Electrophysiologic effects of SB-237376: A new antiarrhythmic compound with dual potassium and calcium channel blocking action

Journal of Cardiovascular Pharmacology

Volumn 41, Issue 3, 2003, Pages 414-421

  Xu, Xiaoping ^a   Yan, Gan Xin ^a   Wu, Ying ^a   Liu, Tengxian ^a   Kowey, Peter R ^b,c  

^a Main Line Health Heart Center   (United States)

^b THOMAS JEFFERSON UNIVERSITY   (United States)

^c Lankenau Medical Office Building East   (United States)

Author keywords

Action potential; Arrhythmia; Electrophysiology; Pharmacology

Indexed keywords

ANTIARRHYTHMIC AGENT; CALCIUM CHANNEL BLOCKING AGENT; CALCIUM CHANNEL L TYPE; N [3 [[2 (3,4 DIMETHOXYPHENYL)ETHYL]AMINO]PROPYL] 4 NITROBENZAMIDE; POTASSIUM CHANNEL BLOCKING AGENT; SOTALOL; UNCLASSIFIED DRUG;

ACTION POTENTIAL; ANIMAL CELL; ARTICLE; CALCIUM CURRENT; CONCENTRATION RESPONSE; CONTROLLED STUDY; DOG; DRUG EFFICACY; ELECTROPHYSIOLOGY; HEART DEPOLARIZATION; HEART PROARRHYTHMIA; HEART REPOLARIZATION; NONHUMAN; POTASSIUM CURRENT; PRIORITY JOURNAL; QT INTERVAL; RABBIT; RISK ASSESSMENT;

ACTION POTENTIALS; ANIMALS; ANTI-ARRHYTHMIA AGENTS; BENZAMIDES; CALCIUM CHANNEL BLOCKERS; CALCIUM CHANNELS; DOGS; DOSE-RESPONSE RELATIONSHIP, DRUG; DRUGS, INVESTIGATIONAL; ELECTROPHYSIOLOGIC TECHNIQUES, CARDIAC; FEMALE; MALE; MYOCYTES, CARDIAC; POTASSIUM CHANNEL BLOCKERS; POTASSIUM CHANNELS;

EID: 0037372528     PISSN: 01602446     EISSN: None     Source Type: Journal    
DOI: 10.1097/00005344-200303000-00010     Document Type: Article

References (26)

