What happens when cardiac Na channels lose their function? 1 - Numerical studies of the vulnerable period in tissue expressing mutant channels

Cardiovascular Research

Volumn 57, Issue 1, 2003, Pages 82-91

  Starmer, C Frank ^a   Colatsky, Thomas J ^b   Grant, Augustus O ^c  

^a MEDICAL UNIVERSITY OF SOUTH CAROLINA   (United States)

^b MEDICAL UNIVERSITY OF SOUTH CAROLINA   (United States)

^c DUKE UNIVERSITY MEDICAL CENTER   (United States)

Author keywords

Arrhythmia (mechanisms); Computer modelling; Conduction (block); Impulse formation; Na channel; Ventricular arrhythmias

Indexed keywords

SODIUM CHANNEL;

ARTICLE; CELL DENSITY; COMPUTER MODEL; HEART EXCITATION; HEART MUSCLE CELL; MUTATION; PRIORITY JOURNAL; REENTRY ARRHYTHMIA; SODIUM CONDUCTANCE;

ARRHYTHMIA; COMPUTER SIMULATION; DEATH, SUDDEN, CARDIAC; HUMANS; MODELS, CARDIOVASCULAR; MUTATION; MYOCYTES, CARDIAC; SODIUM CHANNELS;

EID: 0037215692     PISSN: 00086363     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0008-6363(02)00613-2     Document Type: Article

References (28)

1. Mines G.R. On circulating excitations in heart muscle and their possible relation to tachycardia and fibrillation. Trans R Soc Can. 8:1914;43-52.
2. Wiggers C.F., Wegria R. Ventricular fibrillation due to single localized induction and condenser shocks applied during the vulnerable phase of ventricular systole. Am J Physiol. 128:1940;500-503.
3. Wiener N., Rosenblueth A. The mathematical formulation of the problem of conduction of impulses in a network of connected excitable elements, specifically in cardiac muscle. Arch Inst Cardiol Mex. 16:1946;205-265.
4. Allessie M.A., Bonke F.I.M., Schopman F.J.G. Circus movement in rabbit atrial muscle as a mechanism of tachycardia. Circ Res. 33:1973;54-62.
5. VanCapelle F.J.L., Durrer D. Computer simulation of arrhythmias in a network of coupled excitable elements. Circ Res. 47:1980;454-466.
6. Joyner R.W. Mechanisms of unidirectional block in cardiac tissues. Biophys J. 35:1981;113-125.
7. Quan W., Rudy Y. Unidirectional block and reentry of cardiac excitation: a model study. Circ Res. 66:1990;367-382.
8. 1-subunits. Circ Res. 83:1998;141-146.
9. Dumaine R., Towbin J.A., Brugada P., et al. Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. Circ Res. 85:1999;803-809.
10. Pu J., Boyden P.A. Alterations of Na+ currents in myocytes from epicardial border zone of the infarcted heart: a possible ionic mechanism for reduced excitability and postrepolarization refractoriness. Circ Res. 81:1997;110-119.
11. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. N Engl J Med. 432:1989;406-412.
12. Starmer C.F., Lastra A.A., Nesterenko V.V., Grant A.O. A proarrhythmic response to sodium channel blockade: theoretical model and numerical experiments. Circulation. 84:1991;1364-1377.
13. Starmer C.F., Viktashev V.N., Romashko D.N., Stepanov M.R., Makarova O.N., Krinsky V.I. Vulnerability in an excitable medium: analytical and numerical studies of initiating unidirectional propagation. Biophys J. 65:1993;1775-1787.
14. Starmer C.F., Lancaster A.R., Lastra A.A., Grant A.O. Cardiac instability amplified by use-dependent Na channel blockade. Am J Physiol. 262:1992;H1305-H1310.
15. Nesterenko V.V., Lastra A.A., Rosenshtraukh L.V., Starmer C.F. A proarrhythmic response to sodium channel blockade: modulation of the vulnerable period in guinea pig ventricular myocardium. J Cardiovasc Pharmacol. 19:1992;810-820.
16. Starmer CF, Grant AO, Colatsky TJ. What happens when cardiac Na channel function is compromised? 2: Numerical studies of the vulnerable period in tissue altered by drugs (accepted for publication).
17. Beeler G.W., Reuter H. Reconstruction of the action potential of ventricular myocardial fibers. J Physiol. 268:1977;177-210.
18. Ebijara L, Johnson EA. Fast sodium current in cardiac muscle: a quantitative description. Biophys J 1980;779-790.
19. Bezzina C.R., Rook M.B., Wilde A.A.M. Cardiac sodium channel and inherited arrhythmia syndromes. Cardiovasc Res. 49:2001;257-271.
20. Wan X., Chen S., Sadeghpour A., Wang Q., Kirsch G.E. Accelerated inactivation in a mutant Na+ channel associated with idiopathic ventricular fibrillation. Am J Physiol. 280:2001;H354-H360.
21. Vatta M., Dumaine R., Varghese G., et al. Genetic and biophysical basis of sudden unexplained nocturnal death syndrome (SUNDS), a disease allelic to Brugada syndrome. Hum Mol Genet. 11:2002;337-345.
22. Alessi R., Nusynowitz M., Abildskov J.A., Moe G.K. Non-uniform distribution of vagal effects on the atrial refractory period. Am J Physiol. 194:1958;406-410.
23. Rushton W.A.H. Initiation of the propagated disturbance. Proc R Soc B. 124:1937;210-243.
24. Fozzard H.A., Schoenberg M. Strength-duration curves in cardiac Purkinje fibres: effects of liminal length and charge distribution. J Physiol. 226:1972;593-618.
25. Spach M.S., Dolber P.C., Heidlage J.F. Interaction of inhomogeneities of repolarization with anisotropic propagation in dog atria: a mechanism for both preventing and initiating reentry. Circ Res. 65:1989;1612-1631.
26. Gomez-Gesteira M., Fernandez-Garcia G., Munuzuri A., et al. Vulnerability in an excitable Belousov-Zhabotinsky medium: from 1D to 2D. Physica D. 76:1994;359-368.
27. Hondeghem L.M., Carlsson L., Duker G. Instability and triangulation of the action potential predict serious proarrhythmia, but action potential duration prolongation is antiarrhythmic. Circulation. 103:2001;2004-2013.
28. Yamanouchi Y., Cheng Y., Tchou P.J., Efimov I.R. The mechanism of the vulnerable window: the role of virtual electrodes and shock polarity. Can J Physiol Pharmacol. 79:2001;25-33.