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BACKGROUND: Myocardial fibrosis is observed in multiple cardiac conditions including hypertension and aortic stenosis. Excessive fibrosis is associated with adverse clinical outcomes, but longitudinal human data regarding changes in left ventricular remodelling and fibrosis over time are sparse because of the slow progression, thereby making longitudinal studies challenging. The purpose of this study was to establish and characterize a mouse model to study the development and regression of left ventricular hypertrophy and myocardial fibrosis in response to increased blood pressure and to understand how these processes reverse remodel following normalisation of blood pressure. METHODS: We performed a longitudinal study with serial cardiovascular magnetic resonance (CMR) imaging every 2 weeks in mice (n = 31) subjected to angiotensin II-induced hypertension for 6 weeks and investigated reverse remodelling following normalisation of afterload beyond 6 weeks (n = 9). Left ventricular (LV) volumes, mass, and function as well as myocardial fibrosis were measured using cine CMR and the extracellular volume fraction (ECV) s. RESULTS: Increased blood pressure (65 ± 12 vs 85 ± 9 mmHg; p 

Original publication




Journal article


J cardiovasc magn reson

Publication Date





Cardiovascular magnetic resonance , ECV, Hypertension, T1-mapping, Angiotensin II, Animals, Blood Pressure, Disease Models, Animal, Disease Progression, Fibrosis, Hypertension, Hypertrophy, Left Ventricular, Magnetic Resonance Imaging, Cine, Male, Mice, Inbred C57BL, Myocardium, Time Factors, Ventricular Function, Left, Ventricular Remodeling