Echocardiography-derived left ventricular end-systolic regional wall stress and matrix remodeling after experimental myocardial infarction
View/ Open
Rhode_EchoCardiography-DerivedLeftVentricularEnd-SystolicRegionalWallStressAndMatrixRemodelingAfterExperimentalMyocardialInfarction_JAmCollCardiol_1999.pdf (453.8Kb)
Access Status
Full text of the requested work is not available in DASH at this time ("restricted access"). For more information on restricted deposits, see our FAQ.Author
Rohde, Luis E
Pfeffer, Janice
Note: Order does not necessarily reflect citation order of authors.
Published Version
https://doi.org/10.1016/S0735-1097(98)00602-0Metadata
Show full item recordCitation
Rohde, Luis E, Masanori Aikawa, George C Cheng, Galina Sukhova, Scott D Solomon, Peter Libby, Janice Pfeffer, Marc A Pfeffer, and Richard T Lee. 1999. “Echocardiography-Derived Left Ventricular End-Systolic Regional Wall Stress and Matrix Remodeling after Experimental Myocardial Infarction.” Journal of the American College of Cardiology 33 (3) (March): 835–842. doi:10.1016/s0735-1097(98)00602-0.Abstract
OBJECTIVESWe tested the hypothesis that regional end-systolic left ventricular (ESLV) wall stress is associated with extracellular matrix remodeling activity after myocardial infarction (MI).
BACKGROUND
Increased left ventricular (LV) wall stress is a stimulus for LV enlargement, and echocardiography can be used to estimate regional wall stress. A powerful validation of a noninvasive method of estimating wall stress would be predicting cellular responses after a MI.
METHODS
Echocardiographic images were obtained in rats 1, 7, 14 or 21 days after coronary ligation (n = 11) or sham surgery (n = 5). End-systolic left ventricular wall stress was calculated by finite element analysis in three regions (infarcted, noninfarcted and border) from short-axis images. Matrix metalloproteinase-9 (MMP-9) and macrophage density were determined by immunohistochemistry, and positive cells were counted in high power fields (hpf).
RESULTS
Average ESLV wall stress was higher in rats with MI when compared to shams irrespective of time point (p < 0.01), and ESLV wall stress in the infarcted regions increased with time (25.1 ± 5.9 vs. 69.9 ± 4.4 kdyn/cm2, day 1 vs. 21; p < 0.01). Matrix metalloproteinase-9 expression was higher in infarcted and border regions when compared to noninfarcted regions (22.1 vs. 25.7 vs. 0.10 cells/hpf, respectively; p < 0.01). Over all regions, ESLV wall stress was associated with MMP-9 (r = 0.76; p < 0.001), macrophage density (r = 0.72; p < 0.001) and collagen content (r = 0.67; p < 0.001). End-systolic left ventricular wall stress was significantly higher when MMP-9 positive cell density was greater than 10 cells/hpf (45 ± 20 vs. 14 ± 10 kdyn/cm2; p < 0.001).
CONCLUSIONS
Regional increases in ESLV wall stress determined by echocardiography-based structural analysis are associated with extracellular matrix degradation activity.
Other Sources
http://www.ncbi.nlm.nih.gov/pubmed/10080489Citable link to this page
http://nrs.harvard.edu/urn-3:HUL.InstRepos:35140980
Collections
- HMS Scholarly Articles [17922]
Contact administrator regarding this item (to report mistakes or request changes)