Inhibition of Na+ channels ameliorates arrhythmias in a drug-induced model of Andersen-Tawil syndrome

Heart Rhythm

Volumn 10, Issue 2, 2013, Pages 255-263

  Radwański, Przemysław B ^a   Greer Short, Amara ^a   Poelzing, Steven ^a  

^a UNIVERSITY OF UTAH SCHOOL OF MEDICINE   (United States)

Author keywords

Arrhythmia (mechanisms); Calcium (cytosolic); Mapping; Sodium; Ventricular arrhythmias

Indexed keywords

FLECAINIDE; INDO 1; ISOSORBIDE DINITRATE; RANOLAZINE; SODIUM CALCIUM EXCHANGE PROTEIN; SODIUM CHANNEL; TETRODOTOXIN; 1 (3 SULFONATOPROPYL) 4 (BETA)(2 (DI N BUTYLAMINO) 6 NAPHTHYLVINYL)PYRIDINIUM BETAINE; 1-(3-SULFONATOPROPYL)-4-(BETA)(2-(DI-N-BUTYLAMINO)-6-NAPHTHYLVINYL)PYRIDINIUM BETAINE; ACETANILIDE DERIVATIVE; CALCIUM CHANNEL; PIPERAZINE DERIVATIVE; PYRIDINIUM DERIVATIVE;

ACTION POTENTIAL DURATION; ADULT; ANDERSEN SYNDROME; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CALCIUM BLOOD LEVEL; DECAY TIME CONSTANT; GUINEA PIG MODEL; HEART ARRHYTHMIA; MALE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; SODIUM TRANSPORT; TISSUE PREPARATION; ACTION POTENTIAL; ANIMAL; COMPARATIVE STUDY; CYTOSOL; DISEASE MODEL; DOSE RESPONSE; DRUG EFFECT; ELECTROCARDIOGRAPHY; GUINEA PIG; HEART VENTRICLE TACHYCARDIA; METABOLISM; METHODOLOGY; PATHOPHYSIOLOGY; RANDOMIZATION; SENSITIVITY AND SPECIFICITY;

ACETANILIDES; ACTION POTENTIALS; ANDERSEN SYNDROME; ANIMALS; CALCIUM CHANNELS; CYTOSOL; DISEASE MODELS, ANIMAL; DOSE-RESPONSE RELATIONSHIP, DRUG; ELECTROCARDIOGRAPHY; GUINEA PIGS; MALE; PIPERAZINES; PYRIDINIUM COMPOUNDS; RANDOM ALLOCATION; SENSITIVITY AND SPECIFICITY; SODIUM CHANNELS; SODIUM-CALCIUM EXCHANGER; TACHYCARDIA, VENTRICULAR;

EID: 84877288886     PISSN: 15475271     EISSN: 15563871     Source Type: Journal    
DOI: 10.1016/j.hrthm.2012.10.005     Document Type: Article

References (31)

