Anisotropic repolarization in ventricular tissue

Extracellular recording and stimulation techniques have been used to demonstrate that the effective refractory period of epicardial ventricular cells is significantly influenced by the sequence of activation. Whether myocardial fiber orientation is also important in determining the repolarization process is unclear. To determine the importance of fiber orientation on the repolarization process, we studied 12 blocks of pig right ventricular tissue in vitro. The size of each tissue block was 30 x 30 x 2 mm. Transmembrane action potentials were recorded, and effective refractory periods were measured from the preparation's epicardial surface, which showed nearly uniform fiber orientation. Tissues were paced at 500- and 1,000-ms cycle lengths. Sequential recordings were made at 1, 4, 7, 10, 13, and 16 mm from the stimulation site along and across the fibers. The results show that propagation of depolarization was much slower in the transverse direction than in the longitudinal direction. In the transverse direction, action potential duration was longest at the closest observation point, i.e., 1 mm from the stimulation, site (188 +/- 14 and 267 +/- 18 ms for 500- and 1,000-ms pacing cycle lengths, respectively). Action potential duration progressively shortened as the recording site was moved farther from the stimulation site (P < 0.001). The action potential duration 16 mm from the stimulation site was 165 +/- 11 and 247 +/- 12 ms for 500- and 1,000-ms pacing cycle lengths, respectively. In contrast, the action potential duration in the longitudinal direction did not change as the distance between the recording site and stimulation site increased. We conclude that, at physiological temperature and pacing cycle lengths, sequence of activation significantly influenced action potential duration when the propagation of activation was transverse to myocardial fiber orientation. When activation propagated parallel to fiber orientation, there was little or no change of action potential duration as distance increased.

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Action Potential Duration Maps in Homogeneous Cardiac Ventricular Tissue Slices are Independent of Changes in Stimulation Site

Biophysical Journal ◽

10.1016/j.bpj.2011.11.2966 ◽

2012 ◽

Vol 102 (3) ◽

pp. 543a-544a

Author(s):

Ken Wang ◽

Peter Lee ◽

David Gavaghan ◽

Peter Kohl ◽

Christian Bollensdorff

Keyword(s):

Action Potential ◽

Action Potential Duration ◽

Stimulation Site ◽

Tissue Slices ◽

Ventricular Tissue

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VULNERABILITY TO REENTRY, AND DRIFT, STABILITY AND BREAKDOWN OF SPIRAL WAVES IN A LINEAR GRADIENT OF GK IN A LUO–RUDY 1 VIRTUAL VENTRICULAR TISSUE

International Journal of Bifurcation and Chaos ◽

10.1142/s0218127403009010 ◽

2003 ◽

Vol 13 (12) ◽

pp. 3865-3871 ◽

Cited By ~ 2

Author(s):

O. V. ASLANIDI ◽

R. H. CLAYTON ◽

A. V. HOLDEN ◽

H. K. PHILLIPS ◽

R. J. WARD

Keyword(s):

Action Potential ◽

Velocity Component ◽

Action Potential Duration ◽

Cardiac Tissue ◽

Spiral Wave ◽

Spiral Waves ◽

Linear Gradient ◽

Wave Solutions ◽

Ventricular Tissue ◽

Vulnerable Window

The vulnerable window in a heterogeneous virtual LRl cardiac tissue, with a linear gradient in GK, is wider when following propagation down the gradient, towards tissue with longer action potential duration, than when following propagation up the gradient. Spiral wave solutions in a uniform linear gradient in GK drift, with a velocity component along the gradient of the order of mm/s, towards tissue with a longer APD.

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Effects of Thoracic Epidural Anesthesia with and without Autonomic Nervous System Blockade on Cardiac Monophasic Action Potentials and Effective Refractoriness in Awake Dogs

Anesthesiology ◽

10.1097/00000542-200107000-00023 ◽

2001 ◽

Vol 95 (1) ◽

pp. 132-138 ◽

Cited By ~ 35

Author(s):

Andreas Meissner ◽

Lars Eckardt ◽

Paulus Kirchhof ◽

Thomas Weber ◽

Norbert Rolf ◽

...

