Background: Data from large cardiac surgery registries have been depicting a downward trend of mortality and morbidities in the last 20 years. However, despite decades of medical evolution, cardiac surgery and cardiopulmonary bypass still provoke a systemic inflammatory response, which occasionally leads to worsened outcome. This article seeks to outline the mechanism of the phenomenon.Methods: A thorough review of the literature has been performed. Criteria for considering studies for this non‐systematic review were as follows: observational and interventional studies investigating the systemic inflammatory response to cardiac surgery, experimental studies describing relevant molecular mechanisms, and essential review studies pertinent to the topic.Results: The intrinsic variability of the inflammatory response to cardiac surgery, together with its heterogenous perception among clinicians, as well as the arduousness to early discriminate high‐responder patients from those who will not develop a clinically relevant reaction, concurred to hitherto unconclusive randomized controlled trials. Furthermore, peremptory knowledge about the pathophysiology of maladaptive inflammation following heart surgery is still lacking.Conclusions: Systemic inflammation following cardiac surgery is a frequent entity that occasionally becomes clinically relevant. Specific genomic differences, age, and other preoperative factors influence the magnitude of the response, which elements display extreme redundancy and pleiotropism that the target of a single pathway cannot represent a silver bullet.

High-density lipoproteins (HDLs) are a class of blood particles, principally involved in mediating reverse cholesterol transport from peripheral tissue to liver. Omics approaches have identified crucial mediators in the HDL proteomic and lipidomic profile, which are involved in distinct pleiotropic functions. Besides their role as cholesterol transporter, HDLs display anti-inflammatory, anti-apoptotic, anti-thrombotic, and anti-infection properties. Experimental and clinical studies have unveiled significant changes in both HDL serum amount and composition that lead to dysregulated host immune response and endothelial dysfunction in the course of sepsis. Most SARS-Coronavirus-2-infected patients admitted to the intensive care unit showed common features of sepsis disease, such as the overwhelmed systemic inflammatory response and the alterations in serum lipid profile. Despite relevant advances, episodes of mild to moderate acute kidney injury (AKI), occurring during systemic inflammatory diseases, are associated with long-term complications, and high risk of mortality. The multi-faceted relationship of kidney dysfunction with dyslipidemia and inflammation encourages to deepen the clarification of the mechanisms connecting these elements. This review analyzes the multifaced roles of HDL in inflammatory diseases, the renal involvement in lipid metabolism, and the novel potential HDL-based therapies.

To investigate the impact of systemic inflammatory response syndrome (SIRS) on 30-day mortality following cardiac surgery and develop a machine learning model to predict SIRS. Retrospective cohort study. Single tertiary care hospital. Patients who underwent elective or urgent cardiac surgery with cardiopulmonary bypass (CPB) from 2016 to 2020 (N = 1,908). Mixed cardiac surgery operations were performed on CPB. Data analysis was made of preoperative, intraoperative, and postoperative variables without direct interventions. SIRS, defined using American College of Chest Physicians/Society of Critical Care Medicine parameters, was assessed on the first postoperative day. The primary outcome was 30-day mortality. SIRS incidence was 28.7%, with SIRS-positive patients showing higher 30-day mortality (12.2% v 1.5%, p < 0.001). A multivariate logistic model identified predictors of SIRS. Propensity score matching balanced 483 patient pairs. SIRS was associated with increased mortality (OR 2.77; 95% CI 1.40-5.47, p = 0.003). Machine learning models to predict SIRS were developed. The baseline risk model achieved an area under the curve of 0.77 ± 0.04 in cross-validation and 0.73 (95% CI 0.70-0.85) on the test set, while the procedure-adjusted risk model showed improved performance with an area under the curve of 0.81 ± 0.02 in cross-validation and 0.82 (95% CI 0.76-0.85) on the test set. SIRS is significantly associated with increased 30-day mortality following cardiac surgery. Machine learning models effectively predict SIRS, paving the way for future investigations on potential targeted interventions that may mitigate adverse outcomes.

Thrombocytopenia and impaired platelet function are known as intrinsic drawbacks of cardiac surgery and extracorporeal life supports (ECLS). A number of different factors influence platelet count and function including the inflammatory response to a cardiopulmonary bypass (CPB) or to ECLS, hemodilution, hypothermia, mechanical damage and preoperative treatment with platelet-inhibiting agents. Moreover, although underestimated, heparin-induced thrombocytopenia is still a hiccup in the perioperative management of cardiac surgical and, above all, ECLS patients. Moreover, recent investigations have highlighted how platelet disorders also affect patients undergoing biological prosthesis implantation. Though many hypotheses have been suggested, the mechanism underlying thrombocytopenia and platelet disorders is still to be cleared. This narrative review aims to offer clinicians a summary of their major causes in the cardiac surgery setting.

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