Abstract #3610

Costandi P, Frank L, McCulloch A, Omens J

Genetically engineered murine models of heart failure have proven valuable in characterizing remodeling and its ultimate decompensation to failure. Mice lacking a cytoskeletal protein present with a clinical picture of dilated cardiomyopathy and transition to failure as adults. Longitudinal high field cardiac MRI showed improved ejection fraction and stroke volume temporally concurrent with an abrupt phase of chamber dilatation. Hemodynamic analysis showed elevated end-diastolic volume but decreasing pressures. Computational modeling estimated passive properties revealing that global compliance increased as a function of geometric alterations. Diastolic dysfunction may therefore influence the progression of compensatory remodeling and its eventual transition to failure.