Low coronary driving pressure early in the course of myocardial infarction is associated with subendocardial remodelling and left ventricular dysfunction.
Subendocardial remodelling of the left ventricular (LV) non-infarcted myocardium has been poorly investigated. Previously, we have demonstrated that low coronary driving pressure (CDP) early postinfarction was associated with the subsequent development of remote subendocardial fibrosis. The present study aimed at examining the role of CDP in LV remodelling and function following infarction. Haemodynamics were performed in Wistar rats immediately after myocardial infarction (MI group) or sham surgery (SH group) and at days 1, 3, 7 and 28. Heart tissue sections were stained with HE, Sirius red and immunostained for alpha-actin. Two distinct LV regions remote to infarction were examined: subendocardium (SE) and interstitium (INT). Myocyte necrosis, leucocyte infiltration, myofibroblasts and collagen volume fraction were determined. Compared with SH, MI showed lower CDP and LV systolic and diastolic dysfunction. Necrosis was evident in SE at day 1. Inflammation and fibroplasia predominated in SE as far as day 7. Fibrosis was restricted to SE from day 3 on. Inflammation occurred in INT at days 1 and 3, but at a lower grade than in SE. CDP correlated inversely with SE necrosis (r = -0.65, P = 0.003, at day 1), inflammation (r = -0.76, P < 0.001, at day 1), fibroplasia (r = -0.47, P = 0.04, at day 7) and fibrosis (r = -0.83, P < 0.001, at day 28). Low CDP produced progressive LV expansion. Necrosis at day 1, inflammation at days 3 and 7, and fibroplasia at day 7 correlated inversely with LV function. CDP is a key factor to SE integrity and affects LV remodelling and function following infarction.
Koike
Marcia Kiyomi
MK
LIM 51 - Laboratory of Emergency Medicine, University of São Paulo Medical School, São Paulo, SP, Brazil. mkoike@usp.br
Frimm
Clovis De Carvalho
Cde C
Cúri
Mariana
M
D000818:Animals; D001794:Blood Pressure; D003326:Coronary Circulation; D004699:Endocardium / Q000473:pathology / Q000503:physiopathology; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D032383:Myocytes, Cardiac / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D018487:Ventricular Dysfunction, Left / Q000473:pathology / Q000503:physiopathology*; D020257:Ventricular Remodeling
J Mol Cell Cardiol. 1993 Nov;25(11):1317-23
7507999
J Am Coll Cardiol. 2000 Mar 1;35(3):569-82
10716457
J Mol Cell Cardiol. 1996 May;28(5):851-8
8762025
Cardiovasc Res. 2000 May;46(2):316-23
10773236
Am J Physiol Heart Circ Physiol. 2005 Apr;288(4):H1598-603
15550516
Arq Bras Cardiol. 2003 May;80(5):509-20
12792716
Circulation. 1990 Jan;81(1):238-46
2137045
Circ Res. 1994 Feb;74(2):244-52
8293563
Cell Tissue Res. 2006 Jun;324(3):475-88
16496177
Circulation. 1991 Nov;84(5):2123-34
1934383
Circulation. 2005 Jun 7;111(22):2943-50
15927977
Circ Res. 1961 May;9:589-600
13696612
J Lab Clin Med. 2000 Apr;135(4):316-23
10779047
Ann N Y Acad Sci. 1995 Mar 27;752:286-99
7755273
Am J Respir Cell Mol Biol. 2000 Oct;23(4):475-84
11017912
Circ Res. 1979 Apr;44(4):503-12
428047
Circ Res. 1985 Jul;57(1):84-95
3891127
Coron Artery Dis. 1997 Mar-Apr;8(3-4):155-61
9237025
J Clin Invest. 1991 Nov;88(5):1622-8
1939649
Pathol Res Pract. 2000;196(1):23-33
10674269
Basic Res Cardiol. 1996;91 Suppl 2:79-84
8957549
J Am Coll Cardiol. 2000 Jul;36(1):276-81
10898446
J Mol Cell Cardiol. 1989 Dec;21 Suppl 5:121-31
2534137
J Lab Clin Med. 1997 Apr;129(4):439-46
9104887
Angiology. 1960 Oct;11:398-407
13749954
Cardiovasc Res. 1996 Dec;32(6):1088-95
9015411
Circ Res. 1988 Apr;62(4):641-50
2964944
J Mol Cell Cardiol. 2001 Jun;33(6):1191-207
11444923
J Pathol. 2002 Mar;196(3):335-42
11857498
Cardiovasc Res. 1994 Sep;28(9):1423-32
7954655
J Am Coll Cardiol. 2001 Oct;38(4):1207-15
11583905