RV insertion points and anterolateral wall of the left ventricle. Importantly, prognosis and cardiac function are poorer in DMD patients who have late gadolinium enhancement. In the mdx mouse, standard measures of left ventricular function, including ejection fraction, end systolic volume and wall thickening, do not become abnormal until 9 to 11 months of age. However, MRI has identified early abnormalities in cardiac wall strain and torsion, as well as right ventricular dysfunction at 6–8 months. Imaging studies of cardiac function in the mdx mouse have focused on mice at one specific age, or imaged different groups of mice at different ages, the earliest time point being,5- months. Here we serially imaged the same group of male mdx mice and littermate male wild type controls using MRI at 1 month after birth and at four further timepoints up to 1 year. We assessed left and right ventricular systolic function, diastolic function and response to dobutamine stress. Further, we report the first use of late gadolinium enhancement to identify regions of myocardial fibrosis in mdx mice. In vivo measures of fibrosis correlated with cardiac function, and may offer a sensitive and clinically relevant in vivo method for assessing the efficacy of experimental treatments for muscular dystrophy. In vivo MRI of mouse models of human cardiac disease can give valuable insights into pathology and therapy. Although the mdx mouse model of muscular dystrophy has been studied using ultrasound and haemodynamic measurements, there are limited data from MRI studies and no reports of serial MR imaging of disease progression in the same mdx mice over time. Clinically and experimentally, cardiac MRI is more sensitive to small alterations in cardiac function than other imaging modalities, including ultrasound. Hence, we anticipated that the application of MRI to the mdx mouse, known to have only mild cardiomyopathy when young, may identify subtle changes previously missed by other techniques. In agreement with previous reports, standard cine-MRI did not show altered resting LV function in mdx mice until 9 months of age. However, high temporal resolution cine-MRI indicated that peak LV filling and ejection rates were lower at 3 and 6 months of age, suggesting impaired systolic and diastolic function even in young animals, as has been observed ex vivo in isolated, Nutlin-3 working 3-month-old mdx mouse hearts and in vivo in 8-month-old mice. Interestingly, differences in LV filling and ejection rates were not detected at 12 months, suggesting that progressive remodeling and hypertrophy may compensate for dysfunction and mask the original abnormalities at later time points. This is supported by the study of Li et al, which reported increased regional strain and torsion in the 2-month-old mdx mouse heart and reduced torsion by 10 months. All mice used in this study were male; female mice may have given different results. We have reported RV dysfunction in mdx mice at 8 months that precedes LV dysfunction, probably owing to pulmonary hypertension and dysfunction of the diaphragm muscle. Here, by performing serial imaging, we were able to determine that resting RV function was unaltered at 1 month, but abnormal as early as three months, with RV-ESV increased and RV-EF reduced.