Abstract
Clinical and autopsy studies have suggested that patients with hypothyroidism have more advanced coronary atherosclerosis. The accelerated atherosclerosis has been explained by increases in low density lipoprotein cholesterol, blood pressure and newer risk factors such as homocysteine, C-reactive protein and plasminogen activator inhibitor-1 in hypothyroid state. In addition, recent studies have suggested that thyroid hormone has a direct effect on blood vessel, which may attenuate the progression of atherosclerosis. In addition to a direct relaxation of blood vessel through nongenomic effect, thyroid hormone has been reported to induce production of adrenomedullin and adenosine in vascular smooth muscle cells, which may be involved in vasodilation. Thyroid hormone also inhibits angiotensin II type1 receptor expression and signal transduction, and attenuates neointimal formation after balloon injury. These data suggest that thyroid hormone inhibits atherogenesis through direct effects on the vasculature as well as modifying risk factors.
Keywords: low density lipoprotein, coronary atherosclerosis, vascular smooth muscle factor cell, nitric oxide, C-reactive protein
3