Role of the slow current in cardiac electrophysiology.

Zipes, Douglas P.; Besch, Henry R.; Watanabe, Akira

doi:10.1161/01.cir.51.5.761

Cited by 77 publications

(12 citation statements)

References 49 publications

(10 reference statements)

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“…3) The maximum diastolic potential and the maximum rate of rise of the slow-type AAPs was -54.5 mV and 2.7 V/s, respectively, which agree well with those of the "slow response" with abnormal automaticity (ZIPES et al, 1975). These findings support the notion that activation of 'Ca contributes to the pacemaker potential of the slow-type AAPs.…”

Section: Discussionsupporting

confidence: 78%

Two differential mechanisms of automaticity in diseased human atrial fibers.

et al. 1988

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The ionic mechanisms of automaticity in spontaneously active preparations (n = 38) from "diseased" human atria were investigated. The cycle length (CL) of the automatic action potential (AAP) ranged from 0.6 to 4.5 s (mean + S.D.: 2.0 + 1.0 s). The AAP from preparations obtained from non-digitalized patients (group 1, n = 29) showed various CLs, in that 16 patients had a CL longer than 2.0 s (slow-type AAP) while in tissues from the other 13 patients, the CL was 2.0 s or less (fast-type AAP). On the other hand, all preparations obtained from the digitalized patients prior to cardiac surgery (group 2, n = 9) had the fast-type AAP (CL <_ 2.0 s). The slow-type AAP was accelerated and changed to the fast one after application of ouabain (1 µM) or by perfusing with 50% [Na + ]o Tyrode solution. Ryanodine (1 tiM), a specific inhibitor of calcium release from the sarcoplasmic reticulum (SR), markedly lengthened the CL of fast-type AAP, without affecting the slow-type AAP. In contrast, caffeine (15 mM) shortened the CL of the slow-type AAP and remarkably lengthened the CL of the fast-type AAP, as is the case in ryanodine. The rate of slow-type AAP was enhanced with an increase in [Ca2+]o and depressed with a decrease in [Ca2 +]o or with application of diltiazem, a Ca2 + channel blocker. The slow-type AAP was changed to the fast-type AAP by stretching the preparation by about 20%. In vitro preparations excised from patients with dilated atria revealed a shorter CL of AAPs. We conclude that in "diseased" human atrial preparations, the ionic mechanism responsible for generation of slow-and fast-type automaticity differs. Slow automaticity (CL >2.0 s) perhaps relates to activation of the slow inward Ca2 + current, while the fast-type automaticity (CL <2.0 s) is linked to cyclic increases in [Ca2 +]~.

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Section: Discussionsupporting

confidence: 78%

Two differential mechanisms of automaticity in diseased human atrial fibers.

et al. 1988

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“…The initiation of an onset of triggered activity is thus a cycle length-dependent phenomenon. Nevertheless, shortening of the basic driving cycle length may induce unidirectional block in one pathway and slow conduction in the other pathway, setting up conditions for reentry to occur (13,15,20 suggested that the slow channel action potentials may become dominant under pathologic conditions, such as myocardial ischemia, in regions of the heart ordinarily dominated by the fast sodium channel response (39,40). Such slow channel action potentials have been implicated in the genesis of reentrant ventricular arrhythmias because of their propensity for very slow propagation of impulses (41,42).…”

Section: Discussionmentioning

confidence: 99%

“…It has also been postulated that the calcium-dependent slow channel response may become dominant, and, in turn, may give rise to an automatic rhythm under pathologic conditions (39,40). In this situation, verapamil would be expected to be effective in suppressing such an automatic rhythm.…”

Section: Discussionmentioning

confidence: 99%

Effects of verapamil on ventricular tachycardias possibly caused by reentry, automaticity, and triggered activity.

et al. 1983

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A B S T R A C T To define the role of verapamil in the treatment of ventricular tachycardia (VT), we studied 21 patients with chronic recurrent VT. Electrophysiologic studies were performed before and during intravenous infusion of verapamil (0.15 mg/kg followed by 0.005 mg/kg per min). On the basis of the mode of VT initiation and termination, we identified three groups of patients: (a) 11 patients had VT suggestive of reentry, as VT could be initiated with ventricular extrastimulation and terminated with overdrive ventricular pacing. Verapamil did not affect the inducibility and cycle length of VT. (b) 7 patients had VT suggestive of catecholamine-sensitive automaticity as VT could not be initiated with programmed electrical stimulation but could be provoked by isoproterenol infusion. Moreover, the VT could not be converted to a sustained sinus rhythm with overdrive ventricular pacing and it resolved only with discontinuing isoproterenol infusion. Verapamil exerted no effects on VT. (c) 3 patients had VT with electrophysiologic characteristics suggestive of triggered activity related to delayed afterdepolarizations. Characteristically, after attaining a range of cycle lengths, the sinus, atrial or ventricular paced rhythm could initiate VT without ventricular extrastimulation. The first beat of VT invariably occurred late in the cardiac cycle with a premature coupling interval 0-80 ms shorter than the preceding QRS cycle length; the premature coupling interval gradually decreased as the sinus, atrial or ventricular paced cycle length progressively shortened. Of

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“…n u r d e r l a n g s a m e C a l c i u m k a n a l e x i s t i e r t u n d o b e i n s c h n e l l e r N a t r i u m k ahal fehlt o d e r n u r i n a k t i v ist (41,42,43,44,45,46,47). A r t i f i z i e l l e F r e q u e n zs t e i g e r u n g b r e m s…”

Section: B E I D I E S E N Z E L L E N S I N D C a L C I U M I O N E unclassified

Die Adaptation der transnodalen Erregungsleitung des gesunden menschlichen AV-Knotens an auf- und absteigende atriale Frequenzbelastung vor und nach Blockade des autonomen Nervensystems

et al. 1979

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In 19 patients with healthy AV-nodes the adaptation of the intranodal conduction time (A-H time) to gliding increase and decrease in atrial frequency and to the blockade of the autonomic nervous system was investigated using His bundle electrograms. The measurements were performed during right atrial stimulation with three frequencies, each with a duration of one minute, before and after blockade of the parasympathetic (8 pat.; 1 mg atropine i.v.) and the sympathetic (11 pat.; 0.4 mg Visken i.v.) nervous system. Gliding increase and decrease in atrial frequency results in a staircase pattern of A-H-adaptation in 18 of the patients. The height of the steps was identical in both phases of stimulation in each individual patient. One patient showed functional dissociation of intranodal conduction which was different during increase and decrease of atrial frequency. With parasympathetic blockade the staircase behavior of the A-H time basically remained unchanged with the exception of shorter A-H intervals resulting in lower steps. Atropine abolished the functional dissociation of intranodal conduction; thus the drug might prevent reentrytachycardias due to functional dissociation in the AV-node. Sympathetic blockade lengthens the intranodal conduction time; thus shifting the staircase pattern of the A-H time to higher levels. The results are discussed with respect to the electrophysiological characteristics of AV nodal cells as slow response fibers, and to the changes caused by atrial stimulation, acetylcholine and adrenaline.

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Role of the slow current in cardiac electrophysiology.

Cited by 77 publications

References 49 publications

Two differential mechanisms of automaticity in diseased human atrial fibers.

Two differential mechanisms of automaticity in diseased human atrial fibers.

Effects of verapamil on ventricular tachycardias possibly caused by reentry, automaticity, and triggered activity.

Die Adaptation der transnodalen Erregungsleitung des gesunden menschlichen AV-Knotens an auf- und absteigende atriale Frequenzbelastung vor und nach Blockade des autonomen Nervensystems

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