In line with the ESC mission, newly presented content is made available to all for a limited time (4 months for ESC Congress, 3 months for other events). ESC Professional Members, Association Members (Ivory & above) benefit from year-round access to all the resources from their respective Association, and to all content from previous years. Fellows of the ESC (FESC), and Professionals in training or under 40 years old, who subscribed to a Young Combined Membership package benefit from access to all ESC 365 content from all events, all editions, all year long. Find out more about ESC Memberships here.
Shear stress induced unfolding of von willebrand factor may be involved in the premature development of myocardial infarction
I Melnikov1
,
Y Avtaeva1
,
S Kozlov1
,
D Nozadze1
,
Z Gabbasov1
,
1Cardiology Research and Production Center - Moscow - Russian Federation
,
Citation:
Background: Normally, von Willebrand factor (vWF) becomes highly reactive with platelets upon unfolding into a fibrillar conformation at critical shear rate (more than 5000 s-1), that may occur in stenotic arteries. At shear rates below critical value (1200-1300s-1), which occur in intact coronary arteries, normally there is no conformational rearrangement of vWF. Pathologic unfolding of vWF at shear rates below critical value may increase a risk of the development of coronary thrombosis. There is little information on the role of shear stress induced conformational rearrangement of vWF in the development of myocardial infarction in young individuals. Purpose: to investigate vWF-dependent platelet adhesion of patients with premature myocardial infarction at shear rates below critical value (1200-1300s-1). Methods: Using a microfluidic system, we measured platelet adhesion to a fibrinogen-coated optical surface at shear rates of 1200-1300 s-1 during 10 minutes. We assessed platelet-rich plasma of 8 male persons 40-52 years old, who had previous myocardial infarction at the age of 34-39. The control group comprised 6 healthy male volunteers 30-55 years old. We compared the intensity of scattered laser light measured in volts (V) at 10th minute. To study vWF-dependent platelet adhesion, we blocked GPIb receptor with monoclonal antibody to inhibit platelet interaction with vWF. To compare the intensity of vWF-dependent platelet adhesion with normally occurring adhesion to fibrinogen, we blocked GPIIb/IIIa receptor with monoclonal antibody. Results: The inhibition of GPIb vWF-receptor decreased platelet adhesion to fibrinogen surface at shear rates of 1200-1300s-1 by 17.8±4.7% in healthy volunteers and by 92±2.8% in persons with premature myocardial infarction (p<0.05). Inhibition of GPIIb/IIIa receptor decreased platelet adhesion by 91.5±3.8% in healthy volunteers and by 97.3±3.2% in persons with premature myocardial infarction. Conclusion: Pathologic unfolding of vWF at shear rates below critical value may be involved in the development of premature myocardial infarction.
In line with the ESC mission, newly presented content is made available to all for a limited time (4 months for ESC Congress, 3 months for other events). ESC Professional Members, Association Members (Ivory & above) benefit from year-round access to all the resources from their respective Association, and to all content from previous years. Fellows of the ESC (FESC), and Professionals in training or under 40 years old, who subscribed to a Young Combined Membership package benefit from access to all ESC 365 content from all events, all editions, all year long. Find out more about ESC Memberships here.
ESC 365 is supported by Bayer, Boehringer Ingelheim and Lilly Alliance, Bristol-Myers Squibb and Pfizer Alliance, Novartis Pharma AG and Vifor Pharma in the form of educational grants. The sponsors were not involved in the development of this platform and had no influence on its content.
Our mission: To reduce the burden of cardiovascular disease
