title: Shear-induced platelet aggregation increases in patients with proximal and severe coronary artery stenosis.
abstract: BACKGROUND
  Shear stress generated in stenosed arteries promotes platelet thrombi formation at the stenosed sites by accelerating the binding of von Willebrand factor (vWF) to platelets. Shear-induced platelet aggregation (SIPA) has been studied in acute coronary syndromes, but not in chronic coronary disease.
  
  
  OBJECTIVE
  We investigated the effect of both the site and severity of coronary stenosis on SIPA in patients with chronic coronary artery disease.
  
  
  METHODS
  Shear-induced platelet aggregation was measured using platelet-rich plasma in 49 patients (41 men and 8 women; mean age 61+/-10 years) with coronary artery disease to evaluate the association between the extent of SIPA and coronary angiographic findings. Stenoses > 75% were considered severe. In all, 62 healthy individuals (54 men and 18 women; mean age 45+/-7 years) served as controls. The correlation between SIPA and the site and severity of the coronary lesion, and parameters of coagulation and fibrinolysis were evaluated.
  
  
  RESULTS
  Shear-induced platelet aggregation was increased in the stenosis group (69.0+/-10.6%) compared with the controls (57.7+/-10.3%, p < 0.0001). Patients with severe stenosis in the proximal segments had significantly increased SIPA (p< 0.0001) and vWF larger multimer concentration (p<0.0001) compared with the control group. A significant correlation existed between SIPA and the vWF larger multimer concentration in all subjects studied (r = 0.422, p < 0.0001).
  
  
  CONCLUSIONS
  Shear-induced platelet aggregation is increased in patients with severe stenosis of the proximal coronary arteries and correlates with plasma concentrations of vWF larger multimers, suggesting that severe stenosis in the proximal segments is not only associated with an increased risk of significant myocardial ischemia, but may also generate high shear stress in the stenosed artery and increase plasma vWF larger multimers, thereby promoting the formation of platelet thrombi.
authors: Second Department of Internal Medicine, Kyorin University School of Medicine, Japan.
authors: Koichi
authors: K
authors: Kawano
authors: Hideaki
authors: H
authors: Yoshino
authors: Nobuo
authors: N
authors: Aoki
authors: Hiroshi
authors: H
authors: Udagawa
authors: Atsushi
authors: A
authors: Watanuki
authors: Yoshiko
authors: Y
authors: Hioki
authors: Yukihisa
authors: Y
authors: Hasumura
authors: Toshikaki
authors: T
authors: Yasumura
authors: Masashi
authors: M
authors: Homori
authors: Mitsuru
authors: M
authors: Murata
authors: Yasuo
authors: Y
authors: Ikeda
authors: Kyozo
authors: K
authors: Ishikawa
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000704:Analysis of Variance; D000787:Angina Pectoris / Q000097:blood; D016022:Case-Control Studies; D017023:Coronary Angiography; D023921:Coronary Stenosis / Q000097:blood* / Q000473:pathology; D005260:Female; D018056:Hemorheology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood; D010974:Platelet Aggregation / Q000502:physiology*; D013927:Thrombosis / Q000209:etiology; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D014841:von Willebrand Factor