Our data showed that mice underwent TAC developed cardiac diastolic dysfunction and LVH [15, 17] and for the first time demonstrated that: (1) APN improved active relaxation on a cellular level by increasing the maximal re-lengthening rate and reducing time to 90% re-lengthening of cardiomyocytes in TAC mice; (2) APN exerted positive impacts on myocardial passive stiffness by upregulating titin isoform N2BA/N2B ratios within cardiomyocytes and downregulating collagen I expression, collagen I/III ratios, and Lox expression in extracellular matrix level. This evidence concerns the gene TTN and persistent truncus arteriosus.