title: [High shear stress induced platelet aggregation (h-SIPA) and effects of antiplatelet therapy].
abstract: A physiologic time averaged mean shear stress in stenosed coronary artery reach more than 350 dyne/cm2. Pathologic stenosis can directly lead to shear-induced aggregation of platelets. Platelet aggregation in response to pathologically elevated shear stress is depend on the presence of plasma von Willebrand factor (vWF) and platelet receptor glycoprotein (GP) Ib/IX and GPIIb/IIIa. Fibrinogen bridging thrombus play as key factor at low shear rate, however, vWF is most important factor at high shear rate. When high shear stress are applied to vWF, vWF change the shape round to linear, and bind to extracellular matrix such as collagen type I or III exposed to blood by rupture of atheromatous plaque. Consequently vWF interact with GP Ib/IX for initial adhesion without agonist stimulation, which is followed by activation of GPIIb/IIIa receptor and co-binding with GPIIb/IIIa and vWF. The binding of platelets via vWF is strengthen to sustain the opposing effect of high shear forces in coronary artery. In our study, significant increases of h-SIPA and plasma vWF levels were observed in patients with acute coronary syndrome compared with patients with chronic coronary artery disease. The additional application of ticlopidine or cilostazol to aspirin therapy significantly inhibition of h-SIPA in patient with acute coronary syndrome, however, less effective than patients with chronic coronary artery disease.
authors.affiliation: 1st Internal Medicine, School of Medicine, Mie University.
authors.forename: N
authors.initials: N
authors.lastname: Isaka
authors.forename: T
authors.initials: T
authors.lastname: Tanigawa
authors.forename: M
authors.initials: M
authors.lastname: Nishikawa
authors.forename: T
authors.initials: T
authors.lastname: Nakano
mesh_terms: D000208:Acute Disease; D002986:Clinical Trials as Topic; D003327:Coronary Disease / Q000097:blood / Q000188:drug therapy*; D003328:Coronary Thrombosis / Q000209:etiology; D006801:Humans; D010974:Platelet Aggregation / Q000502:physiology*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000502:physiology; D019038:Platelet Glycoprotein GPIb-IX Complex / Q000502:physiology; D013314:Stress, Mechanical; D013577:Syndrome; D014841:von Willebrand Factor / Q000502:physiology
chemical_list: D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D019038:Platelet Glycoprotein GPIb-IX Complex; D014841:von Willebrand Factor