• Ioanna Oikonomou, Angeliki Papageorgiou, Anne-Lise de Lastic, Athanasios Moulias, Georgia-Andriana Georgopoulou, Athanasia Mouzaki, Eleni-Evangelia Koufou, Grigorios Tsigkas, Charalambos Gogos, Periklis Davlouros, and Stelios F Assimakopoulos.
• Department of Internal Medicine and Division of Infectious Diseases, University of Patras Medical School, Patras, Greece.
• Am. J. Med. Sci. 2024 Nov 1; 368 (5): 485493485-493.

BackgroundGut-derived bacterial and endotoxin translocation induce systemic inflammation, which exerts a pivotal pathogenetic role in all phases of atherosclerosis.ObjectivesTo investigate prospectively the gut barrier function, endotoxin translocation and inflammatory response in ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary artery intervention (PPCI).MethodsTwenty-seven patients with STEMI that underwent successful PPCI were subjected to peripheral blood sampling at 3-time points; before PPCI (day0), 24 h (day1) and 96 h (day4) after PPCI and were compared with 20 chronic coronary syndrome (CCS) patients and 11 healthy controls. Serum ZO-1, I-FABP and endotoxin concentrations were determined by ELISA. Concentrations of cytokines IL-1β, -6, -8, -10 and TNF-α were determined by flow cytometry.ResultsPatients with STEMI before PPCI (day0) had increased serum ZO-1 and endotoxin, both at significantly higher levels compared to CCS patients. STEMI induced also significant increases of the cytokines IL-6, -8 and -10. After PPCI, a significant improvement of gut barrier integrity (ZO-1) and endotoxemia was observed from the first day. At day4 post PPCI, systemic endotoxin and cytokines IL-6, -8 and -10 levels were reduced to control levels. Serum ZO-1 levels were positively correlated with systemic IL-10 concentrations (r = 0.471).ConclusionSTEMI is associated with gut barrier dysfunction, systemic endotoxemia and inflammatory response, which improve rapidly following successful PPCI.Copyright © 2024 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.

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