On-the-Scene Hyaluronan and Syndecan-1 Serum Concentrations and Outcome after Cardiac Arrest and Resuscitation

Abstract

Background. It is not predictable which patients will develop a severe inflammatory response after successful cardiopulmonary resuscitation (CPR), also known as “postcardiac arrest syndrome.” This pathology affects only a subgroup of cardiac arrest victims. Whole body ischemia/reperfusion and prolonged shock states after return of spontaneous circulation (ROSC) may both contribute to this devastating condition. The vascular endothelium with its glycocalyx is especially susceptible to initial ischemic damage and may play a detrimental role in the initiation of postischemic inflammatory reactions. It is not known to date if an immediate early damage to the endothelial glycocalyx, detected by on-the-scene blood sampling and measurement of soluble components (hyaluronan and syndecan-1), precedes and predicts multiple organ failure (MOF) and survival after ROSC. Methods. 15 patients after prehospital resuscitation were included in the study. Serum samples were collected on the scene immediately after ROSC and after 6 h, 12 h, 24 h, and 48 h. Hyaluronan and syndecan-1 were measured by ELISA. We associated the development of multiple organ failure and 30-day survival rates with these serum markers of early glycocalyx damage. Results. Immediate serum hyaluronan concentrations show significant differences depending on 30-day survival. Further, the hyaluronan level is significantly higher in patients developing MOF during the initial and intermediate resuscitation period. Also, the syndecan-1 levels are significantly different according to MOF occurrence. Conclusion. Serum markers of glycocalyx shedding taken immediately on the scene after ROSC can predict the occurrence of multiple organ failure and adverse clinical outcome in patients after cardiac arrest.

Human glycocalyx shedding: Systematic review and critical appraisal

“…227 However, two studies have reported elevations in sdc-1 and HA in patients with cardiovascular disease. 159,184 Support for compensatory reaction(s) can be inferred from an in vivo study of the glycocalyx in sdc-1 knock-out (KO) mice where Savery et al used micro-particle velocimetry to determine the presence of a hydrodynamically significant cell surface layer. 249 They observed no difference in wild-type vs. sdc-1 KO mice and concluded that sdc-1 was not necessary for the existence of an endothelial glycocalyx.…”

“…For example, in one study assessment of the glycocalyx by SDF imaging showed no significant difference in glycocalyx dimensions between patients with and without cardiovascular disease 227 . However, two studies have reported elevations in sdc‐1 and HA in patients with cardiovascular disease 159,184 . Support for compensatory reaction(s) can be inferred from an in vivo study of the glycocalyx in sdc‐1 knock‐out (KO) mice where Savery et al used micro‐particle velocimetry to determine the presence of a hydrodynamically significant cell surface layer 249 .…”

Endothelial Glycocalyx as a Regulator of Fibrotic Processes

“…Syndecan-4 is shed by MMP-9 in a TNF-α-dependent manner [ 49 ]. MMPs are also able to cleave chondroitin sulfate [ 50 ].…”

“…Pathological damage of the glycocalyx occurs in response to mechanical cellular stress, endotoxins, inflammatory mediators, atrial natriuretic peptide, ischemia/reperfusion injury, free oxygen radicals, and hyperglycemia, as well as the novel coronavirus disease 2019 (COVID-19) [ 49 , 66 ]. Degradation of the glycocalyx results in the shedding of some of its components in the blood flow (hyaluronic acid, heparan sulfate, syndecan-1 and 4, and glypicans), and often they correlate with the severity of particular diseases [ 50 , 67 ].…”

Effects of a single aerobic exercise on perfused boundary region and microvascular perfusion: a field study

“…Experimental models of ischaemia/reperfusion and hypoxia/reoxygenation showed that myocardial hypoxia and ischaemia induce an early ESL degradation [3], with purin signalling and perivascular mast cell-derived heparanase being a possible contributing factor [4]. Increased blood levels of shed ESL components such as syndecan-1, hyaluronan and heparan sulphate can be detected in successful cardiopulmonary resuscitation after cardiac arrest, trauma and sepsis and may serve as an early predictor of adverse clinical outcome [5][6][7]. Soluble components of the endothelial glycocalyx may act as damage associated molecular patterns (DAMPs), further augmenting inflammation and tissue damage.…”