HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rohde, L. E. Articles by Lee, R. T. Search for Related Content PubMed PubMed Citation Articles by Rohde, L. E. Articles by Lee, R. T.

EXPERIMENTAL STUDIES

Echocardiography-derived left ventricular end-systolic regional wall stress and matrix remodeling after experimental myocardial infarction

^a Cardiovascular Division, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

Manuscript received January 30, 1998; revised manuscript received September 16, 1998, accepted November 5, 1998.

Reprint requests and correspondence: Dr. Richard T. Lee, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis St., Boston, Massachusetts 02115 USA
rtlee{at}bics.bwh.harvard.edu

OBJECTIVES

We 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.

Abbreviations and Acronyms   ESLV = end-systolic left ventricular   hpf = high power fields   LV = left ventricular   MI = myocardial infarction   MMP = matrix metalloproteinase   TIMP = tissue inhibitor of metalloproteinases

This article has been cited by other articles:

				J. Bian, Z. B. Popovic, C. Benejam, M. Kiedrowski, L. L. Rodriguez, and M. S. Penn Effect of Cell-Based Intercellular Delivery of Transcription Factor GATA4 on Ischemic Cardiomyopathy Circ. Res., June 8, 2007; 100(11): 1626 - 1633. [Abstract] [Full Text] [PDF]

				E. M. Wilson, S. L. Moainie, J. M. Baskin, A. S. Lowry, A. M. Deschamps, R. Mukherjee, T. S. Guy, M. G. St John-Sutton, J. H. Gorman III, L. H. Edmunds Jr, et al. Region- and Type-Specific Induction of Matrix Metalloproteinases in Post-Myocardial Infarction Remodeling Circulation, June 10, 2003; 107(22): 2857 - 2863. [Abstract] [Full Text] [PDF]

				M. St John Sutton, D. Lee, J. L. Rouleau, S. Goldman, T. Plappert, E. Braunwald, and M. A. Pfeffer Left Ventricular Remodeling and Ventricular Arrhythmias After Myocardial Infarction Circulation, May 27, 2003; 107(20): 2577 - 2582. [Abstract] [Full Text] [PDF]

				D. Fraccarollo, P. Galuppo, J. Bauersachs, and G. Ertl Collagen accumulation after myocardial infarction: effects of ETA receptor blockade and implications for early remodeling: Presented in part at the 72nd Scientific Session of the American Heart Association, Atlanta, GA, USA, November 7-10, 1999, and published in abstract form (Circulation 1999;100(Suppl. 1):562) Cardiovasc Res, June 1, 2002; 54(3): 559 - 567. [Abstract] [Full Text] [PDF]

				M. V. Cohen, X.-M. Yang, T. Neumann, G. Heusch, and J. M. Downey Favorable Remodeling Enhances Recovery of Regional Myocardial Function in the Weeks After Infarction in Ischemically Preconditioned Hearts Circulation, August 1, 2000; 102(5): 579 - 583. [Abstract] [Full Text] [PDF]

				J.T. Peterson, H. Li, L. Dillon, and J. W. Bryant Evolution of matrix metalloprotease and tissue inhibitor expression during heart failure progression in the infarcted rat Cardiovasc Res, May 1, 2000; 46(2): 307 - 315. [Abstract] [Full Text] [PDF]