Prolonged Systemic Inflammatory Response Syndrome After Cardiac Surgery.

Objectives: Cardiac surgery induces systemic inflammatory response syndrome (SIRS), leading to higher morbidity and mortality. There are no individualized predictors for worse outcomes or biomarkers for the multifactorial, excessive inflammatory response. The interest of this study was to evaluate whether a systematic use of the SIRS criteria could be used to predict postoperative outcomes beyond infection and sepsis, and if the development of an exaggerated inflammation response could be observed preoperatively.
Design: The study was observational, with prospectively enrolled patients.
Setting: This was a single institution study in a hospital setting combined with laboratory findings.
Participants: The study included a cohort of 261 volunteer patients.
Interventions: Patients underwent cardiac surgery with cardiopulmonary bypass, and were followed up to 90 days. Biomarker profiling was run preoperatively.
Measurements and Main Results: Altogether, 17 of 261 (6.4%) patients had prolonged SIRS, defined as fulfilling at least 2 criteria on 4 consecutive postoperative days. During hospitalization, postoperative atrial fibrillation (POAF) was found in 42.2% of patients, and stroke and transient ischemic attack in 3.8% of patients. Prolonged SIRS was a significant predictor of POAF (odds ratio [OR] 4.5, 95% CI 1.2-17.3), 90-day stroke (OR 4.5, 95% CI 1.1-18.0), and mortality (OR 10.7, 95% CI 1.7-68.8). Biomarker assays showed that preoperative nerve growth factor and interleukin 5 levels were associated with prolonged SIRS (OR 5.6, 95%, CI 1.4-23.2 and OR 0.7, 95%, CI 0.4-1.0, respectively).
Conclusions: Nerve growth factor and interleukin 5 can be used to predict prolonged systemic inflammatory response, which is associated with POAF, stroke, and mortality.
Competing Interests: Declaration of competing interest Joonas Lehto received research grants from the Orion Research Foundation, the Finnish Foundation for Cardiovascular Research, the Finnish Cultural Foundation, the Turku University Foundation, and the Emil Aaltonen Foundation. K. E. Juhani Airaksinen received research grants from the Finnish Foundation for Cardiovascular Research and the Clinical Research Fund (VTR) of Turku University Hospital (Turku, Finland) and lecture fees from Bayer and Boehringer Ingelheim. K. E. Juhani Airaksinen is a member of the advisory boards of Bayer, Astra Zeneca, and Bristol-Myers Squibb-Pfizer. Jarmo Gunn received research grants from the Turku University Research Foundation (Turku, Finland), the Clinical Research Fund (VTR) of Turku University Hospital (Turku, Finland), and an unrestricted grant from Vifor Pharma. Tuomas O. Kiviniemi received lecture fees from Bayer, Boehringer Ingelheim, MSD, Astra Zeneca, St Jude Medical, and Bristol-Myers-Squibb-Pfizer, and research grants from the Finnish Medical Foundation, the Finnish Foundation for Cardiovascular Research, Clinical Research Fund (EVO) of Turku University Hospital (Turku, Finland), Finnish Cardiac Society, the Emil Aaltonen Foundation, the Maud Kuistila Foundation, and an unrestricted grant from Bristol-Myers Squibb-Pfizer. Tuomas O. Kiviniemi is a member of the advisory board of Boehringer-Ingelheim and MSD. Juho Jalkanen owns stock and is employed by Faron Pharmaceuticals Ltd. The other authors declare no competing interests.
(Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)