Duchenne muscular dystrophy (
DMD
), caused by absence of the protein dystrophin, is a common, degenerative muscle disease affecting 1:5000 males worldwide. With recent advances in respiratory care, cardiac dysfunction now accounts for 50% of mortality in
DMD
. Recently, we demonstrated that simvastatin substantially improved skeletal muscle health and function in
mdx
(
DMD
) mice. Given the known cardiovascular benefits ascribed to statins, the aim of this study was to evaluate the efficacy of simvastatin on cardiac function in
mdx
mice. Remarkably, in 12‐month old
mdx
mice, simvastatin reversed diastolic dysfunction to normal after short‐term treatment (8 weeks), as measured by echocardiography in animals anesthetized with isoflurane and administered dobutamine to maintain a physiological heart rate. This improvement in diastolic function was accompanied by increased phospholamban phosphorylation in simvastatin‐treated mice. Echocardiography measurements during long‐term treatment, from 6 months up to 18 months of age, showed that simvastatin significantly improved in vivo cardiac function compared to untreated
mdx
mice, and prevented fibrosis in these very old animals. Cardiac dysfunction in
DMD
is also characterized by decreased heart rate variability (
HRV
), which indicates autonomic function dysregulation. Therefore, we measured cardiac
ECG
and demonstrated that short‐term simvastatin treatment significantly increased heart rate variability (
HRV
) in 14‐month‐old conscious
mdx
mice, which was reversed by atropine. This finding suggests that enhanced parasympathetic function is likely responsible for the improved
HRV
mediated by simvastatin. Together, these findings indicate that simvastatin markedly improves cardiac health and function in dystrophic mice, and therefore may provide a novel approach for treating cardiomyopathy in
DMD
.