Calmodulin Antagonist W‐7 Prevents Sparfloxacin‐Induced Early Afterdepolarizations (EADs) in Isolated Rabbit Purkinje Fibers: Importance of Beat‐to‐Beat Instability of the Repolarization

Introduction: The occurrence of early afterdepolarizations (EADs) has been related to the incidence of torsades de pointes in drug‐induced long QT (LQT). The generation of EADs may be facilitated by Ca2+/calmodulin‐dependent protein kinase II (CaM kinase).

[1]  H. R. Lu,et al.  Are there sex-specific differences in ventricular repolarization or in drug-induced early afterdepolarizations in isolated rabbit purkinje fibers? , 2000, Journal of cardiovascular pharmacology.

[2]  M. Rosen,et al.  Effects of pacing on triggered activity induced by early afterdepolarizations. , 1984, Circulation.

[3]  D. Roden,et al.  Systemic administration of calmodulin antagonist W-7 or protein kinase A inhibitor H-8 prevents torsade de pointes in rabbits. , 1999, Circulation.

[4]  A. Templeton,et al.  Effects of sparfloxacin, grepafloxacin, moxifloxacin, and ciprofloxacin on cardiac action potential duration. , 2000, European journal of pharmacology.

[5]  Mark E. Anderson,et al.  CaM kinase augments cardiac L-type Ca2+ current: a cellular mechanism for long Q-T arrhythmias. , 1999, American journal of physiology. Heart and circulatory physiology.

[6]  H. Schulman,et al.  KN-93, an inhibitor of multifunctional Ca++/calmodulin-dependent protein kinase, decreases early afterdepolarizations in rabbit heart. , 1998, The Journal of pharmacology and experimental therapeutics.

[7]  Hua-rong Lu,et al.  Drug-induced long QT in isolated rabbit Purkinje fibers: importance of action potential duration, triangulation and early afterdepolarizations. , 2002, European journal of pharmacology.

[8]  R. Lazzara,et al.  Afterdepolarizations as a mechanism for the long QT syndrome: electrophysiologic studies of a case. , 1984, Journal of the American College of Cardiology.

[9]  M. Swindells,et al.  Solution structure of calmodulin-W-7 complex: the basis of diversity in molecular recognition. , 1998, Journal of molecular biology.

[10]  Mark E. Anderson,et al.  Calmodulin Inhibitor W-7 Unmasks a Novel Electrocardiographic Parameter That Predicts Initiation of Torsade de Pointes , 2002, Circulation.

[11]  H. Hidaka,et al.  Two types of calcium-dependent protein phosphorylations modulated by calmodulin antagonists. Naphthalenesulfonamide derivatives. , 1982, Molecular pharmacology.

[12]  D. Lacroix,et al.  Electrophysiological and Arrhythmogenic Effects of the Histamine Type 1‐Receptor Antagonist Astemizole on Rabbit Purkinje Fibers: Clinical Relevance , 1995, Journal of cardiovascular pharmacology.

[13]  P. De Koninck,et al.  Sensitivity of CaM kinase II to the frequency of Ca2+ oscillations. , 1998, Science.

[14]  H. R. Lu,et al.  A new method to calculate the beat-to-beat instability of QT duration in drug-induced long QT in anesthetized dogs. , 2005, Journal of pharmacological and toxicological methods.

[15]  R. Bordet,et al.  Sparfloxacin but not levofloxacin or ofloxacin prolongs cardiac repolarization in rabbit Purkinje fibers , 1998, Fundamental & clinical pharmacology.

[16]  H. Hidaka,et al.  Pharmacology of protein kinase inhibitors. , 1992, Annual review of pharmacology and toxicology.

[17]  L. Cubeddu QT prolongation and fatal arrhythmias: a review of clinical implications and effects of drugs. , 2003, American journal of therapeutics.

[18]  G Duker,et al.  Electrophysiological and inotropic effects of H 234/09 (almokalant) in vitro: a comparison with two other novel IK blocking drugs, UK-68,798 (dofetilide) and E-4031. , 1993, Cardiovascular research.

[19]  C. Raehl,et al.  Drug-induced torsade de pointes. , 1985, Clinical pharmacy.

[20]  K. Hashimoto,et al.  Effects of mexiletine on the canine model of sparfloxacin-induced long QT syndrome. , 2003, European journal of pharmacology.

[21]  K. Hiratsuka,et al.  Comparative assessment of prurifloxacin, sparfloxacin, gatifloxacin and levofloxacin in the rabbit model of proarrhythmia. , 2004, The Journal of toxicological sciences.

