This study alms to elucidate the pathophysiological background of the developing heart failure in mice with cardiomyocyte-restricted knockout of survivin (survivin(-/-)). Molecular and functional imaging methods as positron emission tomography (PET) and magnetic resonance imaging (MRI) were used for non-invasive phenotyping. Serial measurements in survivin(-/-) and their littermate controls were performed and combined with histological findings, assessing not only the macroscopic enlargement of heart chambers over time in vivo but also compensatory mechanisms on cellular levels such as hypertrophy and enhancement of glucose metabolism.