Few experimental studies are available on aging, because of the lack of suitable experimental models to test specific pathophysiologic mechanisms. In the present study, the cardiomyopathic Syrian hamster is proposed as experimental model of the aging myocardium. In fact, the hamster myocardium develops an early alpha to beta myosin isoform shifting in ventricles that is independent of hemodynamic overload and repeats the phenomenon physiologically occurring in healthy hamsters during the entire lifespan. At the same time, in atria there is a progressive decline of ANF production that is independent of intracavitary pressure. Conversely, ANF production in ventricles is enhanced before the onset of hemodynamic overload, but parallel to the increase in the fibrotic proportion of the ventricular wall. These characteristics mimic the modifications occurring in otherwise healthy aged mammals and candidate the cardiomyopathic hamster as a model of early myocardial aging.