Endothelial glycocalyx during early reperfusion in patients undergoing cardiac surgery
Arie Passov1, Alexey Schramko1, Ulla-Stina Salminen2
1Division of Anaesthesiology, Department of Anaesthesiology Intensive Care and Pain Medicine, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Insights
During cardiac surgery, aortic declamping causes systemic syndecan-1 release and coronary sequestration. This suggests the glycocalyx may be regenerating after damage during open-heart procedures.
Area of Science:
- Cardiovascular Science
- Biochemistry
- Surgical Research
Background:
- Cardiac ischemia-reperfusion injury damages the glycocalyx, leading to component washout.
- Systemic syndecan-1 and heparan sulfate elevations are known in cardiac surgery.
- Immediate reperfusion events in coronary and systemic circulation remain unclear.
Purpose of the Study:
- To investigate systemic and coronary circulation changes of syndecan-1 and heparan sulfate during immediate reperfusion after aortic declamping.
- To understand the glycocalyx's behavior during early reperfusion in cardiac surgery.
Main Methods:
- Studied 30 patients undergoing aortic valve replacement.
- Measured arterial and coronary sinus concentrations of syndecan-1 and heparan sulfate before and after aortic declamping.
- Calculated trans-coronary gradients to assess component movement.
Main Results:
- Arterial syndecan-1 increased by 18% and heparan sulfate decreased by 14% one minute post-declamping.
- No coronary washout of syndecan-1 or heparan sulfate was observed.
- Trans-coronary sequestration of syndecan-1 occurred at 5 and 10 minutes post-reperfusion.
Conclusions:
- Aortic declamping triggers extracardiac syndecan-1 release and heparan sulfate sequestration.
- Syndecan-1 is sequestered in the coronary circulation during early reperfusion.
- Sequestration may indicate endogenous restoration of the damaged glycocalyx after open-heart surgery.
Background:
Experimental cardiac ischemia-reperfusion injury causes degradation of the glycocalyx and coronary washout of its components syndecan-1 and heparan sulfate. Systemic elevation of syndecan-1 and heparan sulfate is well described in cardiac surgery. Still, the events during immediate reperfusion after aortic declamping are unknown both in the systemic and in the coronary circulation.
Methods:
In thirty patients undergoing aortic valve replacement, arterial concentrations of syndecan-1 and heparan sulfate were measured immediately before and at one, five and ten minutes after aortic declamping (reperfusion). Parallel blood samples were drawn from the coronary sinus to calculate trans-coronary gradients (coronary sinus-artery).
Results:
Compared with immediately before aortic declamping, arterial syndecan-1 increased by 18% [253.8 (151.6-372.0) ng/ml vs. 299.1 (172.0-713.7) ng/ml, p < 0.001] but arterial heparan sulfate decreased by 14% [148.1 (135.7-161.7) ng/ml vs. 128.0 (119.0-138.2) ng/ml, p < 0.001] at one minute after aortic declamping. There was no coronary washout of syndecan-1 or heparan sulfate during reperfusion. On the contrary, trans-coronary sequestration of syndecan-1 occurred at five [-12.96 ng/ml (-36.38-5.15), p = 0.007] and at ten minutes [-12.37 ng/ml (-31.80-6.62), p = 0.049] after reperfusion.
Conclusions:
Aortic declamping resulted in extracardiac syndecan-1 release and extracardiac heparan sulfate sequestration. Syndecan-1 was sequestered in the coronary circulation during early reperfusion. Glycocalyx has been shown to degrade during cardiac surgery. Besides degradation, glycocalyx has propensity for regeneration. The present results of syndecan-1 and heparan sulfate sequestration may reflect endogenous restoration of the damaged glycocalyx in open heart surgery.