Keyword(s):

Action Potential ◽

Epidural Anesthesia ◽

Action Potential Duration ◽

Action Potentials ◽

Monophasic Action Potential ◽

Thoracic Epidural Anesthesia ◽

Thoracic Epidural ◽

Monophasic Action Potentials ◽

Cycle Lengths

Background The effects of thoracic epidural anesthesia (TEA) on myocardial repolarization and arrhythmogenicity are only incompletely understood. This is primarily because of the lack of appropriate experimental models. In most of the studies performed thus far, TEA was used in anesthetized animals. Baseline anesthesia itself may have modified the effects of TEA. This study investigates right atrial and ventricular repolarization by recording monophasic action potentials after TEA in awake dogs. The authors hypothesized that an antiarrhythmic role of TEA exists, which may be related to a direct effect of TEA on myocardial repolarization. Methods The hypothesis was tested in an in vivo canine model, in which atrial and ventricular myocardial action potential duration and refractoriness are recorded by means of monophasic action potential catheters. Results Thoracic epidural anesthesia significantly increased ventricular monophasic action potential duration for cycle lengths shorter than 350 ms. Changes in monophasic action potential duration were paralleled by a concomitant prolongation of effective refractory period (ERP) at higher rates so that the ratio of ERP to action potential duration was unaffected. Conclusions This model helps to study the role of TEA on ventricular repolarization and arrhythmogenicity. Because lengthening of repolarization and prolongation of refractoriness may, in some circumstances, be antiarrhythmic, TEA may be protective against generation of ventricular arrhythmias mediated, e.g., by increased sympathetic tone. The results also imply that the beneficial role of TEA might be stronger at the ventricular site as compared with the atrium. At atrial sites there was only a trend toward prolongation of repolarization even at short cycle lengths.

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Control of action potential duration alternans in canine ventricular tissue

2010 Annual International Conference of the IEEE Engineering in Medicine and Biology ◽

10.1109/iembs.2010.5627828 ◽

2010 ◽

Cited By ~ 3

Author(s):

U Kanu ◽

S Iravanian ◽

R F Gilmour ◽

D J Christini

Keyword(s):

Action Potential ◽

Action Potential Duration ◽

Ventricular Tissue

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Cycle length effect on restitution of action potential duration in dog cardiac fibers

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1983.244.6.h782 ◽

1983 ◽

Vol 244 (6) ◽

pp. H782-H792 ◽

Cited By ~ 28

Author(s):

V. Elharrar ◽

B. Surawicz

Keyword(s):

Steady State ◽

Action Potential ◽

Action Potential Duration ◽

Fiber Types ◽

Ventricular Muscle ◽

Purkinje Fibers ◽

Hyperbolic Curve ◽

Cycle Lengths ◽

Kinetics Of ◽

State Curve

Electrical restitution of action potential duration (APD) was determined in Purkinje (n = 8) and ventricular muscle (n = 6) fibers at two different basic cycle lengths (BCL, 1,500 and 500 ms). Restitution curves, normalized for the longest APD (the plateau of restitution), fitted the sum of a fast (T1) and a slow (T2) exponential component. The T1 was shorter in ventricular muscle than Purkinje fibers (89 +/- 5 and 143 +/- 9; mean +/- SE, P less than 0.05), whereas the T2 did not differ (1,448 +/- 231 and 1,439 +/- 211). The BCL altered the APD value during the plateau of restitution but did not change the two exponential components. In both fiber types, the relation between APD and BCL during steady state fitted a hyperbolic curve that predicts the achievement of the maximum APD at long BCL. The restitution curves crossed the steady-state curve at two points outlining three different zones of APD intervals: early premature, late premature, and postmature. The APD during restitution was longer than the steady state in the late premature zone and shorter than the steady-state APD in the post-mature and early premature zones. The APD per se, independent of BCL, did not influence the kinetics of restitution in Purkinje fibers.

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Dynamic restitution of action potential duration during electrical alternans and ventricular fibrillation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1998.275.5.h1635 ◽

1998 ◽

Vol 275 (5) ◽

pp. H1635-H1642 ◽

Cited By ~ 125

Author(s):

Marcus L. Koller ◽

Mark L. Riccio ◽

Robert F. Gilmour Jr.

