Abstract
Background: Thyroid plays an important role in the regulation of cardiovascular functions. Consistently, hypothyroid patients are at high risk for cardiovascular diseases. Abnormalities in endothelial function play a relevant role in the pathogenesis of cardiovascular diseases. However, the mechanisms of the defects in endothelial function has never been dissected in patients with hypothyroidism.
Aims: To assess vascular function in patients affected by hypothyroidism and to evaluate its mechanisms.
Methods: We selected 3 groups of subjects: 15 healthy controls (group 1), 10 patients affected by primary chronic hypothyroidism (group 2), and 8 patients affected by acute hypothyroidism (post-thyroidectomy for cancer) (group 3). We measured forearm blood flow (FBF) by strain-gauge plethysmography, during intra-brachial graded infusion of acetylcholine (Ach, endothelial-mediated vasodilation), sodium nitroprusside (NP, non-endothelial-mediated vasodilation), norepinephrine (NE) and L-N-monomethylarginine (L-NMMA).
Results: At the highest Ach rate, FBF was significantly reduced in groups 2 (8.5±1.62 ml/dl/min) and 3 (15.7±3.0) compared with group 1 (23.2±3.4 ml/dl/min). Also, NO and cGMP production was significantly reduced in patients with both acute and chronic hypothyroidism. NP infusion induced a reduced response in group 2 and 3 vs group 1 (15.4±2.2, 11.6±1.7 and 22.1±1.7 ml/dl/min, respectively). In contrast, the response to NE and L-NMMA infusion were comparable in the three groups.
Conclusions: Patients affected by hypothyroidism show severe vascular dysfunction, with the involvement of both endothelial and smooth muscle cells. Specifically, short term hypothyroidism is sufficient to impair vascular function, although chronic hypothyroidism can further damage the vessel wall. The data suggest that maintaining and restoring normal thyroid hormone plasma levels should be considered of primary importance to minimize the progression of vascular damage.