Shear‐induced platelet aggregation increases in patients with proximal and severe coronary artery stenosis

Abstract

SummaryBackground: 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.Hypothesis: 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).

Intracoronary shear-related up-regulation of platelet P-selectin and platelet-monocyte aggregation despite the use of aspirin and clopidogrel

“…31 Our results support a direct relationship between stenosis severity, shear stress, and in situ platelet activation in human coronaries but show that atheroma burden per se, as measured by plaque volume, does not correlate with platelet activation in stable patients. This suggests that in stable coronary disease, shear stress is a more important determinant of platelet activation within coronary arteries rather than the amount of atheroma.…”

Enhanced Shear-Induced Platelet Aggregation in Patients Who Experience Subacute Stent Thrombosis

“…Shear-induced platelet aggregation is increased in chronic coronary artery disease (7,8) and myocardial infarction (7) and has been shown to be insensitive to aspirin (9) but sensitive to the combined therapy with aspirin and thienopyridine (7,10). We performed a prospective study of individuals (identified post hoc) with SAT to test the hypothesis that SIPA might identify differences between patients with or without SAT despite dual antiplatelet therapy.…”

Impact of small thrombus formation in restenotic bare-metal stent lesions associated with acute coronary syndrome: Identification by optical coherence tomography

“…To clarify the different phenotypes of ISR with its thrombogenicity or thrombogenic tissue component is difficult by using such high-resolution devices as OCT because of no direct comparison for ISR lesions between histopathology and OCT appearance. The enhanced shear stress at a severe stenotic lesion activates platelets and invites an increasing risk of platelet aggregation in the native coronary artery [23][24][25]. High shear stress also has a vicious influence on the endothelial cell function preventing thrombus formation [26].…”