Effect of serum from patients with ST-segment elevation myocardial infarction on endothelial cells.

Grupos y Plataformas de I+D+i

• Grupo de Investigación en Electrofisiología cardiaca experimental

  

  Leading Researcher

  Antonio M. Alberola Aguilar

• Grupo de Investigación en Enfermedades Respiratorias, Neuromusculares y Daño Pulmonar

  

  Leading Researcher

  Jaime Signes-Costa Miñana

• Grupo de Investigación Traslacional en Cardiopatía Isquémica

  

  Leading Researcher

  Vicent Bodí Peris

Abstract

INTRODUCTION AND OBJECTIVES: Clinical and experimental studies have shown that, in patients with reperfused ST-segment elevation myocardial infarction (STEMI), abnormalities in the endothelial monolayer are initiated during ischemia but rapidly intensify upon restoration of blood perfusion to the ischemic area. We aimed to evaluate the effect of serum isolated after revascularization from STEMI patients on the degree of endothelial permeability in vitro, by promoting endothelial cell apoptosis and necrosis in vitro. We also investigated the association between the percentage of serum-induced endothelial cell apoptosis or necrosis in vitro and the extent of cardiovascular magnetic resonance (CMR)-derived parameters of reperfusion injury (edema, hemorrhage, and microvascular obstruction). METHODS: Human coronary artery endothelial cells were incubated with serum isolated 24hours after revascularization from 43 STEMI patients who underwent CMR and 14 control participants. We assessed the effect of STEMI serum on activation of apoptosis and necrosis, as well as on the permeability and structure of the endothelial monolayer. RESULTS: Serum from STEMI patients increased apoptosis (P <.01) and necrosis (P <.05) in human coronary artery endothelial cells and caused increased permeability of the endothelial monolayer in vitro (P <.01), due to enlarged intercellular spaces (P <.05 vs control in all cases). Higher serum-induced necrosis was associated with greater endothelial permeability in vitro (P <.05) and with more extensive CMR-derived indices of reperfusion injury and infarct size. CONCLUSIONS: Postreperfusion serum activates necrosis and apoptosis in endothelial cells and increases the degree of endothelial permeability in vitro. The more potent the necrosis-triggering effect of serum, the more deleterious the consequences in terms of the resulting cardiac structure.

Copyright © 2023 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.

Keywords

• Células endoteliales; Daño por reperfusión; Endothelial cells; Endothelial permeability; Infarto de miocardio; Myocardial infarction; Permeabilidad endotelial; Reperfusion injury