Effect of trimetazidine and verapamil on the cardiomyopathic hamster myosin phenotype

In this study we investigated whether long‐term trimetazidine (anti‐ischaemic drug) therapy alters the ventricular myosin heavy chain (MHC) isoform composition in a model of cardiomyopathy. MHC isoforms were analysed in the native state by electrophoresis in a pyrophosphate buffer. Myosin isoform patterns were studied in cardiac muscle from cardiomyopathic hamsters (CMH) of the BIO 14 : 6 strain during the time course of the disease and compared with those of healthy golden hamsters (F1B). The correlation between myosin profile and Ca2+‐activated ATPase activity was determined from 220 days. At the stage of insufficiency (350 days), CMH presented the most abnormal phenotype with 53% V1‐24% V3 compared to 79% V1‐7% V3 (P