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[Progressively acting antithrombins and plasma heparin resistance in ischemic heart disease]
Insights
Antithrombin activity is often impaired in patients with angina and myocardial infarction. A "self-coagulogram" revealed reduced antithrombin activity in 80% of patients, impacting thrombin inactivation.
Area of Science:
- Cardiology
- Hematology
- Biochemistry
Background:
- Antithrombin is a key regulator of coagulation.
- Its activity can be affected in cardiovascular diseases like angina and myocardial infarction.
Purpose of the Study:
- To compare antithrombin activity and heparin cofactor activity in patients with angina pectoris and myocardial infarction.
- To assess the impact of these conditions on thrombin inactivation.
Main Methods:
- Activity of progressively acting antithrombin and heparin-cofactor activity were measured.
- Thrombin inactivation was assessed using the Abiligaard method and a "self-coagulogram".
- Heparin-thrombin test was employed to compute antithrombin activity and plasma reserve indices.
Main Results:
- The Abiligaard method showed normal thrombin inactivation in most patients, with exceptions in those with primary antithrombin III deficiency and acute myocardial infarction.
- The "self-coagulogram" revealed decreased antithrombin activity in 80% of patients.
- Heparin-cofactor activity was significantly disrupted, independent of platelet antiheparin factor levels.
Conclusions:
- A significant portion of patients with angina and myocardial infarction exhibit impaired antithrombin activity.
- The "self-coagulogram" and heparin-thrombin tests are valuable for detecting these coagulation disorders.
- These findings highlight the role of antithrombin dysfunction in thrombotic events associated with cardiovascular diseases.
Abstract:
A comparative study of activity of the progressively acting antithrombin and their heparin-cofactor activity was undertaken in 27 patients with angina pectoris and 46 with macrofocal myocardial infarction. It was established that the count of thrombin inactivation during 5 minutes (Abiligaard method) shows no disorders in the majority of patients. Only in 3 patients with the primary antithrombin III and 3 (40% of patients with acute myocardial infarction showed a marked decrease of this parameter. Inactivation count of the endogenous thrombin according to the "self-coagulogram" during one hour enabled one to show decrease of activity of antithrombin in of 80% of patients. The heparin-cofactor activity in the serial heparin-thrombin test is markedly disrupted, which was used to compute the indices of activity of antithrombin and of the antithrombin plasma reserve. This disorder did not depend much on the increase of the antiheparin factor of thrombocytes in plasma.