Increased serum vWF and sVCAM-1 levels are associated with late or very late angiographic stent thrombosis after sirolimus-eluting stent implantation.
BACKGROUND
This study sought to examine whether circulatory levels of endothelial dysfunction biomarkers [vascular cell adhesion molecule (sVCAM-1), intercellular adhesion molecule (sICAM-1), sE-selectin, von Willebrand factor (vWF), tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1)] are associated with occurrence of late or very late stent thrombosis (ST) after percutaneous coronary intervention with sirolimus-eluting stent implantation, and to assess the possible influence of genetic variants of these proteins on ST.


METHODS
Serum levels of sVCAM-1, sICAM-1, sE-selectin, vWF, t-PA and PAI-1 were measured, and polymorphisms of vWF (-1234C/T, -1185A/G and -1051G/A), t-PA (insertion/deletion) and PAI-1 genes (4G/5G) were determined in 41 patients who experienced at least one episode of late or very late ST. Eighty-two patients without ST randomly selected from the same study period served as controls.


RESULTS
Serum levels of vWF, sVCAM-1 and sICAM-1 were significantly increased in patients with ST than in controls (all P<0.01). No significant difference was observed in the genotype and allele distribution of the vWF, t-PA and PAI-1 gene polymorphisms. Multivariable logistic regression analysis showed that vWF, sVCAM-1, discontinuation of clopidogrel therapy and left ventricular ejection fraction of less than 50% were independent determinants of late ST.


CONCLUSIONS
Increased serum vWF and sVCAM-1 levels are associated with late ST, suggesting that endothelial dysfunction contributes to the development of late or very late ST.
Department of Cardiology, Rui Jin Hospital, Medical School of Jiaotong University, Shanghai, PR China.
Cao
C
Jin
Lin
L
Lu
Zheng Bin
ZB
Zhu
Rui Yan
RY
Zhang
Qi
Q
Zhang
Run
R
Du
Feng Hua
FH
Ding
Qiu Jing
QJ
Chen
Wei Feng
WF
Shen
D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects* / Q000295:instrumentation*; D015415:Biomarkers / Q000097:blood; D002317:Cardiovascular Agents / Q000008:administration & dosage*; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D002681:China; D017023:Coronary Angiography; D054855:Drug-Eluting Stents; D019040:E-Selectin / Q000097:blood; D005260:Female; D005787:Gene Frequency; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood / Q000235:genetics; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011110:Polymorphism, Genetic; D018570:Risk Assessment; D012307:Risk Factors; D020123:Sirolimus / Q000008:administration & dosage*; D013318:Stroke Volume; D013927:Thrombosis / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000097:blood / Q000235:genetics; D016896:Treatment Outcome; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood*; D016277:Ventricular Function, Left; D014841:von Willebrand Factor / Q000235:genetics / Q000378:metabolism*
D015415:Biomarkers; D002317:Cardiovascular Agents; D019040:E-Selectin; D017395:Plasminogen Activator Inhibitor 1; D010975:Platelet Aggregation Inhibitors; C546936:SELE protein, human; C051321:SERPINE1 protein, human; D019010:Vascular Cell Adhesion Molecule-1; D014841:von Willebrand Factor; D018799:Intercellular Adhesion Molecule-1; D010959:Tissue Plasminogen Activator; D020123:Sirolimus