BACKGROUND: Complex cardiovascular procedures may initiate a systemic inflammatory response syndrome (SIRS) with a massive cytokine release, which is involved in postoperative myocardial injury. Intraoperative cytokine hemoadsorption (HA) mitigates the inflammatory response. Micro ribonucleic acids (miRNAs) are emerging as a marker of myocardial injury. METHODS: This study evaluated if intraoperative cytokine reduction by HA modulates SIRS and affects myocardial injury as measured by miRNA-126, 223 and miRNA-1, 133a, respectively. Twenty-eight patients were assigned into HA (n = 15) and control (C) (n = 13) groups. HA was performed by integrating CytoSorb™ into the extracorporeal circuit. RESULTS: MiRNA-133a plasma levels were increased postoperatively in both groups but were much higher in the HA group than in the C group at 3 h (P = 0.037) and 18 h (P = 0.017) after reperfusion. MiRNA-1 and miRNA-223 plasma levels were significantly increased postoperatively, but did not differ between groups. The vascular miRNA-126 was not affected. CONCLUSION: Intraoperative cytokine HA in cardiovascular operations increased the plasma levels of miRNA-133a, suggesting higher myocardial injury.

• Keywords
• Cardiac operations, Cytokines, Hemoadsorption, MicroRNA, Myocardial injury, Systemic inflammatory response syndrome,
• Publication type
• Journal Article MeSH

Cardiac surgery patients are now more risky in terms of age, comorbidities, and the need for complex procedures. It brings about reperfusion injury, which leads to dysfunction and/or loss of part of the myocardium. These groups of patients have a higher incidence of postoperative complications and mortality. One way of augmenting intraoperative myocardial protection is the phenomenon of myocardial conditioning, elicited with brief nonlethal episodes of ischaemia-reperfusion. In addition, drugs are being tested that mimic ischaemic conditioning. Such cardioprotective techniques are mainly focused on reperfusion injury, a complex response of the organism to the restoration of coronary blood flow in ischaemic tissue, which can lead to cell death. Extensive research over the last three decades has revealed the basic mechanisms of reperfusion injury and myocardial conditioning, suggesting its therapeutic potential. But despite the enormous efforts that have been expended in preclinical studies, almost all cardioprotective therapies have failed in the third phase of clinical trials. One reason is that evolutionary young cellular mechanisms of protection against oxygen handling are not very robust. Ischaemic conditioning, which is among these, is also limited by this. At present, the prevailing belief is that such options of treatment exist, but their full employment will not occur until subquestions and methodological issues with the transfer into clinical practice have been resolved.

• MeSH
• Adjuvants, Pharmaceutic therapeutic use   MeSH
• Ischemic Postconditioning MeSH
• Cardiac Surgical Procedures * adverse effects   MeSH
• Cardiotonic Agents therapeutic use   MeSH
• Clinical Trials as Topic MeSH
• Humans MeSH
• Treatment Outcome MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Names of Substances
• Adjuvants, Pharmaceutic MeSH
• Cardiotonic Agents MeSH