Blood viscosity and platelet function in thrombolytic therapy of acute myocardial infarction.
The mechanisms by which thrombolytic drugs accomplish their impressive clinical effects in the treatment of acute myocardial infarction are as yet incompletely appreciated. Factors other than lysis of thrombi and restoration of blood flow most likely play a role, and blood viscosity and platelet function probably are important factors. Blood viscosity is inversely related to oxygen supply to myocardial tissue and therefore a decrease in viscosity might contribute to preservation of myocardial function. Since fibrinogen is a major determinant of blood viscosity and this protein is largely degraded by some thrombolytic drugs, it is conceivable that a systemic fibrinogenolytic state is of additional benefit for the patient. Fibrinogen and other plasma proteins which change during thrombolytic therapy are also essential for adequate platelet function. Besides, thrombolytic drugs can directly affect platelet activity. Although the exact effects are still unknown, it is certain that changes in platelet function induced by thrombolytic drugs are important for the clinical efficacy and probably for the side-effects of thrombolytic therapy.
Hoffmann
J J
JJ
Department of Clinical Laboratories, Catharina Hospital, Eindhoven, The Netherlands.
D016255:Anistreplase / Q000627:therapeutic use*; D001792:Blood Platelets / Q000187:drug effects*; D001809:Blood Viscosity / Q000187:drug effects*; D006801:Humans; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy*; D013300:Streptokinase / Q000627:therapeutic use*; D015912:Thrombolytic Therapy; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use*; D014568:Urokinase-Type Plasminogen Activator / Q000627:therapeutic use*
D016255:Anistreplase; D013300:Streptokinase; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator