Abstract
In some patients with stable and unstable angina pectoris and in some donors without clinical manifestations of cardiovascular diseases and other pathologies, spontaneous platelet aggregation was completely suppressed by glycoprotein IIb-IIIa antagonists blocking the interaction of this glycoprotein with fibrinogen. Antibodies inhibiting binding of glycoprotein Ib with von Willebrand factor had no effect on the level and rate of spontaneous platelet aggregation. In the donor group, the level of spontaneous aggregation was almost 1.5-fold higher in persons with a certain genetic polymorphism (Leu-->Pro substitution in position 33 of glycoprotein IIIa). The level of spontaneous aggregation correlated with the amount of glycoprotein IIb-IIIa on the platelet surface (r = 0.41).
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antibodies, Monoclonal / pharmacology
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Antibodies, Monoclonal / therapeutic use
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Aspirin / pharmacology
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Aspirin / therapeutic use
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Blood Platelets / drug effects
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Blood Platelets / metabolism*
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Cardiovascular Diseases / blood
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Cardiovascular Diseases / drug therapy
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Fibrinogen / metabolism
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Humans
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Mutation
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Peptide Fragments / pharmacology
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Peptide Fragments / therapeutic use
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Platelet Aggregation / drug effects
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Platelet Aggregation / genetics
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Platelet Aggregation / physiology*
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Platelet Glycoprotein GPIIb-IIIa Complex / antagonists & inhibitors
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Platelet Glycoprotein GPIIb-IIIa Complex / genetics
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Platelet Glycoprotein GPIIb-IIIa Complex / metabolism*
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Polymorphism, Genetic
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Protein Binding / drug effects
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von Willebrand Factor / metabolism
Substances
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Antibodies, Monoclonal
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Peptide Fragments
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Platelet Glycoprotein GPIIb-IIIa Complex
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monafram
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von Willebrand Factor
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Fibrinogen
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Aspirin