2026 FSA Podium and Poster Abstracts

Introduction/Background: The endothelial glycocalyx is a critical regulator of vascular permeability, shear-stress signaling, microcirculatory flow, and inflammatory homeostasis. During cardiac surgery, particularly in the setting of cardiopulmonary bypass (CPB), the glycocalyx is disrupted by ischemia-reperfusion injury, hemodilution, oxidative stress, and inflammatory activation, leading to shedding of key components such as syndecan-1 and heparan sulfate. Emerging evidence suggests that glycocalyx degradation contributes to vasoplegia, myocardial dysfunction, acute kidney injury (AKI), and multiorgan impairment. Although the underlying mechanisms are increasingly understood, glycocalyx injury is not routinely factored into anesthetic management strategies. This systematic review evaluates the glycocalyx as both a therapeutic and diagnostic target in cardiac anesthesia and explores strategies for its preservation.

Methods: A systematic literature review was conducted using PubMed, Embase, and the Cochrane Library from 2000 to 2024. Search terms included (“glycocalyx” AND “cardiac surgery”), (“syndecan-1” AND “cardiopulmonary bypass”), (“endothelial injury” AND “AKI”), and (“microcirculation” AND “anesthesia”). Eligible studies included randomized controlled trials, observational cohorts, and mechanistic studies involving adult patients undergoing cardiac surgery with CPB that reported glycocalyx biomarkers, microcirculatory measures, or postoperative cardiac and renal outcomes. Data were synthesized to identify consistent associations between glycocalyx injury, anesthetic/perfusion factors, and clinical outcomes rather than pooled effect estimates alone.

Results: Twenty-five studies met inclusion criteria. CPB was consistently associated with measurable glycocalyx shedding, with circulating syndecan-1 levels commonly increasing 2 to 5-fold from baseline. Elevated glycocalyx degradation markers were associated with higher vasopressor requirements, impaired microcirculatory measures, increased postoperative troponin release, and a reported 1.8 to 2.5-fold increased risk of AKI in several cohorts. Perfusion-related factors, including non-pulsatile flow, hemodilution, and longer CPB duration, were associated with greater biomarker elevation. Interventions such as pulsatile perfusion, reduced crystalloid exposure, albumin administration, corticosteroids, and antioxidant strategies demonstrated attenuation of glycocalyx shedding in select studies, though findings were not uniform. Biomarker-guided associations suggested that early glycocalyx injury may precede clinically overt organ dysfunction.

Discussion/Conclusion: This systematic review highlights the endothelial glycocalyx as a potentially important contributor to postoperative cardiac and renal dysfunction in cardiac anesthesia. Preservation of glycocalyx integrity represents a promising therapeutic target through perfusion optimization, anti-inflammatory modulation, and endothelial-protective adjuncts. Furthermore, glycocalyx biomarkers such as syndecan-1 hold potential as early diagnostic tools for risk stratification and personalized perioperative management. Future prospective studies should evaluate targeted glycocalyx-preserving interventions and validate biomarker-guided anesthetic and perfusion strategies aimed at reducing vasoplegia, myocardial injury, and AKI following cardiac surgery.