Shear-induced platelet aggregation increases in patients with proximal and severe coronary artery stenosis.
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.
Kawano
Koichi
K
Second Department of Internal Medicine, Kyorin University School of Medicine, Japan.
Yoshino
Hideaki
H
Aoki
Nobuo
N
Udagawa
Hiroshi
H
Watanuki
Atsushi
A
Hioki
Yoshiko
Y
Hasumura
Yukihisa
Y
Yasumura
Toshikaki
T
Homori
Masashi
M
Murata
Mitsuru
M
Ikeda
Yasuo
Y
Ishikawa
Kyozo
K
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
D014841:von Willebrand Factor