Atherogenesis in hypothyroid patients

Abstract

Hypothyroidism may lead to circulatory system impairment, which could appear as atherosclerotic lesions in blood vessels and ischemic heart disease. Thyroid hormones deficiency directly affects on heart and blood vessels functions, or they may promote metabolic changes, which affect atherosclerosis. Hypothyroidism influences in decreasing stroke volume and cardiac contractility, arterial media intima thickness, and arterial smooth muscles diastole disorders. Atherogenesis is characterized by lipoprotein metabolism disorders, which increase total cholesterol, LDL cholesterol, apoprotein B–100 and triglycerides. High LDL levels during hypothyroidism may be the result of LDL receptors reduction. The lipid profile alterations could be the consequence of specific enzymes and proteins decreased activity: hepatic lipase, lipoprotein lipase and cholesteryl ester transfer protein, which maintain correct lipid metabolism. Hypothyroidism may contribute to oxidative LDL modifications, thus tyroxine has antioxidant effect on lipoproteins. Increased atherosclerosis risk in the course of hypothyroidism may be caused also by elevated lipoprotein (a) level. Atherogenesis is often associated with chronic inflammation, which leads to increased C-reactive protein level. Moreover, it may be connected with hyperhomocysteinemia, which is caused by decreasing activity of enzymes remethylating homocysteine, and by reducing renal clearance of homocysteine. Regarding to hemostatic system, patients suffering from hypothyroidism are characterized by impaired coagulation factors synthesis and by intensified fibrynolysis, which manifest as increased bleeding tendency. Atherogenesis in hypothyroid patients is a compound mechanism. The coexistence of lipid abnormalities, intensified inflammation, and hyperhomocysteinemia amplifies atherogenesis in the course of hypothyroidism. However changes, which are observed in hemostatic system may prevent escalating of atherosclerosis.