Study of copeptin and brain natriuretic peptide in patients with thyroid dysfunction: relation to cardiovascular performance

Background Thyroid disorders are the second most common endocrine disorders after type 2 diabetes mellitus. Copeptin, the C-terminal part of pre-pro arginine vasopressin, and brain natriuretic peptide (BNP) are new markers of cardiac and endothelial diseases. The relationship between thyroid status and copeptin has not been studied yet. Serum BNP levels are also affected by thyroid function status; however, its value in the presence of thyroid dysfunction has been recently questioned. Aim of the work The aim of this work was to assess the alteration of serum copeptin and BNP in patients with thyroid dysfunction and the relationship between this alteration and cardiovascular performance in patients with thyroid dysfunction. Materials and methods This study included 60 patients who were divided into two groups: group 1 included 30 patients with hyperthyroidism and group 2 included 30 patients with primary hypothyroidism. A total of 20 healthy euthyroid individuals served as the control group (group 3). All patients and controls were subjected to estimation of serum and urine osmolarity and electrolyte study and evaluation of T3, T4, thyroid-stimulating hormone, serum copeptin, and serum BNP using enzyme-linked immunosorbent assay. Echocardiographic study was conducted to assess left ventricle (LV) systolic and diastolic functions. In addition, endothelial function was assessed by measuring flow-mediated dilatation of the brachial artery. Results In patients with hyperthyroidism, serum copeptin was significantly lower than that in controls (mean = 2.24 ± 1.68 vs. 3.34 ± 2.93 pmol/l, P = 0.03). However, it was significantly higher in hypothyroid patients in comparison with controls (mean = 18.78 ± 11.29 vs. 3.34 ± 2.93 pmol/l, P = 0.0001). Serum BNP in the hypothyroid group was significantly higher than that in the control group (mean = 15.02 ± 6.9 vs. 3.60 ± 1.38 ng/l, P = 0.028). E ′/ A ′ was significantly lower in hypothyroid patients in comparison with the control group (mean = 1.15 ± 0.72 vs. 1.48 ± 0.48, P = 0.03), and more than half of the patients (53%) had E ′/ A ′ less than 1, suggesting the presence of diastolic dysfunction in hypothyroid patients. There was a significant negative correlation between ejection fraction ( P = 0.002), fractional shortening ( P = 0.01), and copeptin in the hypothyroid group. There was a significant positive correlation between copeptin and flow-mediated dilatation ( P = 0.01) in the hyperthyroid group. Conclusion Serum copeptin and BNP were significantly increased in hypothyroid patients, whereas serum copeptin was significantly decreased in hyperthyroid patients. In hyperthyroid patients, LV systolic function was increased. More than half of the hypothyroid patients with high serum copeptin levels had impaired LV filling.