title: Platelet expression of stromal-cell-derived factor-1 (SDF-1): an indicator for ACS?
abstract: BACKGROUND
  Acute coronary syndrome (ACS) along with myocardial ischemic injury are the leading causes for chest pain. Platelet surface expression of stromal-cell-derived factor-1 (SDF-1) is enhanced during ischemic events and may play an important role in trafficking hematopoietic progenitor cells for tissue regeneration and neovascularization. This study examined the platelet surface expression of SDF-1 in patients with chest pain.
  
  
  METHODS
  We consecutively evaluated 1000 patients, who were admitted to the emergency department with chest pain. Platelet surface expression of GPIb and SDF-1 was determined by two-color whole blood flow cytometry.
  
  
  RESULTS
  Patients with ACS showed significantly enhanced SDF-1 expression on admission compared to patients with other causes such as stable angina pectoris (SAP) and other origin of chest pain (CPO) (ACS vs. SAP/CPO (mean fluorescence intensity (MFI)± SD): 39.7 ± 26.3 vs. SAP: 37.6 ± 31.5;P=0.045; arterial hypertension: 27.3 ± 12.7;P=0.003; orthopedic disease: 22.1 ± 6.5;P=0.014; pulmonary embolism: 26.6 ± 19.1;P=0.003; Da Costa's syndrome: 22.1 ± 12.5;P=0.021; inflammatory cardiomyopathy: 19.8 ± 11.5;P=0.025). Logistic regression analysis showed that surface expression of platelet SDF-1 was significantly associated with ACS (P=0.026), however, the superiority of troponin-I in predicting ACS remains on a high level (P=0.001). Areas under the curve of receiver operating characteristic analysis revealed 0.718 (95% confidence interval (CI):0.680-0.757) using SDF-1, and 0.795 (95%CI:0.760-0.829) applying troponin-I baseline serum levels. Patients with enhanced SDF-1 levels (cutoff:MFI ≥ 27.7) had a 1.4-fold relative risk (95%CI:1.17-1.52) for ACS.
  
  
  CONCLUSIONS
  Platelet SDF-1 surface expression was significantly enhanced in patients with ACS compared to SAP or CPO. Determination of platelet SDF-1 may be useful as an early additional biomarker for cardiovascular risk stratification.
authors: Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard-Karls-Universität Tübingen, Germany.
authors: Thomas
authors: T
authors: Wurster
authors: Konstantinos
authors: K
authors: Stellos
authors: Michael
authors: M
authors: Haap
authors: Peter
authors: P
authors: Seizer
authors: Tobias
authors: T
authors: Geisler
authors: James
authors: J
authors: Otton
authors: Andreas
authors: A
authors: Indermuehle
authors: Masaki
authors: M
authors: Ishida
authors: Andreas
authors: A
authors: Schuster
authors: Eike
authors: E
authors: Nagel
authors: Meinrad
authors: M
authors: Gawaz
authors: Boris
authors: B
authors: Bigalke
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood / Q000378:metabolism*; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000378:metabolism*; D054377:Chemokine CXCL12 / Q000096:biosynthesis* / Q000097:blood; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged
chemical_list: D015415:Biomarkers; D054377:Chemokine CXCL12