1. Hohnloser SH, Singh BN. Proarrhythmia with class III antiarrhythmic drugs: definition, electrophysiologic mechanisms, incidence, predisposing factors, and clinical implications. J Cardiovasc Electrophysiol. 1995;6:920-36.
2. Yan GX, Wu Y, Liu T, et al. Phase 2 early after depolarization as a trigger of polymorphic ventricular tachycardia in acquired long-QT syndrome: Direct evidence from intracellular recordings in the intact left ventricular wall. Circulation. 2001;103:2851-6.
3. Liu DW, Gintant GA, Antzelevitch C. Ionic bases for electrophysiological distinctions among epicardial, midmyocardial, and endocardial myocytes from the free wall of the canine left ventricle. Circ Res. 1993;72:671-87.
4. Anyukhovsky EP, Sosunov EA, Rosen MR. Regional differences in electrophysiological properties of epicardium, midmyocardium, and endocardium: in vitro and in vivo correlations. Circulation. 1996;94:1981-8.
5. Yan GX, Shimizu W, Antzelevitch C. The characteristics and distribution of M cells in arterially-perfused canine left ventricular wedge preparations. Circulation. 1998;98:1921-7.
6. Akar FG, Yan GX, Antzelevitch C, et al. Unique topographical distribution of M cells underlies reentrant mechanism of torsade de pointes in the long-QT syndrome. Circulation. 2002;105:1247-53.
7. Ks heterogeneity on action potential duration and its rate dependence: a simulation study. Circulation. 1999;99:2466-74.
8. Yan GX, Antzelevitch C. Cellular basis for the normal T wave and the electrocardiographic manifestations of the long-QT syndrome. Circulation. 1998;98:1928-36.
9. + channel opener to reduce transmural dispersion of repolarization and prevent torsade de pointes in LQT1, LQT2, and LQT3 models of the long-QT syndrome. Circulation. 2000;102:706-12.
10. Gillis AM, Traboulsi M, Hii JTY, et al. Antiarrhythmic drug-induced dispersion of ventricular repolarization predicts outcome of serial electropharmacologic studies in patients with malignant ventricular arrhythmias. Am J Cardiol. 1998;81:588-93.
11. El-Sherif N, Chinushi M, Caref EB, et al. Electrophysiological mechanism of the characteristic electrocardiographic morphology of torsade de pointes tachyarrhythmias in the long-QT syndrome: detailed analysis of ventricular tridimensional activation patterns. Circulation. 1997;96:4392-99.
12. Bril A, Faivre JF, Forest MC, et al. Electrophysiological effect of BRL-32872, a novel antiarrhythmic agent with potassium and calcium channel blocking properties, in guinea-pig cardiac isolated preparations. J Pharmacol Exp Ther. 1995;273:1264-72.
13. Bril A, Gout B, Bonhomme M, et al. Combined potassium and calcium channel blocking activities as basis for antiarrhythmic efficacy with low proarrhythmic risk: experimental profile of BRL-32872. J Pharmacol Exp Ther. 1996;276:637-46.
14. Gout B, Bonhomme M, Jean J, et al. In vivo efficacy of SB-237376, a dual potassium and calcium channel antagonist, against atrial and ventricular arrhythmias. Naunyn Schmiedebergs Arch Pharmacol. 1998;358:R701.
15. Faivre JF, Gout B, Landais L, et al. SB-237376, a new antiarrhythmic compound with dual potassium and calcium channel blocking action has improved antiarrhythmic properties. Naunyn Schmiedebergs Arch Pharmacol. 1998;358:R700.
16. Rials SJ, Wu Y, Xu X, et al. Regression of left ventricular hypertrophy with captopril restores normal ventricular action potential duration, dispersion of refractoriness, and vulnerability to inducible ventricular fibrillation. Circulation. 1997;96:1330-6.
17. Yan GX, Antzelevitch C. Cellular basis for the electrocardiographic J wave. Circulation. 1996;93:372-9.
18. Yan GX, Rials SJ, Wu Y, et al. Ventricular hypertrophy amplifies transmural dispersion of repolarization and induces phase 2 early afterdepolarization. Am J Physiol Heart Circ Physiol. 2001;281:H1968-75.
19. Fermini B, Jurkiewicz NK, Jow B, et al. Use-dependent effects of the class III antiarrhythmic agent NE-10064 (azimilide) on cardiac repolarization: block of delayed rectifier potassium and L-type calcium currents. J Cardiovasc Pharmacol. 1995;26:259-71.
20. Yao JA, Tseng G-N. Azimilide (NE-10064) can prolong or shorten the action potential duration in canine ventricular myocytes: dependence on blockade of K, Ca, and Na Channels. J Cardiovasc Electrophysiol. 1997;8:184-98.
21. Gintant GA. Azimilide causes reverse rate-dependent block while reducing both components of delayed-rectifier current in canine ventricular myocytes. J Cardiovasc Pharmacol. 1998;31:945-53.
22. Bril A, Forest MC, Cheval B, et al. Combined potassium and calcium channel antagonistic activities as a basis for neutral frequency dependent increase in action potential duration: comparison between BRL-32872 and azimilide. Cardiovasc Res. 1998;37:130-40.
23. Xu X, Rials SJ, Wu Y, et al. Left ventricular hypertrophy decreases slowly but not rapidly activating delayed rectifier potassium currents of epicardial and endocardial myocytes in rabbits. Circulation. 2001;103:1585-90.
24. MacNeil DJ, Davies RO, Deitchman D. Clinical safety profile of sotalol in the treatment of arrhythmias. Am J Cardiol. 1993;72:44A-50A.
25. Lehmann MH, Hardy S, Archibald D, et al. Sex difference in risk of torsades de pointes with d,l-sotalol. Circulation. 1996;94:2535-41.
26. Connolly SJ, Schnell DJ, Page RL, et al. Dose-response relations of azimilide in the management of symptomatic, recurrent, atrial fibrillation. Am J Cardiol. 2001;88:974-9.