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Published on: October 12, 2017
Hyperlipoproteinemia, hemostatic variables and thromboatherosclerosis
1Medical Clinic No. 1, Cluj-Napoca, Romania.
Endogenous hypertriglyceridemia is linked to altered hemostasis, promoting fibrin deposition and arterial clots. This suggests a mechanism contributing to the development of thromboatherosclerosis.
Area of Science:
- Cardiovascular Science
- Hematology
- Metabolic Disorders
Background:
- Hyperlipoproteinemia is increasingly associated with hemostatic imbalances.
- These imbalances can promote fibrin deposition and microthrombi formation within arterial walls.
Purpose of the Study:
- To investigate the relationship between endogenous hypertriglyceridemia and hemostatic variables.
- To explore the potential mechanisms linking hypertriglyceridemia to thromboatherosclerosis.
Main Methods:
- Clinical and laboratory observations were utilized.
- Plasma levels of fibrin stabilizing factor XIII, fibronectin, and fibrinolytic inhibitors were assessed.
- Activity of vitamin K-dependent clotting factors and antithrombin III levels were measured.
Main Results:
- Endogenous hypertriglyceridemia correlated with elevated plasma levels of fibrin stabilizing factor XIII, fibronectin, and fibrinolytic inhibitors.
- Fibrin clots showed increased resistance to fibrinolysis and enhanced adherence to the subendothelial layers.
- Increased activity of vitamin K-dependent clotting factors was observed, partially offset by high antithrombin III levels.
Conclusions:
- Accelerated lipoprotein synthesis and turnover in endogenous hypertriglyceridemia may stimulate hepatic production of specific hemostatic factors.
- The resulting hemostatic imbalance favors fibrin deposition and microthrombi, contributing to the localized and slow progression of thromboatherosclerosis.
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