Key result
Low coronary driving pressure early post-infarction correlated inversely with subendocardial necrosis and fibrosis, driving progressive LV expansion.
Why the study?
Does low coronary driving pressure early post-myocardial infarction affect subendocardial remodelling and left ventricular function in Wistar rats?
Does low coronary driving pressure early post-myocardial infarction affect subendocardial remodelling and left ventricular function in Wistar rats?
Low coronary driving pressure early after myocardial infarction is associated with progressive left ventricular expansion, subendocardial necrosis, inflammation, and fibrosis, negatively impacting LV function.
Answers are grounded in this paper and cite their sources.
Should not change post-MI practice; extends rat data linking low driving pressure to adverse remodeling.
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.
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Koike et al. (2007) studied Myocardial infarction. Myocardial infarction vs. Sham surgery was evaluated on Subendocardial necrosis, inflammation, fibroplasia, fibrosis, and LV function. Low coronary driving pressure early post-infarction correlated inversely with subendocardial necrosis and fibrosis, driving progressive LV expansion.
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