Your new experience awaits. Try the new design now and help us make it even better

ORIGINAL RESEARCH article

Front. Med.

Sec. Intensive Care Medicine and Anesthesiology

Volume 12 - 2025 | doi: 10.3389/fmed.2025.1561886

This article is part of the Research TopicInnovative Monitoring and Management of Perioperative Complications in Cardiac SurgeryView all 9 articles

Elevated serum levels of monocyte chemoattractant protein-1 (MCP-1) in 71 patients three months after elective cardiac surgery suggest a potential link to persistent inflammation but not an increased propensity for postoperative cerebrovascular events

Provisionally accepted
  • Mayo Clinic, Rochester, Minnesota, United States

The final, formatted version of the article will be published soon.

Monocyte chemoattractant protein 1(MCP-1)plays a critical role in the transmigration of peripheral monocytes,a central mechanism underlying chronic inflammation.In this study,we investigate postoperative serum kinetics of MCP-1 as a potential contributor to postoperative neurocognitive decline,arteriosclerosis,and the development of organ failures.Seventy-one patients undergoing elective cardiac surgery were included in this study.Serum samples were collected preoperatively (tbaseline),and postoperatively at 24 hours (t24h),7 days (t7d),and 3 months (t3m). MCP-1 levels were quantified in conjunction with other inflammatory markers and alarmins.Whole blood samples underwent lipopolysaccharide(LPS)stimulation to evaluate MCP-1 production capacity,and peripheral monocyte transcriptomes were analyzed.Surrogate markers of end-organ dysfunction,including markers of neurodegeneration,neuroinjury,vasculitis,and atherosclerosis,were assessed.Acute kidney failure was defined per the RIFLE criteria,and occurrences of cerebrovascular accidents (CVA),pulmonary embolism (PE),deep venous thrombosis (DVT),and dispositions were documented.Cardiac surgery resulted in an acute increase in serum MCP-1 at 24 hours,7 days,and three months as compared to the presurgical baseline.MCP-4 levels were unchanged,while Regulated on Activation Normal T Cell Expressed and Secreted cytokine (RANTES) was significantly depleted after surgery. Except for a prior history of cerebrovascular accidents, other preoperative clinical conditions, duration of anesthesia, surgery, cross-clamp, estimated fluid loss, and transfusions did not influence t24h MCP-1 serum level. Perioperative use of non-steroidal anti-inflammatory drugs and opioids affected acute serum MCP-1 levels. At three months, patients undergoing coronary artery bypass graft (CABG) surgery exhibited the most pronounced elevation in MCP-1 compared to other cardiac surgery. Serum IL-6 at 24 hours positively correlated with MCP-1 levels measured at hours, 7 days, and 3 months. Additionally, markers of neurodegeneration (τ protein and amyloid β-1-40), some vascular inflammation (FGF-23 and FGF-21), and atherosclerosis (LOX-1) demonstrated correlational relationships with MCP-1. Finally, patients experiencing postoperative cerebrovascular accidents demonstrated depressed levels of MCP-1 at 24 hours, 7 days, and 3 months as compared to patients recovering uneventfully.Serum MCP-1 levels were elevated for up to three months following cardiac surgery, even in patients who experienced an uneventful recovery. MCP-4 was unchanged, while RANTES depressed postsurgery. A significant correlation between MCP-1 and serum surrogate markers of brain injury, vascular inflammation, and atherosclerosis highlights MCP-1 as a potential biomarker and a possible mediator of adverse outcomes after cardiac surgery.

Keywords: cardiac surgery, Monocyte chemoattractant protein 1, Long-term outcome, Vasculitis, Neuroinflammation, neurodegeneration, Stroke

Received: 16 Jan 2025; Accepted: 10 Jul 2025.

Copyright: © 2025 Laudanski, Antar and Gad. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Krzysztof Laudanski, Mayo Clinic, Rochester, 55902, Minnesota, United States

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.