Keyword(s):

Ventricular Fibrillation ◽

Action Potential ◽

Action Potential Duration ◽

Cycle Length ◽

Strong Relationship ◽

Standard Protocol ◽

Diastolic Interval ◽

Cycle Lengths ◽

Electrical Alternans ◽

Kinetics Of

The restitution kinetics of action potential duration (APD) were investigated in paced canine Purkinje fibers (P; n = 9) and endocardial muscle (M; n = 9), in isolated, perfused canine left ventricles during ventricular fibrillation (VF; n = 4), and in endocardial muscle paced at VF cycle lengths (simulated VF; n = 4). Restitution was assessed with the use of two protocols: delivery of a single extrastimulus after a train of stimuli at cycle length = 300 ms (standard protocol), and fixed pacing at short cycle lengths (100–300 ms) that induced APD alternans (dynamic protocol). The dynamic protocol yielded a monotone increasing restitution function with a maximal slope of 1.13 ± 0.13 in M and 1.14 ± 0.17 in P. Iteration of this function reproduced the APD dynamics found experimentally, including persistent APD alternans. In contrast, the standard protocol yielded a restitution relation with a maximal slope of 0.57 ± 0.18 in M and 0.84 ± 0.20 in P, and iteration of this function did not reproduce the APD dynamics. During VF, the restitution kinetics at short diastolic interval were similar to those determined with the dynamic protocol (maximal slope: 1.72 ± 0.47 in VF and 1.44 ± 0.49 in simulated VF). Thus APD dynamics at short coupling intervals during fixed pacing and during VF were accounted for by the dynamic, but not the standard, restitution relation. These results provide further evidence for a strong relationship among the kinetics of electrical restitution, the occurrence of APD alternans, and complex APD dynamics during VF.

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Control of Action Potential Duration Alternans in Canine Cardiac Ventricular Tissue

IEEE Transactions on Biomedical Engineering ◽

10.1109/tbme.2010.2089984 ◽

2011 ◽

Vol 58 (4) ◽

pp. 894-904 ◽

Cited By ~ 13

Author(s):

Uche B Kanu ◽

Shahriar Iravanian ◽

Robert F Gilmour ◽

David J Christini

Keyword(s):

Action Potential ◽

Action Potential Duration ◽

Ventricular Tissue

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Isoproterenol antagonizes drug-induced prolongation of action potential duration in humans

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y93-113 ◽

1993 ◽

Vol 71 (10-11) ◽

pp. 755-760 ◽

Cited By ~ 13

Author(s):

David Newman ◽

Paul Dorian ◽

Randi Feder-Elituv

Keyword(s):

Steady State ◽

Action Potential ◽

Action Potential Duration ◽

Refractory Period ◽

Cycle Length ◽

Monophasic Action Potential ◽

Class Iii ◽

State Action ◽

Cycle Lengths ◽

Prolongation Of Action Potential

The effects of an isoproterenol infusion on the duration of the human right ventricular endocardial monophasic action potential at 90% repolarization were recorded in the absence and in the presence of an antiarrhythmic drag regimen containing class III effects in two similar groups of patients. The drugs used were amiodarone (N = 3, 300 ± 50 mg), sotalol plus quinidine (N = 11, 156 ± 13 mg sotalol, 1688 ± 594 mg quinidine), and sotalol alone (N = 3, 300 ± 20 mg). All patients had underlying coronary disease but no evidence of inducible ischemia. In the absence of antiarrhythmic drug, isoproterenol did not significantly change the relationship of action potential duration at 90% repolarization to cycle length; there was a linear decrease in action potential duration by 19.8% between a paced cycle length of 600 and 300 ms. Isoproterenol did not significantly shorten the action potential duration at any cycle length. However, isoproterenol decreased the ventricular effective refractory period at 400 ms drive from 240 ± 5.0 to 225 ± 6.0 ms (p < 0.05) accompanied by no change in the ratio of refractory period to steady-state action potential duration. In the presence of class III drug effects, the action potential duration was increased by an average of 9.2% at all paced cycle lengths longer than 300 ms (p < 0.05). The ventricular refractory period was increased from 240 ± 5 to 269 ± 9.0 ms (p < 0.05 compared with baseline) with a concomitant increase in the ratio of refractory period to action potential duration from 96 ± 2 to 103 ± 2% (p < 0.05 compared with baseline). With infusion of isoproterenol in the presence of a class III containing regimen, the drug-prolonged action potential duration was shortened (p < 0.05) by an average of 8.1% at all cycle lengths longer than 300 ms. These results suggest that isoproterenol simulation of enhanced sympathetic tone can antagonize drug prolongation of action potential duration and that in the absence of drugs, the effects of isoproterenol on the steady-state action potential duration are modest. The clinical utility of class III agents may be augmented by the addition of concomitant β-blockade.Key words: action potential duration, antiarrhythmic drugs, isoproterenol.

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