Ranolazine Prevents Phenotype Development in a Mouse Model of Hypertrophic Cardiomyopathy.

ABSTRACT:

Background

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.

Methods and results

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

SUBMITTER: Coppini R 

PROVIDER: S-EPMC6284403 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature