Ranolazine Prevents Phenotype Development in a Mouse Model of Hypertrophic Cardiomyopathy
Current therapies are ineffective in preventing the development of cardiac phenotype in young carriers of mutations associated with hypertrophic cardiomyopathy (HCM). Ranolazine, a late Na current blocker, reduced the electromechanical dysfunction of human HCM myocardium in vitro. To test whether lo...
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| Published in | Circulation. Heart failure Vol. 10; no. 3 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
01.03.2017
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 1941-3289 1941-3297 1941-3297 |
| DOI | 10.1161/CIRCHEARTFAILURE.116.003565 |
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| Abstract | Current therapies are ineffective in preventing the development of cardiac phenotype in young carriers of mutations associated with hypertrophic cardiomyopathy (HCM). Ranolazine, a late Na
current blocker, reduced the electromechanical dysfunction of human HCM myocardium in vitro.
To test whether long-term treatment prevents cardiomyopathy in vivo, transgenic mice harboring the R92Q troponin-T mutation and wild-type littermates received an oral lifelong treatment with ranolazine and were compared with age-matched vehicle-treated animals. In 12-months-old male R92Q mice, ranolazine at therapeutic plasma concentrations prevented the development of HCM-related cardiac phenotype, including thickening of the interventricular septum, left ventricular volume reduction, left ventricular hypercontractility, diastolic dysfunction, left-atrial enlargement and left ventricular fibrosis, as evaluated in vivo using echocardiography and magnetic resonance. Left ventricular cardiomyocytes from vehicle-treated R92Q mice showed marked excitation-contraction coupling abnormalities, including increased diastolic [Ca
] and Ca
waves, whereas cells from treated mutants were undistinguishable from those from wild-type mice. Intact trabeculae from vehicle-treated mutants displayed inotropic insufficiency, increased diastolic tension, and premature contractions; ranolazine treatment counteracted the development of myocardial mechanical abnormalities. In mutant myocytes, ranolazine inhibited the enhanced late Na
current and reduced intracellular [Na
] and diastolic [Ca
], ultimately preventing the pathological increase of calmodulin kinase activity in treated mice.
Owing to the sustained reduction of intracellular Ca
and calmodulin kinase activity, ranolazine prevented the development of morphological and functional cardiac phenotype in mice carrying a clinically relevant HCM-related mutation. Pharmacological inhibitors of late Na
current are promising candidates for an early preventive therapy in young phenotype-negative subjects carrying high-risk HCM-related mutations. |
|---|---|
| AbstractList | Current therapies are ineffective in preventing the development of cardiac phenotype in young carriers of mutations associated with hypertrophic cardiomyopathy (HCM). Ranolazine, a late Na
current blocker, reduced the electromechanical dysfunction of human HCM myocardium in vitro.
To test whether long-term treatment prevents cardiomyopathy in vivo, transgenic mice harboring the R92Q troponin-T mutation and wild-type littermates received an oral lifelong treatment with ranolazine and were compared with age-matched vehicle-treated animals. In 12-months-old male R92Q mice, ranolazine at therapeutic plasma concentrations prevented the development of HCM-related cardiac phenotype, including thickening of the interventricular septum, left ventricular volume reduction, left ventricular hypercontractility, diastolic dysfunction, left-atrial enlargement and left ventricular fibrosis, as evaluated in vivo using echocardiography and magnetic resonance. Left ventricular cardiomyocytes from vehicle-treated R92Q mice showed marked excitation-contraction coupling abnormalities, including increased diastolic [Ca
] and Ca
waves, whereas cells from treated mutants were undistinguishable from those from wild-type mice. Intact trabeculae from vehicle-treated mutants displayed inotropic insufficiency, increased diastolic tension, and premature contractions; ranolazine treatment counteracted the development of myocardial mechanical abnormalities. In mutant myocytes, ranolazine inhibited the enhanced late Na
current and reduced intracellular [Na
] and diastolic [Ca
], ultimately preventing the pathological increase of calmodulin kinase activity in treated mice.
