These observations are reinforced by studies in the general population showing associations between subclinical thyroid hormone alterations and an increased coronary calcification.[14] The increased cardiovascular risk due to non-thyroidal illness could be explained by the promotion of endothelial dysfunction, vasoconstriction and lipid alterations by a systemic low thyroid hormone state.[15] These pathways seem, however, not fully able to explain the specific presence of media calcification. This evidence concerns the gene TG and endothelial dysfunction.