Endothelial activation and infarct size at the acute phase of myocardial infarction

Abstract

Acute myocardial infarction (MI) leads to an intense inflammatory response with endothelial cell activation. Vascular cell adhesion protein 1 (VCAM-1), E-selectin, intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein 1 (MCP-1) promote the adherence of leucocytes especially monocytes, in the infarcted area which may increase infarct size (IS). Our objective was to evaluate the kinetic of endothelial cell activation markers at the acute phase of ST-elevated MI (STEMI) and their relationship with IS and Major Adverse Cardiac Event (MACE). Blood sample of 182 STEMI patients were collected at admission and four hours after reperfusion. Infarct Size (IS) was assessed in all patients using cardiac Magnetic Resonance Imaging (cMRI) one month after discharge. We performed ELISA quantification of the main markers of endothelial cell activation in serum: VCAM-1, E-selectin, ICAM-1 and MCP-1. Patients mean age was 58 ± 11 years with 77% males. Median levels of each marker at admission reached 165.3 ng/mL interquartile range (IQR) [127.0–193.3] for VCAM-1, 140.6 ng/mL IQR [104.6–196.6] for ICAM-1, 15.3 ng/mL IQR [10.2–23.3] for E-selectin and 53.8 pg/mL IQR [34.7–90.5] for MCP-1. VCAM-1 and MCP-1 serum levels significantly increased four hours after admission (respectively +6% and +32%). E-selectin and ICAM-1 levels did not change four hours after admission compared to admission. Only VCAM-1 was significantly correlated with IS assessed by cMRI ( r = 0.26, P = 0.0004) and inversely correlated with left ventricular ejection fraction ( r = −0.16, P = 0.04). However, VCAM-1 level and other markers were not associated with MACE. MI is associated with endothelial cell activation. VCAM-1 and MCP-1 significantly increased at the acute phase of MI whereas E-selectin and ICAM-1 levels are stable. Only VCAM-1 serum level was correlated with IS. However, none of these markers was associated with the occurrence of MACE.