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Role of Thyroid Hormone and Oxidant Stress in Cardiovascular Diseases
Mobidullah Khan1, Suchismita Mukherjee1, Sarbashri Bank1
1Post Graduate Department of Biochemistry, Cell & Molecular Therapeutics Laboratory, Oriental Institute of Science and Technology, Rangamati, Midnapore, WB, 721102, India.
Insights
Thyroid hormones, particularly Triiodothyronine (T3), are linked to cardiovascular disease (CVD) risk factors like dyslipidemia and high glucose. Elevated T3 and thyroid-stimulating hormone (TSH) correlate with CVD severity and pathogenesis.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Metabolic Disorders
Background:
- Cardiovascular diseases (CVD) stem from metabolic issues like hypertension, dyslipidemia, and diabetes.
- Thyroid hormones, which regulate metabolic rate, are increasingly implicated in CVD development.
Purpose of the Study:
- To investigate the correlation between thyroid hormones (T3, T4, TSH) and metabolic/cardiovascular risk factors in cardiac patients.
- To explore the role of thyroid hormones in the pathogenesis and severity of cardiovascular disease.
Main Methods:
- Blood samples from 59 males (>45 yrs) including cardiac patients (trop-T+), high-risk individuals, and controls were analyzed.
- Evaluated lipid profiles, thyroid hormones (T3/T4/TSH), glucose, oxidative stress markers (MDA/NPSH), and hsCRP using biochemical methods and ELISA.
Main Results:
- In cardiac and high-risk groups, thyroid hormones correlated with glucose, triglycerides, and uric acid, indicating a hypermetabolic state.
- Elevated Triiodothyronine (T3) and thyroid-stimulating hormone (TSH) were significantly associated with increased cardiovascular risk factors and disease markers (hsCRP).
- T3 levels were notably higher in high-glucose, high-cholesterol, and trop-t+ groups, suggesting a role in pathogenesis and severity.
Conclusions:
- Dyslipidemia and oxidative stress, in conjunction with elevated T3, contribute to cardiovascular pathogenesis.
- Thyroid hormone levels are significantly associated with key risk factors and disease progression in cardiovascular conditions.
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.
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