Background: Postoperative delirium (POD) is a neurocognitive syndrome affecting patients undergoing surgery. It is a frequent complication of coronary artery bypass grafting (CABG) and is associated with higher morbidity, mortality and treatment costs. This study aimed to investigate the relationship between gaseous microemboli (GME) load during cardiopulmonary bypass (CPB) and subsequent POD in patients undergoing CABG. Methods: In total, 102 patients undergoing elective on-pump CABG were evaluated in this observational study. An ultrasonic microbubble counter, with probes placed on the arterial and venous lines, was used during CPB to evaluate the GME load for each patient. During the first postoperative week, the patients were examined for the presence of POD. Results: Patients diagnosed with POD had higher number of bubbles in the arterial CPB line (5382.8 (4127.8–6637.8) vs. 2389.4 (2033.9–2745.0), p < 0.001), higher volume of bubbles in both the venous (24.2 µL (16.8–31.6) vs. 12.4 µL (9.7–15.1), p = 0.004) and arterial lines (1.82 µL (1.43–2.21) vs. 0.29 µL (0.22–0.36), p < 0.001), lower quality factor (QF) values (p = 0.039), a lower venoarterial reduction in bubble number (83.0% (77.8–88.1) vs. 92.4% (90.9–93.8), p = 0.001) and a lower venoarterial reduction in bubble volume (88.8% (85.4–92.2) vs. 96.3% (95.2–97.3), p < 0.001) compared to the patients without POD. Older age (p = 0.005), a lower reduction in bubble volume (p < 0.001) and lower QF values (p = 0.004) were significant independent predictors of POD. Conclusions: Our findings indicate a strong association between GME and the occurrence of POD, which entails that all available actions should be implemented to prevent their generation and facilitate the elimination of GME from the CPB circuit.

Coronary artery bypass grafting (CABG) utilizing cardiopulmonary bypass (CPB) remains a cornerstone of treatment for advanced multivessel coronary artery disease. However, exposure of blood components toDuring the ischemic period, myocardial cells become injured and increasingly depend on anaerobic metabolism. After reperfus artificial surfaces, combined with ischemia-reperfusion injury, surgical trauma, and gut translocation of endotoxins, triggers a complex systemic inflammatory response syndrome (SIRS). This inflammatory cascade involves a tightly regulated network of humoral cascades (complement, contact, coagulation, and fibrinolytic systems) and cellular effectors (neutrophils, monocytes, endothelial cells, and platelets). Molecular signaling pathways, notably Toll-like receptor 4 (TLR4) activation, nuclear factor kappa B (NF-κB) nuclear translocation, mitogen-activated protein kinase (MAPK) phosphorylation, and NLRP3 inflammasome assembly, drive a cytokine storm characterized by massive releases of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-8 (IL-8). These molecular events lead to endothelial barrier disruption, vasoplegic shock, acute lung injury, myocardial dysfunction, and acute kidney injury. This comprehensive narrative review provides a detailed synthesis of the cellular and molecular mechanisms underlying CPB-induced SIRS, highlights recent advances in neutrophil extracellular trap (NET) dynamics and microvascular injury, and evaluates contemporary pharmacological and bioengineering therapeutic strategies designed to mitigate postoperative organ dysfunction.

Coronary artery disease is a leading cause of morbidity and mortality in modern medicine. In contrast, surgical myocardial revascularization via coronary artery bypass grafting (CABG) remains the gold standard of treatment for complex multivessel disease. The great saphenous vein remains the most frequently used conduit due to its availability and technical simplicity, but its long-term patency is significantly inferior to that of arterial grafts. The primary pathological process responsible for vein graft failure is intimal hyperplasia, which represents a complex response of the vascular wall to surgical trauma, vein arterialization, inflammation, and hemodynamic stress. This process is characterized by endothelial dysfunction, inflammatory cell activation, proliferation and migration of vascular smooth muscle cells, and extracellular matrix remodeling. Underpinning these alterations are numerous molecular pathways, including NF-κB, MAPK, PI3K/Akt, TGF-β, and mTOR signaling, as well as substantial contributions from oxidative stress, cytokines, growth factors, and microRNAs. Contemporary research indicates that the phenotypic transformation of vascular smooth muscle cells constitutes the central event in the development of intimal hyperplasia. Understanding the cellular and molecular mechanisms underlying this disease’s onset enables the development of novel therapeutic strategies to preserve long-term graft patency. This review paper aims to provide a systematic overview of current knowledge regarding the molecular and cellular mechanisms of intimal hyperplasia development in vein grafts following CABG.

Coronary artery disease is a leading cause of morbidity and mortality in modern medicine. In contrast, surgical myocardial revascularization via coronary artery bypass grafting (CABG) remains the gold standard of treatment for complex multivessel disease. The great saphenous vein remains the most frequently used conduit due to its availability and technical simplicity, but its long-term patency is significantly inferior to that of arterial grafts. The primary pathological process responsible for vein graft failure is intimal hyperplasia, which represents a complex response of the vascular wall to surgical trauma, vein arterialization, inflammation, and hemodynamic stress. This process is characterized by endothelial dysfunction, inflammatory cell activation, proliferation and migration of vascular smooth muscle cells, and extracellular matrix remodeling. Underpinning these alterations are numerous molecular pathways, including NF-κB, MAPK, PI3K/Akt, TGF-β, and mTOR signaling, as well as substantial contributions from oxidative stress, cytokines, growth factors, and microRNAs. Contemporary research indicates that the phenotypic transformation of vascular smooth muscle cells constitutes the central event in the development of intimal hyperplasia. Understanding the cellular and molecular mechanisms underlying this disease's onset enables the development of novel therapeutic strategies to preserve long-term graft patency. This review paper aims to provide a systematic overview of current knowledge regarding the molecular and cellular mechanisms of intimal hyperplasia development in vein grafts following CABG.

Coronary artery bypass grafting (CABG) utilizing cardiopulmonary bypass (CPB) remains a cornerstone of treatment for advanced multivessel coronary artery disease. During the ischemic period, myocardial cells become injured and increasingly depend on anaerobic metabolism. After reperfusion, exposure of blood components to artificial surfaces, combined with ischemia–reperfusion injury, surgical trauma, and gut translocation of endotoxins, triggers a complex systemic inflammatory response syndrome (SIRS). This inflammatory cascade involves a tightly regulated network of humoral cascades (complement, contact, coagulation, and fibrinolytic systems) and cellular effectors (neutrophils, monocytes, endothelial cells, and platelets). Molecular signaling pathways, notably Toll-like receptor 4 (TLR4) activation, nuclear factor kappa B (NF-κB) nuclear translocation, mitogen-activated protein kinase (MAPK) phosphorylation, and NLRP3 inflammasome assembly, drive a cytokine storm characterized by massive releases of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-8 (IL-8). These molecular events lead to endothelial barrier disruption, vasoplegic shock, acute lung injury, myocardial dysfunction, and acute kidney injury. This comprehensive narrative review provides a detailed synthesis of the cellular and molecular mechanisms underlying CPB-induced SIRS, highlights recent advances in neutrophil extracellular trap (NET) dynamics and microvascular injury, and evaluates contemporary pharmacological and bioengineering therapeutic strategies designed to mitigate postoperative organ dysfunction.