Echocardiography-derived left ventricular end-systolic regional wall stress and matrix remodeling after experimental myocardial infarction
Luis E. Rohde, MD, MSca,
Masanori Aikawa, MD, PhDa,
George C. Cheng, MD, PhDa,
Galina Sukhova, PhDa,
Scott D. Solomon, MD, FACCa,
Peter Libby, MD, FACCa,
Janice Pfeffer, PhDa,
Marc A. Pfeffer, MD, PhD, FACCa and
Richard T. Lee, MD, FACCa
a Cardiovascular Division, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA
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Figure 1 Representative examples of finite element meshes and color stress maps demonstrating the global and regional differences in left ventricular end-systolic wall stress between a sham-operated rat (A and B) and an infarcted rat (C and D) 21 days after the procedures. Each triangle designates the subdivisions of infarcted, border and noninfarcted regions, respectively. The same color scale was applied for both models. The left ventricle from the infarcted rat is dilated with focal areas of high ESLV stress concentrated in the regions that connect normal with infarcted tissue (arrowheads).
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Figure 2 Temporal evolution of regional ESLV wall stress from day 1 to day 21 after the infarctions. Values for sham-operated rats are expressed as average of the entire transverse section. *p < 0.05 refers to comparisons within the infarcted segments between different time points. Regional wall stress increases progressively up to 3 weeks after the MI in the infarcted regions.
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Figure 3 Immunohistochemistry for MMP-9 (A) and macrophages (B) in high power fields (x40, reduced by 65%). Matrix metalloproteinase-9 positive cells (arrowheads) are spread homogeneously throughout the infarcted region, and macrophages are shown infiltrating the border region next to myocardial cells (arrow). Scale bars in (A) and (B) represent 55 µm. Double immunolabeling (C) for macrophages (blue-stained cells) and MMP-9 (red-stained cells) in high power fields (x100, reduced by 65%) demonstrates double-stained cells (purple cells, arrow). Scale bar in (C) represents 12 µm.
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Figure 4 Sections of an infarcted segment 21 days after the surgery showing MMP-9 (A) and TIMP-1 (B) immunoreactivity. Parallel sections demonstrate collagen accumulation under direct (C) and under polarized light (D). Note dissociation between the areas that express MMP-9 (arrowheads) and the areas that express TIMP-1 (arrow) and are rich in collagen (arrow). Scale bars represent 70 µm.
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Figure 5 The relationship between ESLV wall stress with MMP-9 and macrophage content dichotomized according to the density of positive cells. "N" represents the number of segments analyzed. Regions with more than 10 cells/high power field (hpf) have a threefold increase in regional ESLV wall stress when compared to regions with fewer positive cells.
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