title: Platelet reactivity in coronary ostial blood: a reflection of the thrombotic state accompanying plaque rupture and of the adequacy of anti-thrombotic therapy.
abstract: BACKGROUND
  Optimal anti-thrombotic therapy for acute coronary syndromes (ACS) should suppress pro-thrombotic activity at the site of plaque rupture. We sought to determine whether platelet reactivity is increased in blood in the immediate vicinity of a ruptured plaque and is apparent even when blood is obtained by sampling from a catheter placed proximal to the lesion.
  
  
  METHODS
  Blood was obtained from a catheter placed in the aorta and from the same catheter after engaging the culprit coronary artery. Platelet reactivity was determined with the use of flow cytometry by surface expression of P-selectin.
  
  
  RESULTS
  In preliminary studies we demonstrated that a marker of thrombin activity, fibrinopeptide A, was similarly increased in blood taken from the coronary sinus and coronary arterial ostium of patients with ACS. Subsequently blood was obtained from the aorta and coronary arterial ostium through a coronary guide catheter for assessment of platelet reactivity in 23 subjects with ACS and 22 subjects with stable angina. The percentage of platelets expressing P-selectin in response to 0.2 microM adenosine diphosphate (ADP) was greater in coronary arterial samples from patients with ACS (aorta=6.1+/-1%, coronary artery=8.8+/-1.6%, p=0.02) compared with that in patients with stable symptoms (aorta=6.9+/-1.2, coronary artery=6.5+/-1.4, p=NS).
  
  
  CONCLUSIONS
  Coronary arterial blood obtained from the ostium through a coronary guide catheter can be used to determine whether thrombin activity and platelet reactivity are increased in the immediate vicinity of a ruptured atherosclerotic plaque. The simplicity of the approach developed should facilitate its use in future studies designed to determine the impact of optimal suppression of platelet reactivity and the pro-thrombotic state before coronary interventions on short- and long-term clinical outcomes.
authors.affiliation: The University of Vermont, Burlington, VT, USA.
authors.forename: S S
authors.initials: SS
authors.lastname: Kabbani
authors.forename: M W
authors.initials: MW
authors.lastname: Watkins
authors.forename: P A
authors.initials: PA
authors.lastname: Holoch
authors.forename: E F
authors.initials: EF
authors.lastname: Terrien
authors.forename: B E
authors.initials: BE
authors.lastname: Sobel
authors.forename: D J
authors.initials: DJ
authors.lastname: Schneider
mesh_terms: D000208:Acute Disease; D000368:Aged; D001011:Aorta; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000150:complications* / Q000473:pathology; D003326:Coronary Circulation; D003331:Coronary Vessels; D005343:Fibrinolytic Agents / Q000008:administration & dosage; D005344:Fibrinopeptide A / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood; D015539:Platelet Activation / Q000187:drug effects; D012422:Rupture, Spontaneous / Q000097:blood* / Q000209:etiology; D019851:Thrombophilia / Q000097:blood / Q000209:etiology
chemical_list: D005343:Fibrinolytic Agents; D019007:P-Selectin; D005344:Fibrinopeptide A