RESUMO
BACKGROUND: Cardiovascular-diseases (CVD) are caused by different metabolic-anomalies related to hypertension/sedentary lifestyle/drug-addiction/dyslipidemia and diabetes. The scanty report suggests that metabolic-rate regulating thyroid hormones are linked to CVD. METHODS: A total of 59 individuals (male, >45 yrs) were involved in this study. Blood-samples from diagnosed cardiac-patients troponin (N=13, trop-T+), individuals with high-risk (N=15) (high glucose/cholesterol/triglycerides), and with age-matched 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. RESULTS: Correlation-data suggest that in normal conditions, there is no significant correlation between thyroid-hormones and other parameters. On the contrary, blood-glucose/triglyceride/uric-acid/ proteins are correlated in cardiac and high-risk patients, suggesting hypermetabolic conversion of nutrients by biochemical connectors like the TCA cycle and gluconeogenesis pathways. Further, the hypermetabolic-state is favored by the rise in the thyroid hormones level. In the 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 pathogenesis and severity. CONCLUSION: Dyslipidemia, oxidant-stress in association with T3, augments cardiac-pathogenesis.
