Abstract: The present invention relates to a method for the treatment or prevention of atrial fibrillation and/or atrial flutter comprising coadministration of a synergistically therapeutic amount of dronedarone or a pharmaceutically acceptable salt or salts thereof and a synergistically therapeutic amount of ranolazine or a pharmaceutically acceptable salt or salts thereof. Also provided are methods for modulating ventricular and atrial rhythm and rate. This invention also relates to pharmaceutical formulations that are suitable for such combined administration.

Abstract: The present invention relates to a method for the treatment or prevention of atrial fibrillation and/or atrial flutter comprising coadministration of a synergistically therapeutic amount of dronedarone or a pharmaceutically acceptable salt or salts thereof and a synergistically therapeutic amount of ranolazine or a pharmaceutically acceptable salt or salts thereof. Also provided are methods for modulating ventricular and atrial rhythm and rate. This invention also relates to pharmaceutical formulations that are suitable for such combined administration.

Abstract: The present invention relates to a method for the treatment or prevention of atrial fibrillation and/or atrial flutter comprising coadministration of a synergistically therapeutic amount of dronedarone or a pharmaceutically acceptable salt or salts thereof and a synergistically therapeutic amount of ranolazine or a pharmaceutically acceptable salt or salts thereof. Also provided are methods for modulating ventricular and atrial rhythm and rate. This invention also relates to pharmaceutical formulations that are suitable for such combined administration.

Abstract: The present invention relates to a method for the treatment or prevention of atrial fibrillation and/or atrial flutter comprising coadministration of a synergistically therapeutic amount of dronedarone or a pharmaceutically acceptable salt or salts thereof and a synergistically therapeutic amount of ranolazine or a pharmaceutically acceptable salt or salts thereof. Also provided are methods for modulating ventricular and atrial rhythm and rate. This invention also relates to pharmaceutical formulations that are suitable for such combined administration.

Abstract: The present invention relates to a method for the treatment or prevention of atrial fibrillation and/or atrial flutter comprising coadministration of a synergistically therapeutic amount of dronedarone or a pharmaceutically acceptable salt or salts thereof and a synergistically therapeutic amount of ranolazine or a pharmaceutically acceptable salt or salts thereof. Also provided are methods for modulating ventricular and atrial rhythm and rate. This invention also relates to pharmaceutical formulations that are suitable for such combined administration.

Abstract: Methods are provided for treating arrhythmias including tachycardias, such as idiopathic ventricular tachycardia, ventricular fibrillation, and Torsade de Pointes (TdP) in a manner that minimizes undesirable side effects.

Abstract: The present invention relates to a method for the treatment or prevention of atrial fibrillation and/or atrial flutter comprising coadministration of a synergistically therapeutic amount of dronedarone or a pharmaceutically acceptable salt or salts thereof and a synergistically therapeutic amount of ranolazine or a pharmaceutically acceptable salt or salts thereof. Also provided are methods for modulating ventricular and atrial rhythm and rate. This invention also relates to pharmaceutical formulations that are suitable for such combined administration.

Abstract: Previously unknown mutations of the CACNA1C and CACNB2b genes are disclosed which are involved in ion channel disruptions associated with shorter than normal QT interval and ST segment elevation syndrome. These mutations are utilized to diagnose and screen for shorter than normal QT interval and ST segment elevation syndrome, thus providing modalities for diagnosing syncope and/or sudden cardiac death and/or predicting susceptibility to syncope and/or sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant polypeptides described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: Previously unknown mutations of the CACNA1C and CACNB2b genes are disclosed which are involved in ion channel disruptions associated with shorter than normal QT interval and ST segment elevation syndrome. These mutations are utilized to diagnose and screen for shorter than normal QT interval and ST segment elevation syndrome, thus providing modalities for diagnosing syncope and/or sudden cardiac death and/or predicting susceptibility to syncope and/or sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant polypeptides described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: Previously unknown mutations of the CACNA1C and CACNB2b genes are disclosed which are involved in ion channel disruptions associated with shorter than normal QT interval and ST segment elevation syndrome. These mutations are utilized to diagnose and screen for shorter than normal QT interval and ST segment elevation syndrome, thus providing modalities for diagnosing syncope and/or sudden cardiac death and/or predicting susceptibility to syncope and/or sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant polypeptides described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: Previously unknown mutations of the KCNH2, SCN5A and KCNQ1 genes are disclosed which are involved in ion channel disruptions associated with short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease. These mutations are utilized to diagnose and screen for short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease, thus providing modalities for diagnosing sudden cardiac death and/or predicting susceptibility to sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant proteins described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: The present invention relates to a method for the treatment of atrial fibrillation comprising the coadministration of a synergistic therapeutically effective amount of amiodarone and synergistic therapeutically effective amount ranolazine. This invention also relates to pharmaceutical formulations that are suitable for such combined administration.

Abstract: Methods are provided for treating arrhythmias including tachycardias, such as idiopathic ventricular tachycardia, ventricular fibrillation, and Torsade de Pointes (TdP) in a manner that minimizes undesirable side effects.

Abstract: Previously unknown mutations of the KCNH2, SCN5A and KCNQ1 genes are disclosed which are involved in ion channel disruptions associated with short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease. These mutations are utilized to diagnose and screen for short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease, thus providing modalities for diagnosing sudden cardiac death and/or predicting susceptibility to sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant proteins described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: Previously unknown mutations of the KCNH2, SCN5A and KCNQ1 genes are disclosed which are involved in ion channel disruptions associated with short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease. These mutations are utilized to diagnose and screen for short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease, thus providing modalities for diagnosing sudden cardiac death and/or predicting susceptibility to sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant proteins described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: Previously unknown mutations of the CACNA1C and CACNB2b genes are disclosed which are involved in ion channel disruptions associated with shorter than normal QT interval and ST segment elevation syndrome. These mutations are utilized to diagnose and screen for shorter than normal QT interval and ST segment elevation syndrome, thus providing modalities for diagnosing syncope and/or sudden cardiac death and/or predicting susceptibility to syncope and/or sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant polypeptides described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: Methods are provided for treating arrhythmias including tachycardias, such as idiopathic ventricular tachycardia, ventricular fibrillation, and Torsade de Pointes (TdP) in a manner that minimizes undesirable side effects.

Abstract: Previously unknown mutations of the KCNH2, SCN5A and KCNQ1 genes are disclosed which are involved in ion channel disruptions associated with short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease. These mutations are utilized to diagnose and screen for short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease, thus providing modalities for diagnosing sudden cardiac death and/or predicting susceptibility to sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant proteins described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: Methods are provided for treating arrhythmias including tachycardias, such as idiopathic ventricular tachycardia, ventricular fibrillation, and Torsade de Pointes (TdP) in a manner that minimizes undesirable side effects.