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.
Jin
Cao
C
Department of Cardiology, Rui Jin Hospital, Medical School of Jiaotong University, Shanghai, PR China.
Lu
Lin
L
Zhu
Zheng Bin
ZB
Zhang
Rui Yan
RY
Zhang
Qi
Q
Du
Run
R
Ding
Feng Hua
FH
Chen
Qiu Jing
QJ
Shen
Wei Feng
WF
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