were observed with saline and multiple inductions of fibrillation. In another six pigs, ventricular fibrillation after propranolol was compared with a preceding control episode of fibrillation. Ventricular fibrillation alter propranolol exhibited a decreased activation rate per epicardial recording site and fewer activation fronts per second. There was no change in the amount of tissue excited by each activation front or the number of reentry cycles per activation front compared with control. In addition, there was no change in the maximum negative dV/dt detected per activation at an epicardial site. In six pigs ventricular fibrillation during isoproterenol was compared with control episodes of ventricular fibrillation before and 45 minutes after washout of the drug. The control episodes of fibrillation were not different from each other. Compared with control, ventricular fibrillation during isoproterenol exhibited an increased activation rate per epicardial site, an increased amount of tissue excited by each activation front, and an increased maximum negative dV/dt for each activation. There was no change in the number of activation fronts per second or the number of reentry cycles per activation front compared with control.Conclusions:Quantitative analysis revealed that propranolol and isoproterenol do not have symmetrically opposite effects on ventricular fibrillation. Propranolol decreased the number of activation fronts while isoproterenol increased the amount of tissue excited by each activation front. Thus, drugs that alter ventricular refractoriness or excitability alter ventricular fibr

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00420.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Ablation of Interfascicular Reentrant Tachycardia.Introduction:Fascicular reentrant ventricular tachycardia (VT) using the anterior fascicle of the left bundle anterogradely is rare and may produce identical QRS morphology during sinus rhythm and VT. Catheter ablation of this type of VT has not been described in detail.Methods and Results:In a postinfarct patient with dilated left ventricle and recurrent VT (showing a QRS configuration of right bundle branch, left posterior fascicular block), endocardial recordings from the His‐Purkinje system showed that VT was due to interfascicular reentry. Induction of VT occurred after progressive retrograde conduction delay on increasing the prematurity of the extrastimulus. Anterograde conduction occurred exclusively over the left anterior fascicle, which caused identical QRS morphology during sinus rhythm and VT. During VT, the left posterior fascicle was used retrogradely. The usual target for bundle branch reentry ablation, the right bundle, did not participate in the reentrant circuit. While performing left ventricular endocardial mapping, VT was interrupted when positioning the catheter on the left anterior fascicle, and “reversed” nonsustained bundle branch reentry occurred with anterograde conduction over the posterior fascicle and retrograde conduction over the anterior fascicle. Ablation of conduction in the anterior fascicle led to cure of the VT.Conclusion:Interfascicular reentrant VT with right bundle branch block, right‐axis QRS configuration can be cured by catheter ablation of anterior fascicle con

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00421.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AV Conduction in WPW. We report an unusual case of a relatively regular wide QRS complex tachycardia alternating with periods of an irregular narrow QRS complex tachycardia during atrial fibrillation in a patient with Wolff‐Parkinson‐White syndrome. Both tachycardias resulted from atrial fibrillation, the wide QRS complex tachycardia being due to 2:1 AV conduction of a type I atrial fibrillation across a posteroseptal accessory AV connect

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00422.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Role of Gap Junctions in Anisotropic Conduction. Electrical activation of the heart requires transfer of current from one discrete cardiac myocyte to another, a process that occurs at gap junctions. Recent advances in knowledge have established that, like most differentiated cells, individual cardiac myocytes express multiple gap junction channel proteins that are members of a multigene family of channel proteins called connexins. These proteins form channels with unique biophysical properties. Furthermore, functionally distinct cardiac tissues such as the nodes and bundles of the conduction system and atrial and ventricular muscle express different combinations of connexins. Myocytes in these tissues are interconnected by gap junctions that differ in a tissue‐specific manner in terms of their number, size, and three‐dimensional distribution. These observations suggest that both molecular and structural aspects of gap junctions are critical determinants of the anisotropic conduction properties of different cardiac tissues. Expression of multiple connexins also creates the possibility that “hybrid” channels composed of more than one connexin protein type can form, thus greatly increasing the potential for fine control of intercellular ion flow and communication within th

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00423.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY