3 EXPERIMENTAL ANIMAL MODEL FOR ANTHRACYCLINE-INDUCED HEART FAILURE

The paper by Simunek et al. in this issue of the Journal describes a rabbit model for heart failure (HF), in which HF is caused by anthracycline-induced cardiomyocyte damage.1 The discovery of the presence of both apoptosis,2 and proliferation3 in cardiac myocytes in the human heart, contested the general assumption that the heart is a terminally differentiated organ. With this in mind, animal models of cardiomyocyte injury, such as the rabbit model described by Simunek et al. in this issue, may be of great interest to evaluate alternative, previously unexplored pathophysiologic mechanisms of HF and to test new cardioprotective treatment modalities. The authors describe that systolic and diastolic cardiac function were impaired in daunorubicin treated rabbits, in contrast to saline-treated controls. Assessment of cardiac function was performed by cardiac catheterization, phonocardiography, echocardiography, biochemistry, and histological examinations of the rabbit hearts after sacrifice.1 It was possible to adequately quantify severity of HF, and higher cumulative doses of daunorubicin resulted in increased impairment of cardia