Few experimental studies are available on aging, because of the lack of sui
table experimental models to test specific pathophysiologic mechanisms. In
the present study, the cardiomyopathic Syrian hamster is proposed as experi
mental model of the aging myocardium. In fact, the hamster myocardium devel
ops an early alpha to beta myosin isoform shifting in ventricles that is in
dependent of hemodynamic overload and repeats the phenomenon physiologicall
y occurring in healthy hamsters during the entire lifespan. At the same tim
e, in atria there is a progressive decline of ANF production that is indepe
ndent of intracavitary pressure. Conversely, ANF production in ventricles i
s enhanced before the onset of hemodynamic overload, but parallel to the in
crease in the fibrotic proportion of the ventricular wall. These characteri
stics mimic the modifications occurring in otherwise healthy aged mammals a
nd candidate the cardiomyopathic hamster as a model of early myocardial agi
ng.