Low coronary driving pressure early in the course of myocardial infarction is associated with subendocardial remodelling and left ventricular dysfunction

Abstract

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.

Borage oil attenuates progression of cardiac remodeling in rats after myocardial infarction

“…After myocardial infarction, remote subendocardial lesions are associated with ventricular dilation, as previously demonstrated, indicating its importance to cardiac remodeling 14 .…”

“…Left ventricular expansion index = (left ventricular cavity area/left ventricular total area) x (interventricular septum thickness/infarct wall thickness) 14 The same formula was used to calculate left ventricular expansion index in sham animals, replacing the infarct wall thickness by the left ventricular free wall thickness.…”

“…In the remote portions not subendocardial, middle and outer fabric myocardial infarction, changes are become more apparent in the chronic phase, and appear to be the result of remote subendocardial lesions and refer to the deterioration of cardiac function 14 .…”

Methotrexate carried in lipid core nanoparticles reduces myocardial infarction size and improves cardiac function in rats

“…19,20 Briefly, with the rats under ketamine (Cristália, Itapira, Brazil) (50 mg/kg) and xylazine (CEVA, Paulínia, Brazil) (10 mg/kg) anesthesia, and positive pressure ventilation (rodent ventilator model 683, Harvard, Holliston, MA, USA), a left thoracotomy was performed. The left coronary artery was occluded, and the thoracic incision was sutured.…”

“…The SEN area was defined as the inner third of the non-infarcted LV area and the INT area as the remaining outer two-thirds. 20,25 The ratios of endocardial infarct surface length to total LV endocardial circumference, and between epicardial infarct surface length to total LV epicardial circumference were averaged to calculate the MI size.…”