Relations between myocardial contractility, myosin phenotype, and plasma angiotensin-converting enzyme activity in the cardiomyopathic hamster.

Angiotensin-converting enzyme (ACE) inhibitors have been shown to preserve myocardial contractility in the cardiomyopathic Syrian hamster (CSH). To determine if this was related to changes in myosin heavy-chain (MHC) phenotype, myosin isoform patterns and mechanical properties were studied in the same left ventricular papillary muscle from CSH of the Bio 53.58-dilated strain. From age 1 to 6 months, 22 CSH randomly received either perindopril 1 mg/kg/day in distilled water (PE, n = 11) or distilled water only (PL, n = 11), and seven control golden Syrian hamsters (C) received distilled water by force-feeding. Compared to C, PL had a lower Vmax (p < 0.01), a lower amount of alpha-MHC (p < 0.01), and an unchanged twitch duration. In PE, as compared to PL, there was a higher Vmax (p < 0.05), a higher alpha-MHC (p < 0.05), and an unchanged twitch duration. There was a positive relationship between Vmax and alpha-MHC in the population taken as a whole (p < 0.01), and when muscles from C and PL groups were plotted together (p < 0.001), but neither within each group, nor when PL and PE were plotted together. Our study indicates that in CSH (a) the preserved contractility with ACE-inhibitor treatment is associated with limitation of isomyosin shift induced by the myopathic process, but no cause-to-effect relationship could be demonstrated on the basis of our data, and (b) adaptive changes in twitch duration were not observed either in untreated CSH or in perindopril-treated CSH, despite significant changes in alpha-MHC content.