, and Wolfgang R. Bauer. Multimodal functional cardiac MRI in creatine kinasedeficient mice reveals subtle abnormalities in myocardial perfusion and mechanics. Am J Physiol Heart Circ Physiol 290: H2516-H2521, 2006. First published January 13, 2006; doi:10.1152/ajpheart.01038.2005.-A decrease in the supply of ATP from the creatine kinase (CK) system is thought to contribute to the evolution of heart failure. However, previous studies on mice with a combined knockout of the mitochondrial and cytosolic CK (CK Ϫ/Ϫ ) have not revealed overt left ventricular dysfunction. The aim of this study was to employ novel MRI techniques to measure maximal myocardial velocity (Vmax) and myocardial perfusion and thus determine whether abnormalities in the myocardial phenotype existed in CK Ϫ/Ϫ mice, both at baseline and 4 wk after myocardial infarction (MI Ϫ/Ϫ MI, 3.71 Ϯ 0.57 ml/g ⅐ min, P ϭ NS, P Ͻ 0.05 vs. baseline), paralleled by a significantly reduced capillary density (histology). In conclusion, myocardial function in transgenic mice may appear normal when only gross indexes of performance such as EF are assessed. However, the use of a combination of novel MRI techniques to measure myocardial perfusion and mechanics allowed the abnormalities in the CK Ϫ/Ϫ phenotype to be detected. The myocardium in CK-deficient mice is characterized by reduced perfusion and reduced maximal contraction velocity, suggesting that the myocardial hypertrophy seen in these mice cannot fully compensate for the absence of the CK system. magnetic resonance imaging; contractility; myocardial infarction CHANGES IN myocardial energetics, including reduced levels of phosphocreatine, creatine kinase (CK) (10, 16), and ATP (20), have been documented in the failing heart. However, whether these alterations in myocardial energetics are a causal mechanism contributing to left ventricular (LV) remodeling and dysfunction or an adaptive phenomenon has yet to be resolved. Recently, our group reported that deletion of the CK enzyme system [double knockout of the mitochondrial and cytosolic CK (CK Ϫ/Ϫ )] leads to adaptive changes of the murine heart, consisting of LV hypertrophy and mild dilatation of the LV. However, cardiac output and LV ejection fraction remained normal in these mice (15). Furthermore, when CK Ϫ/Ϫ mice were examined 4 wk after the induction of myocardial infarction (MI), no evidence of adverse LV remodeling was seen (15). Therefore, the aim of the current study was to determine whether the use of novel techniques in mouse cardiac MRI, such as perfusion imaging and the imaging of myocardial mechanics, would allow subtle abnormalities of the myocardial phenotype to be detected.A phase-contrast MRI pulse sequence, recently developed by our group (21) to measure myocardial contraction velocity and mechanics in mice, was used in this study. In addition, a second novel MR technique to quantify myocardial perfusion, which has also recently been modified to work in the small and rapidly beating mouse heart (12, 22), was employed to assess myocardial p...