期刊
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
卷 143, 期 4, 页码 962-966出版社
MOSBY-ELSEVIER
DOI: 10.1016/j.jtcvs.2011.12.028
关键词
-
资金
- NHLBI NIH HHS [1R01HL089315-01, T32-HL-007843-13, T32 HL007843, R01 HL089315, K08 HL072812] Funding Source: Medline
Objectives: Ventricular remodeling after myocardial infarction begins with massive extracellular matrix deposition and resultant fibrosis. This loss of functional tissue and stiffening of myocardial elastic and contractile elements starts the vicious cycle of mechanical inefficiency, adverse remodeling, and eventual heart failure. We hypothesized that stromal cell-derived factor 1 alpha (SDF-1 alpha) therapy to microrevascularize ischemic myocardium would rescue salvageable peri-infarct tissue and subsequently improve myocardial elasticity. Methods: Immediately after left anterior descending coronary artery ligation, mice were randomly assigned to receive peri-infarct injection of either saline solution or SDF-1 alpha. After 6 weeks, animals were killed and samples were taken from the peri-infarct border zone and the infarct scar, as well as from the left ventricle of noninfarcted control mice. Determination of tissues' elastic moduli was carried out by mechanical testing in an atomic force microscope. Results: SDF-1 alpha-treated peri-infarct tissue most closely approximated the elasticity of normal ventricle and was significantly more elastic than saline-treated peri-infarct myocardium (109 +/- 22.9 kPa vs 295 +/- 42.3 kPa; P<.0001). Myocardial scar, the strength of which depends on matrix deposition from vasculature at the peri-infarct edge, was stiffer in SDF-1 alpha-treated animals than in controls (804 +/- 102.2 kPa vs 144 +/- 27.5 kPa; P<.0001). Conclusions: Direct quantification of myocardial elastic properties demonstrates the ability of SDF-1 alpha to reengineer evolving myocardial infarct and peri-infarct tissues. By increasing elasticity of the ischemic and dysfunctional peri-infarct border zone and bolstering the weak, aneurysm-prone scar, SDF-1 alpha therapy may confer a mechanical advantage to resist adverse remodeling after infarction. (J Thorac Cardiovasc Surg 2012;143:962-6)
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