Owing to the sustained reduction of intracellular Ca
and calmodulin kinase activity, ranolazine prevented the development of morphological and functional cardiac phenotype in mice carrying a clinically relevant HCM-related mutation. Pharmacological inhibitors of late Na
current are promising candidates for an early preventive therapy in young phenotype-negative subjects carrying high-risk HCM-related mutations. Current therapies are ineffective in preventing the development of cardiac phenotype in young carriers of mutations associated with hypertrophic cardiomyopathy (HCM). Ranolazine, a late Na+ current blocker, reduced the electromechanical dysfunction of human HCM myocardium in vitro.BACKGROUNDCurrent therapies are ineffective in preventing the development of cardiac phenotype in young carriers of mutations associated with hypertrophic cardiomyopathy (HCM). Ranolazine, a late Na+ current blocker, reduced the electromechanical dysfunction of human HCM myocardium in vitro.To test whether long-term treatment prevents cardiomyopathy in vivo, transgenic mice harboring the R92Q troponin-T mutation and wild-type littermates received an oral lifelong treatment with ranolazine and were compared with age-matched vehicle-treated animals. In 12-months-old male R92Q mice, ranolazine at therapeutic plasma concentrations prevented the development of HCM-related cardiac phenotype, including thickening of the interventricular septum, left ventricular volume reduction, left ventricular hypercontractility, diastolic dysfunction, left-atrial enlargement and left ventricular fibrosis, as evaluated in vivo using echocardiography and magnetic resonance. Left ventricular cardiomyocytes from vehicle-treated R92Q mice showed marked excitation-contraction coupling abnormalities, including increased diastolic [Ca2+] and Ca2+ waves, whereas cells from treated mutants were undistinguishable from those from wild-type mice. Intact trabeculae from vehicle-treated mutants displayed inotropic insufficiency, increased diastolic tension, and premature contractions; ranolazine treatment counteracted the development of myocardial mechanical abnormalities. In mutant myocytes, ranolazine inhibited the enhanced late Na+ current and reduced intracellular [Na+] and diastolic [Ca2+], ultimately preventing the pathological increase of calmodulin kinase activity in treated mice.METHODS AND RESULTSTo test whether long-term treatment prevents cardiomyopathy in vivo, transgenic mice harboring the R92Q troponin-T mutation and wild-type littermates received an oral lifelong treatment with ranolazine and were compared with age-matched vehicle-treated animals. In 12-months-old male R92Q mice, ranolazine at therapeutic plasma concentrations prevented the development of HCM-related cardiac phenotype, including thickening of the interventricular septum, left ventricular volume reduction, left ventricular hypercontractility, diastolic dysfunction, left-atrial enlargement and left ventricular fibrosis, as evaluated in vivo using echocardiography and magnetic resonance. Left ventricular cardiomyocytes from vehicle-treated R92Q mice showed marked excitation-contraction coupling abnormalities, including increased diastolic [Ca2+] and Ca2+ waves, whereas cells from treated mutants were undistinguishable from those from wild-type mice. Intact trabeculae from vehicle-treated mutants displayed inotropic insufficiency, increased diastolic tension, and premature contractions; ranolazine treatment counteracted the development of myocardial mechanical abnormalities. In mutant myocytes, ranolazine inhibited the enhanced late Na+ current and reduced intracellular [Na+] and diastolic [Ca2+], ultimately preventing the pathological increase of calmodulin kinase activity in treated mice.Owing to the sustained reduction of intracellular Ca2+ and calmodulin kinase activity, ranolazine prevented the development of morphological and functional cardiac phenotype in mice carrying a clinically relevant HCM-related mutation. Pharmacological inhibitors of late Na+ current are promising candidates for an early preventive therapy in young phenotype-negative subjects carrying high-risk HCM-related mutations.CONCLUSIONSOwing to the sustained reduction of intracellular Ca2+ and calmodulin kinase activity, ranolazine prevented the development of morphological and functional cardiac phenotype in mice carrying a clinically relevant HCM-related mutation. Pharmacological inhibitors of late Na+ current are promising candidates for an early preventive therapy in young phenotype-negative subjects carrying high-risk HCM-related mutations. |
| Author | Rotellini, Matteo Belardinelli, Luiz Cerbai, Elisabetta Coppini, Raffaele Tesi, Chiara Tardiff, Jil Sacconi, Leonardo Mugelli, Alessandro Gentile, Francesca Santini, Lorenzo Crocini, Claudia Laurino, Annunziatina Ferrantini, Cecilia Bartolucci, Gianluca Mazzoni, Luca Poggesi, Corrado Pioner, Josè Manuel Bargelli, Valentina Olivotto, Iacopo |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28255011$$D View this record in MEDLINE/PubMed |
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| Copyright | 2017 American Heart Association, Inc. |
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| Keywords | sodium remodeling calcium drug therapy arrhythmias cardiomyocyte prevention |
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| PublicationTitle | Circulation. Heart failure |
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| SubjectTerms | Animals Blotting, Western Calcium-Calmodulin-Dependent Protein Kinases - metabolism Cardiomyopathy, Hypertrophic - genetics Cardiomyopathy, Hypertrophic - metabolism Cardiomyopathy, Hypertrophic - physiopathology Cardiomyopathy, Hypertrophic - prevention & control Disease Models, Animal Echocardiography, Doppler Excitation Contraction Coupling - drug effects Genetic Predisposition to Disease Heart Rate Hypertrophy, Left Ventricular - genetics Hypertrophy, Left Ventricular - metabolism Hypertrophy, Left Ventricular - prevention & control Magnetic Resonance Imaging Male Membrane Potentials Mice, Inbred C57BL Mice, Transgenic Microscopy, Confocal Mutation Myocardial Contraction - drug effects Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Phenotype Ranolazine - pharmacology Sodium - metabolism Sodium Channel Blockers - pharmacology Time Factors Troponin T - genetics Ventricular Dysfunction, Left - genetics Ventricular Dysfunction, Left - metabolism Ventricular Dysfunction, Left - prevention & control Ventricular Function, Left - drug effects |
| Title | Ranolazine Prevents Phenotype Development in a Mouse Model of Hypertrophic Cardiomyopathy |
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