Role of Thyroid Hormone and Oxidant Stress in Cardiovascular Diseases
Background: Cardiovascular-diseases (CVD) are caused by different metabolic-anomalies related to hypertension/sedentary life-style/drug-addiction/dyslipidemia and diabetes. Scanty report suggests that metabolic-rate regulating thyroid hormones are linked to CVD. Methods: A total 59 individuals (male, >45 yrs) were involved in this study. Blood-samples from diagnosed cardiacpatients troponin (N=13, trop-T+), individuals with high-risk (N=15) (high glucose/cholesterol/triglycerides) with agematched controls (N=31) were tested for the evaluation of lipid-profiles/thyroid-hormones; Triiodothyronine, Thyroxine and thyroid stimulating hormone (T3/T4/TSH), blood-glucose/oxidative-stress indicators like malondialdehyde(MDA)/non-protein-soluble-thiol(NPSH) and metabolic inflammatory-marker; human C-reactive protein hsCRP by biochemical-methods/ELISA. Result: Correlation-data suggest that in normal-condition there is no significant correlation between thyroid-hormones and other parameters. In contrary, blood-glucose/triglyceride/uric-acid/proteins are correlated in cardiac and high-risk patients suggesting hypermetabolic conversion of nutrients by biochemical connectors like TCA cycle and gluconeogenesis pathways. Further, the hypermetabolic-state is favored by the rise in the thyroid hormones level. In high-glucose group there is a significant correlation between metabolic-parameter and oxidative-stress indices like uric-acid/NPSH/MDA. T3 and T4 have also been linked to the serum-protein. But in the trop t+ group all thyroid hormones have been significantly associated with blood cholesterol/triglyceride and glucose suggesting the increasing involvement of thyroid-hormone in risk-factors and disease groups. The hsCRP level was ~100% and ~5-fold higher in high cholesterol and trop t+ groups, respectively. T3 was also ~70%, ~4.5-fold and ~3.5-fold higher in high-glucose/high-cholesterol/trop-t+ groups, respectively. This suggests that T3/TSH is linked to the pathogenesis and severity. Conclusion: Dyslipidemia, oxidant-stress in association with T3 augment cardiac-pathogenesis.