Abstract #2198

Cardiac MRI for quantifying myocardial perfusion deficits in a mouse model of hypertrophic cardiomyopathy

Min-Chi Ku^1,2, Frank Kober³, Andreas Pohlmann¹, Qadri Fatimunnisa⁴, Michael Bader^2,4, and Thoralf Niendorf^1,2,5

¹Berlin Ultrahigh Field Facility (B.U.F.F.), Max Delbrueck Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany, ²German Centre for Cardiovascular Research (DZHK), parter site Berlin, Berlin, Germany, ³Centre de Résonance Magnétique Biologique et Médicale (CRMBM), Aix-Marseille Université, Marseille, France, ⁴Molecular Biology of Peptide Hormones, Max Delbrueck Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany, ⁵Experimental and Clinical Research Center, Charite Medical Faculty and the Max Delbrueck Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany

Measuring the myocardial morphological and functional changes is not sufficient to assess the underlying subclinical myocardial microstructural changes in hypertrophic cardiomyopathy (HCM). Despite cardiac MRI (CMR) is advanced in characterizing the changes in myocardial microstructure, in vivo assessment of the kinetics of microstructural changes including microvasculature deficits and the mechanism underlying disease progression is still missing. We hypothesize that the impairment of myocardial perfusion may contribute to the microstructural changes in HCM. To test this, we used state-of-the-art arterial spin labeling (ASL) based CMR method to quantify the myocardial perfusion changes in a HCM mouse model.

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