Document Detail

Myocardial tissue elastic properties determined by atomic force microscopy after stromal cell-derived factor 1α angiogenic therapy for acute myocardial infarction in a murine model.
MedLine Citation:
PMID:  22264415     Owner:  NLM     Status:  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 1α (SDF-1α) 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-1α. 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-1α-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-1α-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-1α to re-engineer 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-1α therapy may confer a mechanical advantage to resist adverse remodeling after infarction.
William Hiesinger; Matthew J Brukman; Ryan C McCormick; J Raymond Fitzpatrick; John R Frederick; Elaine C Yang; Jeffrey R Muenzer; Nicole A Marotta; Mark F Berry; Pavan Atluri; Y Joseph Woo
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2012-01-20
Journal Detail:
Title:  The Journal of thoracic and cardiovascular surgery     Volume:  143     ISSN:  1097-685X     ISO Abbreviation:  J. Thorac. Cardiovasc. Surg.     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-03-19     Completed Date:  2012-05-07     Revised Date:  2014-09-09    
Medline Journal Info:
Nlm Unique ID:  0376343     Medline TA:  J Thorac Cardiovasc Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  962-6     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2012 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.
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MeSH Terms
Angiogenesis Inducing Agents / pharmacology*
Biomechanical Phenomena
Chemokine CXCL12 / pharmacology*
Disease Models, Animal
Elastic Modulus
Elasticity Imaging Techniques / methods*
Heart Ventricles / drug effects*,  pathology,  physiopathology
Microscopy, Atomic Force*
Myocardial Infarction / drug therapy*,  pathology,  physiopathology
Myocardium / pathology*
Neovascularization, Physiologic / drug effects*
Time Factors
Ventricular Remodeling / drug effects
Grant Support
1R01HL089315-01/HL/NHLBI NIH HHS; K08 HL072812/HL/NHLBI NIH HHS; R01 HL089315/HL/NHLBI NIH HHS; T32-HL-007843-13/HL/NHLBI NIH HHS
Reg. No./Substance:
0/Angiogenesis Inducing Agents; 0/Chemokine CXCL12

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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