Hypothyroidism and Risk of Cardiovascular Disease
Нема приказа
Аутори
Gluvić, ZoranZafirović, Sonja
Obradović, Milan M.
Sudar-Milovanović, Emina
Rizzo, Manfredi
Isenović, Esma R.
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт
Thyroid hormones (TH) have a significant impact on cellular oxidative metabolism. Besides that,they maintain vascular homeostasis by positive effects on endothelial and vascular smooth muscle cells. Subclinical(SCH) and clinical (CH) hypothyroidism influences target organs by changing their morphology andfunction and impaired blood and oxygen supply induced by accelerated atherosclerosis. The increased risk ofacceleration and extension of atherosclerosis in patients with SCH and CH could be explained by dyslipidemia,diastolic hypertension, increased arterial stiffness, endothelial dysfunction, and altered blood coagulation. Instabilityof atherosclerotic plaque in hypothyroidism could cause excessive activity of the elements of innateimmunity, which are characterized by the significant presence of macrophages in atherosclerotic plaques, increasednuclear factor kappa B (NFkB) expression, and elevated levels of tumor necrosis factor α (TNF-α) andmatrix metalloproteinase (MMP) 9, with redu...ced interstitial collagen; all of them together creates inflammationmilieu, resulting in plaque rupture. Optimal substitution by levothyroxine (LT4) restores biochemical euthyroidism.In postmenopausal women and elderly patients with hypothyroidism and associated vascularcomorbidity, excessive LT4 substitution could lead to atrial rhythm disorders and osteoporosis. Therefore, it isof interest to maintain thyroid-stimulating hormone (TSH) levels in the reference range, thus eliminating thedeleterious effects of lower or higher TSH levels on the cardiovascular system. This review summarizes the recentliterature on subclinical and clinical hypothyroidism and atherosclerotic cardiovascular disease and discussesthe effects of LT4 replacement therapy on restoring biochemical euthyroidism and atherosclerosis processes.
Кључне речи:
thyroid hormones / atherosclerosis / biochemical euthyroidism / cardiovascular diseases / hypothyroidism / levothyroxineИзвор:
Current Pharmaceutical Design, 2022, 28, 25, 2065-2072
DOI: 10.2174/1381612828666220620160516
ISSN: 1381-6128
PubMed: 35726428
WoS: 00085137620000
Scopus: 2-s2.0-85136794506
Институција/група
VinčaTY - JOUR AU - Gluvić, Zoran AU - Zafirović, Sonja AU - Obradović, Milan M. AU - Sudar-Milovanović, Emina AU - Rizzo, Manfredi AU - Isenović, Esma R. PY - 2022 UR - https://vinar.vin.bg.ac.rs/handle/123456789/10409 AB - Thyroid hormones (TH) have a significant impact on cellular oxidative metabolism. Besides that,they maintain vascular homeostasis by positive effects on endothelial and vascular smooth muscle cells. Subclinical(SCH) and clinical (CH) hypothyroidism influences target organs by changing their morphology andfunction and impaired blood and oxygen supply induced by accelerated atherosclerosis. The increased risk ofacceleration and extension of atherosclerosis in patients with SCH and CH could be explained by dyslipidemia,diastolic hypertension, increased arterial stiffness, endothelial dysfunction, and altered blood coagulation. Instabilityof atherosclerotic plaque in hypothyroidism could cause excessive activity of the elements of innateimmunity, which are characterized by the significant presence of macrophages in atherosclerotic plaques, increasednuclear factor kappa B (NFkB) expression, and elevated levels of tumor necrosis factor α (TNF-α) andmatrix metalloproteinase (MMP) 9, with reduced interstitial collagen; all of them together creates inflammationmilieu, resulting in plaque rupture. Optimal substitution by levothyroxine (LT4) restores biochemical euthyroidism.In postmenopausal women and elderly patients with hypothyroidism and associated vascularcomorbidity, excessive LT4 substitution could lead to atrial rhythm disorders and osteoporosis. Therefore, it isof interest to maintain thyroid-stimulating hormone (TSH) levels in the reference range, thus eliminating thedeleterious effects of lower or higher TSH levels on the cardiovascular system. This review summarizes the recentliterature on subclinical and clinical hypothyroidism and atherosclerotic cardiovascular disease and discussesthe effects of LT4 replacement therapy on restoring biochemical euthyroidism and atherosclerosis processes. T2 - Current Pharmaceutical Design T1 - Hypothyroidism and Risk of Cardiovascular Disease VL - 28 IS - 25 SP - 2065 EP - 2072 DO - 10.2174/1381612828666220620160516 ER -
@article{ author = "Gluvić, Zoran and Zafirović, Sonja and Obradović, Milan M. and Sudar-Milovanović, Emina and Rizzo, Manfredi and Isenović, Esma R.", year = "2022", abstract = "Thyroid hormones (TH) have a significant impact on cellular oxidative metabolism. Besides that,they maintain vascular homeostasis by positive effects on endothelial and vascular smooth muscle cells. Subclinical(SCH) and clinical (CH) hypothyroidism influences target organs by changing their morphology andfunction and impaired blood and oxygen supply induced by accelerated atherosclerosis. The increased risk ofacceleration and extension of atherosclerosis in patients with SCH and CH could be explained by dyslipidemia,diastolic hypertension, increased arterial stiffness, endothelial dysfunction, and altered blood coagulation. Instabilityof atherosclerotic plaque in hypothyroidism could cause excessive activity of the elements of innateimmunity, which are characterized by the significant presence of macrophages in atherosclerotic plaques, increasednuclear factor kappa B (NFkB) expression, and elevated levels of tumor necrosis factor α (TNF-α) andmatrix metalloproteinase (MMP) 9, with reduced interstitial collagen; all of them together creates inflammationmilieu, resulting in plaque rupture. Optimal substitution by levothyroxine (LT4) restores biochemical euthyroidism.In postmenopausal women and elderly patients with hypothyroidism and associated vascularcomorbidity, excessive LT4 substitution could lead to atrial rhythm disorders and osteoporosis. Therefore, it isof interest to maintain thyroid-stimulating hormone (TSH) levels in the reference range, thus eliminating thedeleterious effects of lower or higher TSH levels on the cardiovascular system. This review summarizes the recentliterature on subclinical and clinical hypothyroidism and atherosclerotic cardiovascular disease and discussesthe effects of LT4 replacement therapy on restoring biochemical euthyroidism and atherosclerosis processes.", journal = "Current Pharmaceutical Design", title = "Hypothyroidism and Risk of Cardiovascular Disease", volume = "28", number = "25", pages = "2065-2072", doi = "10.2174/1381612828666220620160516" }
Gluvić, Z., Zafirović, S., Obradović, M. M., Sudar-Milovanović, E., Rizzo, M.,& Isenović, E. R.. (2022). Hypothyroidism and Risk of Cardiovascular Disease. in Current Pharmaceutical Design, 28(25), 2065-2072. https://doi.org/10.2174/1381612828666220620160516
Gluvić Z, Zafirović S, Obradović MM, Sudar-Milovanović E, Rizzo M, Isenović ER. Hypothyroidism and Risk of Cardiovascular Disease. in Current Pharmaceutical Design. 2022;28(25):2065-2072. doi:10.2174/1381612828666220620160516 .
Gluvić, Zoran, Zafirović, Sonja, Obradović, Milan M., Sudar-Milovanović, Emina, Rizzo, Manfredi, Isenović, Esma R., "Hypothyroidism and Risk of Cardiovascular Disease" in Current Pharmaceutical Design, 28, no. 25 (2022):2065-2072, https://doi.org/10.2174/1381612828666220620160516 . .