Figure 2
Figure 2. Monotherapy and combination treatment of DNase I and rhADAMTS13 improve cardiac function after 24 hours of MI/R. (A) Echocardiography analysis displayed a significant decrease in EF (%) in all treated groups of mice after 24 hours MI/R in contrast to control group (##P < .01; ###P < .001; # represents comparison with control). EF decreased significantly less in all groups of treated mice as compared with vehicle-treated animals, respectively (*P < .05; **P < .01; ***P < .001). (B) Correlation analysis including all experimental groups revealed a significant inverse relationship between the infarct size (% of LV) and EF (%) (Spearman r coefficient = −0.441, P = .027). In contrast to all mice assigned to the vehicle arm of the study (●), mice treated with either DNase I monotherapy (▲), rhADAMTS13 (▼), or combination therapy (♦) showed a significantly smaller myocardial infarction after MI/R injury and markedly improved LV systolic function.

Monotherapy and combination treatment of DNase I and rhADAMTS13 improve cardiac function after 24 hours of MI/R. (A) Echocardiography analysis displayed a significant decrease in EF (%) in all treated groups of mice after 24 hours MI/R in contrast to control group (##P < .01; ###P < .001; # represents comparison with control). EF decreased significantly less in all groups of treated mice as compared with vehicle-treated animals, respectively (*P < .05; **P < .01; ***P < .001). (B) Correlation analysis including all experimental groups revealed a significant inverse relationship between the infarct size (% of LV) and EF (%) (Spearman r coefficient = −0.441, P = .027). In contrast to all mice assigned to the vehicle arm of the study (●), mice treated with either DNase I monotherapy (▲), rhADAMTS13 (▼), or combination therapy (♦) showed a significantly smaller myocardial infarction after MI/R injury and markedly improved LV systolic function.

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