Mice that were treated with intramyocardial injections of different NPs, including CHIR + FGF1-NPs, CHIR-NPs, FGF1-NPs, and empty NPs (nonloaded); MI-only control mice; and sham-operated control mice were subjected to echocardiographic assessments of left ventricular (LV) function (A). Ejection fraction (EF) (B), fractional shortening (FS) (C), end-systolic diameter of the left ventricle (D), and end-diastolic diameter of the left ventricle (E) were assessed before MI induction (pre-S) and on post-MI day 28 (post-S). On day 28 after MI, CHIR + FGF1-NP treatment groups presented significantly greater EF and FS compared with other treatment as well as control groups (B and C) and significantly lower values of systolic/diastolic diameters of the left ventricle. Data are given as means ± SEM. There were 10–12 animals per group. Statistical analysis: 2-way ANOVA with Dunn’s multiple comparisons test. *P < 0.01 vs. sham; ^†P < 0.01 vs. MI; ^‡P < 0.05 vs. empty NPs; ^§P < 0.05 vs. CHIR-NPs, ^||P < 0.01 vs. FGF1-NPs. Sirius Red/Fast Green histochemical staining revealing areas of infarcted (red, nonviable) and noninfarcted (green, viable) zones in post-MI day 28 ventricular tissue sections (F). The infarct size was quantified as the ratio of the scar area to the total surface area of the left ventricle and expressed as a percentage, for day 28 samples (G). At day 28, the CHIR + FGF1-NP treatment group showed significant reduction in infarct size compared with other NP treatment groups or the untreated control MI animals. Scale bar: 1 mm (panels in F). Data are given as means ± SEM. There were 10–12 animals per group. Statistical analysis: 1-way ANOVA with Dunn’s multiple comparisons test. *P < 0.01 vs. MI; ^†P < 0.01 vs. empty NP; ^‡P < 0.01 vs. CHIR-NP; ^§P < 0.01 vs. FGF1-NP.