Perturbation of the endothelial glycocalyx in post cardiac arrest syndrome.
BACKGROUND
The prognosis of immediate survivors of cardiac arrest remains poor, as the majority of these patients develops an inflammatory disorder known as the post-cardiac arrest syndrome (PCAS). Recently, the endothelial glycocalyx has been shown to be a key modulator of vascular permeability and inflammation, but its role in PCAS remains unknown.


METHODS
Plasma levels of the glycocalyx components syndecan-1, heparan sulfate and hyaluronic acid were measured in 25 patients after immediate survival of cardiac arrest during different phases of PCAS. Twelve hemodynamically stable patients with acute coronary syndrome served as controls.


RESULTS
Cardiac arrest resulted in a significant increase in syndecan-1, heparan sulfate and hyaluronic acid levels compared to controls, indicating a shedding of the endothelial glycocalyx as a pathophysiological component of the post cardiac arrest syndrome. The time course differed between the individual glycocalyx components, with a higher increase of syndecan-1 in the early phase of PCAS (2.8-fold increase vs. controls) and a later peak of heparan sulfate (1.7-fold increase) and hyaluronic acid (2-fold increase) in the intermediate phase. Only the plasma levels of syndecan-1 correlated positively with the duration of CPR and negatively with the glycocalyx-protective protease inhibitor antithrombin III. Plasma levels of both syndecan-1 and heparan sulfate were higher in eventual non-survivors than in survivors of cardiac arrest.


CONCLUSIONS
Our data for the first time demonstrates a perturbation of the endothelial glycocalyx in immediate survivors of cardiac arrest and indicate a potential important role of this endothelial surface layer in the development of post-cardiac arrest syndrome.
Department of Internal Medicine III, University Hospital Freiburg, Germany. sebastian.grundmann@uniklinik-freiburg.de
Sebastian
S
Grundmann
Katrin
K
Fink
Lyubomira
L
Rabadzhieva
Natascha
N
Bourgeois
Tilmann
T
Schwab
Martin
M
Moser
Christoph
C
Bode
Hans-Joerg
HJ
Busch
D000368:Aged; D001798:Blood Proteins / Q000032:analysis; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D019276:Glycocalyx / Q000378:metabolism*; D006323:Heart Arrest / Q000150:complications / Q000378:metabolism*; D006497:Heparan Sulfate / Q000097:blood; D006801:Humans; D006820:Hyaluronic Acid / Q000097:blood; D008297:Male; D053668:Syndecan-1 / Q000097:blood
D001798:Blood Proteins; D006497:Heparan Sulfate; D006820:Hyaluronic Acid; D053668:Syndecan-1