1. Tristani-Firouzi, M., Jensen, J.L., Donaldson, M.R., et al. Functional and clinical characterization of KCNJ2 mutations associated with LQT7 (Andersen syndrome). J Clin Invest 110 (2002), 381–388.
2. Radwański, P.B., Veeraraghavan, R., Poelzing, S., Cytosolic calcium accumulation and delayed repolarization associated with ventricular arrhythmias in a guinea pig model of Andersen-Tawil syndrome. Heart Rhythm 7 (2010), 1428–1435.
3. Morita, H., Zipes, D.P., Morita, S.T., Wu, J., Mechanism of U wave and polymorphic ventricular tachycardia in a canine tissue model of Andersen-Tawil syndrome. Cardiovasc Res 75 (2007), 510–518.
4. Radwański, P.B., Poelzing, S.N.C.X., is an important determinant for premature ventricular activity in a drug-induced model of Andersen-Tawil syndrome. Cardiovasc Res 92 (2011), 57–66.
5. + channels. J Physiol 588 (2010), 4249–4260.
6. Haufe, V., Chamberland, C., Dumaine, R., The promiscuous nature of the cardiac sodium current. J Mol Cell Cardiol 42 (2007), 469–477.
7. Antzelevitch, C., Burashnikov, A., Sicouri, S., Belardinelli, L., Electrophysiologic basis for the antiarrhythmic actions of ranolazine. Heart Rhythm 8 (2011), 1281–1290.
8. Veeraraghavan, R., Salama, M.E., Poelzing, S., Interstitial volume modulates the conduction velocity-gap junction relationship. Am J Physiol Heart Circ Physiol 302 (2012), H278–H286.
9. Bayly, P.V., KenKnight, B.H., Rogers, J.M., Hillsley, R.E., Ideker, R.E., Smith, W.M., Estimation of conduction velocity vector fields from epicardial mapping data. IEEE Trans Biomed Eng 45 (1998), 563–571.
10. Girouard, S.D., Pastore, J.M., Laurita, K.R., Gregory, K.W., Rosenbaum, D.S., Optical mapping in a new guinea pig model of ventricular tachycardia reveals mechanisms for multiple wavelengths in a single reentrant circuit. Circulation 93 (1996), 603–613.
11. Maier, S.K.G., Westenbroek, R.E., McCormick, K.A., Curtis, R., Scheuer, T., Catterall, W.A., Distinct subcellular localization of different sodium channel alpha and beta subunits in single ventricular myocytes from mouse heart. Circulation 109 (2004), 1421–1427.
12. Liu, N., Denegri, M., Ruan, Y., et al. Short communication: flecainide exerts an antiarrhythmic effect in a mouse model of catecholaminergic polymorphic ventricular tachycardia by increasing the threshold for triggered activity. Circ Res 109 (2011), 291–295.
13. 2+ transient: evidence from NCX knockout mice. J Physiol 588 (2010), 3267–3276.
14. Leblanc, N., Hume, J.R., Sodium current-induced release of calcium from cardiac sarcoplasmic reticulum. Science 248 (1990), 372–376.
15. Wasserstrom, J.A., Sharma, R., O'Toole, M.J., et al. Ranolazine antagonizes the effects of increased late sodium current on intracellular calcium cycling in rat isolated intact heart. J Pharmacol Exp Ther 331 (2009), 382–391.
16. Watanabe, H., Chopra, N., Laver, D., et al. Flecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humans. Nat Med 15 (2009), 380–383.
17. Shimizu, W., Antzelevitch, C., Sodium channel block with mexiletine is effective in reducing dispersion of repolarization and preventing torsade de pointes in LQT2 and LQT3 models of the long-QT syndrome. Circulation 96 (1997), 2038–2047.
18. Shaw, R.M., Rudy, Y., Ionic mechanisms of propagation in cardiac tissue: roles of the sodium and L-type calcium currents during reduced excitability and decreased gap junction coupling. Circ Res 81 (1997), 727–741.
19. Veeraraghavan, R., Poelzing, S., Mechanisms underlying increased right ventricular conduction sensitivity to flecainide challenge. Cardiovasc Res 77 (2008), 749–756.
20. Kumar, K., Nearing, B.D., Carvas, M., et al. Ranolazine exerts potent effects on atrial electrical properties and abbreviates atrial fibrillation duration in the intact porcine heart. J Cardiovasc Electrophysiol 20 (2009), 796–802.
21. max in guinea pig myocardium. Circ Res 56 (1985), 696–703.
22. Wang, Z., Fermini, B., Nattel, S., Mechanism of flecainide's rate-dependent actions on action potential duration in canine atrial tissue. J Pharmacol Exp Ther 267 (1993), 575–581.
23. Wu, L., Rajamani, S., Li, H., January, C.T., Shryock, J.C., Belardinelli, L., Reduction of repolarization reserve unmasks the proarrhythmic role of endogenous late Na(+) current in the heart. Am J Physiol Heart Circ Physiol 297 (2009), H1048–H1057.
24. Lipp, P., Niggli, E., Sodium current-induced calcium signals in isolated guinea-pig ventricular myocytes. J Physiol 474 (1994), 439–446.
25. 2+ release from the sarcoplasmic reticulum during action potentials in guinea-pig ventricular myocytes. J Physiol 489 (1995), 1–17.
26. Armoundas, A.A., Hobai, I.A., Tomaselli, G.F., Winslow, R.L., O'Rourke, B., Role of sodium-calcium exchanger in modulating the action potential of ventricular myocytes from normal and failing hearts. Circ Res 93 (2003), 46–53.
27. Noble, D., Noble, P.J., Late sodium current in the pathophysiology of cardiovascular disease: consequences of sodium-calcium overload. Heart, 92, 2006 iv1–iv5.
28. 2+, calmodulin, and CaMKII in normal and failing dog cardiomyocytes: similarities and differences. Am J Physiol Heart Circ Physiol 294 (2008), H1597–H1608.
29. 2+ spark mass. J Mol Cell Cardiol 48 (2010), 293–301.
30. 2+ release channels (RyR2) determines efficacy of class I antiarrhythmic drugs in catecholaminergic polymorphic ventricular tachycardia. Circ Arrhythm Electrophysiol 4 (2011), 128–135.
31. Starmer, C.F., Lastra, A.A., Nesterenko, V.V., Grant, A.O., Proarrhythmic response to sodium channel blockade: theoretical model and numerical experiments. Circulation 84 (1991), 1364–1377.