[22]  D. A. Brown,et al.  The naphthalenesulphonamide calmodulin antagonist W7 and its 5-iodo-1-C8 analogue inhibit potassium and calcium currents in NG108-15 neuroblastoma × glioma cells in a manner possibly unrelated to their antagonism of calmodulin , 1991, Neuroscience Letters.

[23]  Ard Teisman,et al.  Choice of cardiac tissue plays an important role in the evaluation of drug-induced prolongation of the QT interval in vitro in rabbit. , 2005, Journal of pharmacological and toxicological methods.

[24]  Dan M Roden,et al.  Calmodulin Kinase II and Arrhythmias in a Mouse Model of Cardiac Hypertrophy , 2002, Circulation.

[25]  Craig T. January,et al.  Early Afterdepolarizations: Mechanism of Induction and Block A Role for L‐Type Ca2+ Current , 1989, Circulation research.

[26]  H. Lode,et al.  Sparfloxacin in the treatment of drug resistant tuberculosis or intolerance of first line therapy. , 2001, The European respiratory journal.

[27]  K. Sunagawa,et al.  Cellular and ionic mechanism for drug-induced long QT syndrome and effectiveness of verapamil. , 2005, Journal of the American College of Cardiology.

[28]  H. Wellens,et al.  Progress in the understanding of cardiac early afterdepolarizations and torsades de pointes: time to revise current concepts. , 2000, Cardiovascular research.

[29]  O. Pongs,et al.  Effects of fluoroquinolones on HERG currents. , 2000, European journal of pharmacology.

[30]  D. Zipes,et al.  Electrophysiological Mechanisms in a Canine Model of Erythromycin‐Associated Long QT Syndrome , 1993, Circulation.

[31]  Guy Salama,et al.  Cytosolic Ca2+ triggers early afterdepolarizations and torsade de pointes in rabbit hearts with type 2 long QT syndrome , 2002, The Journal of physiology.

[32]  D. Roden,et al.  Potassium current antagonist properties and proarrhythmic consequences of quinolone antibiotics. , 2001, The Journal of pharmacology and experimental therapeutics.

[33]  R. Lazzara,et al.  Early Afterdepolarizations Produced by d,1‐Sotalol and Clofilium , 1997, Journal of cardiovascular electrophysiology.

[34]  C. Antzelevitch,et al.  Effects of Sodium Channel Block with Mexiletine to Reverse Action Potential Prolongation in In Vitro Models of the Long QT Syndrome , 1997, Journal of cardiovascular electrophysiology.

[35]  S. Viskin,et al.  Long QT syndrome caused by noncardiac drugs. , 2003, Progress in cardiovascular diseases.

[36]  S. Heinemann,et al.  Inhibition of human ether à go‐go potassium channels by Ca2+/calmodulin , 2000, The EMBO journal.

[37]  J. Kimura Effects of various calmodulin antagonists on Na/Ca exchange current of single ventricular cells of guinea-pig , 1993, Pflügers Archiv.

[38]  Hua-rong Lu,et al.  Species Plays an Important Role in Drug‐Induced Prolongation of Action Potential Duration and Early Afterdepolarizations in Isolated Purkinje Fibers , 2001, Journal of cardiovascular electrophysiology.

[39]  Charles Antzelevitch,et al.  Reinduction of Atrial Fibrillation Immediately After Termination of the Arrhythmia Is Mediated by Late Phase 3 Early Afterdepolarization–Induced Triggered Activity , 2003, Circulation.

[40]  B. Souweine,et al.  Torsades de pointe probably related to sparfloxacin , 1996, European Journal of Clinical Microbiology and Infectious Diseases.

[41]  R. Shah,et al.  Pharmacogenetic Aspects of Drug-Induced Torsade de Pointes , 2004, Drug safety.

[42]  L. Carlsson,et al.  Proarrhythmic effects of the class III agent almokalant: importance of infusion rate, QT dispersion, and early afterdepolarisations. , 1993, Cardiovascular research.

[43]  M. Anderson Calmodulin kinase and L-type calcium channels; a recipe for arrhythmias? , 2004, Trends in cardiovascular medicine.

[44]  R. Gilmour,et al.  Depressant effect of magnesium on early afterdepolarizations and triggered activity induced by cesium, quinidine, and 4-aminopyridine in canine cardiac Purkinje fibers. , 1989, American heart journal.

[45]  D J Triggle,et al.  Interactions of a series of fluoroquinolone antibacterial drugs with the human cardiac K+ channel HERG. , 2001, Molecular pharmacology.

[46]  Milan Stengl,et al.  Increased Short-Term Variability of Repolarization Predicts d-Sotalol–Induced Torsades de Pointes in Dogs , 2004, Circulation.