Changes in syndecan-1 concentration in the coronary sinus immediately after cardiac reperfusion reflect postoperative myocardial injury

Abstract

Objectives: Endothelial glycocalyx (eGCX) is shed into the bloodstream during reperfusion injury and ischemia, and its core proteins, syndecan-1 and glypican-1, can be measured in the blood. However, no studies have measured cardiac serum syndecan-1 concentrations in blood from the coronary sinus. Therefore, we aimed to examine the relationship between the degree and changes in eGCX damage and postoperative clinical outcomes using blood drawn from the coronary sinus.

Methods: Serum eGCX concentrations in the coronary sinus of 56 patients who underwent cardiac and thoracic aortic surgery with combined ante- and retrograde cardioplegia were analyzed. The association between maximum postoperative troponin T (TnT) level, as a myocardial damage marker, and eGCX injury markers, including syndecan-1 and glypican-1, measured in coronary sinus blood drawn immediately after reperfusion, was assessed. The association between eGCX injury markers and duration of cardioplegic arrest was also investigated.

Results: An association between degree of change in coronary sinus serum syndecan-1 concentration during reperfusion and postoperative maximum serum TnT levels was observed. No such association was found between the degree of change in coronary sinus serum glypican-1 concentration during reperfusion and postoperative serum TnT levels. Similar results were obtained for somatic circulation. Moreover, an association between maximum change in serum syndecan-1 concentration in the coronary sinus during reperfusion and cardioplegic arrest duration was observed. No such association was found for glypican-1 concentration.

Conclusions: The degree of endothelial damage to the coronary sinuses during reperfusion may predict myocardial injury following cardiac surgery.

Keywords: Cardioplegic arrest; Coronary sinus; Endothelial glycocalyx; Glypican-1; Reperfusion injury; Syndecan-1; Troponin T.