Effects on cardiac function, remodeling and inflammation following myocardial ischemia–reperfusion injury or unreperfused myocardial infarction in hypercholesterolemic APOE*3-Leiden mice

Figures

• 

  Figure 1. Contrast-enhanced MR imaging. After 2 days no significant difference in infarct size was observed between the MI and MI-R group. However, after 3 weeks the MI group displayed a significant increased infarct size as compared to the MI-R group (a; n = 15–16 per group). Typical example of contrast-enhanced MR image 2 days following non-transmural MI-R (b) and transmural MI (c). Red line indicates epicardial border, green line indicates endocardial border and yellow line indicates infarct area. Individual data points are presented in Supplemental Fig. S1. Data are mean ± SEM. ##p < 0.01 versus MI.

• 

  Figure 2. Cardiac MR imaging of LV volumes and function. Assessment of LV volumes and function after 2 days and 3 weeks (n = 13–16 per group). MI-R caused a decreased EDV (a) and ESV (b) compared to MI. EF did not significantly differ between the MI-R and MI group but was reduced in both groups as compared to sham (c). Typical transversal short-axis MR images at end-diastole (ED) and end-systole (ES) 2 days (d) and 3 weeks (e) after infarction in the sham, MI-R and MI groups. Individual data points are presented in Supplemental Fig. S2. Data are mean ± SEM. ##p < 0.01 versus MI; *p < 0.05, ***p < 0.001 both versus sham.

• 

  Figure 3. LV fibrous content and wall thickness. Histological analysis after 3 weeks (n = 9–10 per group) showed no significant difference in LV fibrous content between the MI and MI-R group (a). This could possibly be explained since transmural infarction in the MI group caused substantial LV wall thinning which underestimated the fibrous content as a percentage of the total LV when compared to MI-R. LV wall thickness was significantly decreased in the MI group as compared to the MI-R group (b). Sirius red staining of transversal short-axis sections showing typical non-transmural infarction in the MI-R (c) and transmural infarction with substantial LV wall thinning in the MI (d) group. Scale bar: 500 μm. Individual data points are presented in Supplemental Fig. S3. Data are mean ± SEM. ##p < 0.01 versus MI; ***p < 0.001 versus sham.

• 

  Figure 4. Systemic inflammatory response. FACS analysis after 2 days (n = 5–8 per group) showed increased levels of circulating monocytes in both the MI-R and MI group as compared to sham (a) with a different distribution pattern of Ly-6Chi and Ly-6Clo monocytes in both groups (b and c). Circulating eosinophils were obviously decreased in both the MI-R and MI group compared to sham (d). Individual data points are presented in Supplemental Fig. S4. Data are mean ± SEM. *p < 0.05 versus sham.

• 

  Figure 5. Local inflammatory response. Both MI-R and MI resulted in an increased number of infiltrated leukocytes 3 weeks after infarction as compared to sham (b; n = 9–10 per group). After 2 days numbers of local infiltrated leukocytes in the infarct area were higher in the MI group compared to the MI-R group (a; n = 5 per group). Individual data points are presented in Supplemental Fig. S5 Data are mean ± SEM. #p < 0.05 versus MI-R; *p < 0.05, **p < 0.01, ***p < 0.001 all versus sham.