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pdf) Footnotes Contributors: WvdB, DMdB and BGM conceived the trial concept and designed the protocol. IMV, AAK, PJZ, MPLP, DPV, CDSH, MRWE, HW and TMdR helped develop the trial design and protocol. JJMCHdlR inhibitor bulk is the principal investigator and takes overall responsibility for all aspects of trial design, the protocol and trial conduct. All authors read and approved the final manuscript. Competing interests: JJMCHdlR is paid consultant to AngioDynamics. Ethics approval: Ethics Committe of Academic Medical Center Amsterdam and Athens Medical University. Provenance and peer review: Not commissioned; internally peer reviewed.
Epidemiological studies have demonstrated that cardiac surgery is a known risk factor for acute respiratory distress syndrome (ARDS).1–3 Over 300 000 patients undergo cardiac surgery every year in the USA, and up to 20% will experience ARDS.4 The risk factors include the type of surgery, cardiopulmonary bypass, ischaemia-reperfusion injury,

transfusion-related acute lung injury and drug toxicity. The mortality rate associated with ARDS is approximately 40% in the general population; however, this rate is considerably higher (up to 80%) among postcardiac surgery patients.5 6 Moderate-to-severe ARDS causes the majority of deaths associated with this syndrome, and the possible therapeutic choices differ for the varying severities of ARDS. Patients with mild ARDS typically only require non-invasive treatments, whereas patients with

moderate to severe ARDS are more likely to require more aggressive interventions, including prone positioning, recruitment manoeuvres, neuromuscular blockage agents, inhaled nitric oxide, high frequency oscillatory ventilation and even extracorporeal membrane oxygenation. Thus, the identification of patients with moderate to severe ARDS is clinically meaningful. Although cardiac surgery with cardiopulmonary bypass (CPB) is considered a highly sterile type of surgery, it can lead to a systemic inflammatory response syndrome (SIRS).7 The possible causes of SIRS include the exposure of blood to non-physiological surfaces, ischaemia-reperfusion injury due to aortic clamping Carfilzomib and extracorporeal circulation.8 In addition, the translocation of gut endotoxins to the bloodstream after the release of the aortic clamp is another potential cause9 that can activate inflammatory cascades similar to those observed in sepsis. Cytokines, such as interleukin (IL)-6, IL-8, tumour necrosis factor-α and C reactive protein (CRP), lipoprotein-binding protein and procalcitonin (PCT) potentially play important roles in immune reactions, whereas PCT liberation is predominantly dependent on the use of CPB.10 PCT is initially described as an early, sensitive and specific marker for sepsis associated with bacterial infection.