Blood Thrombogenicity Is Independently Associated With Serum TSH Levels in Post–Non-ST Elevation Acute Coronary Syndrome

Viswanathan, Girish; Balasubramaniam, K.; Hardy, Richard; Marshall, Sally M.; Zaman, Azfar; Razvi, Salman

doi:10.1210/jc.2013-3062

Cited by 25 publications

(24 citation statements)

References 21 publications

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“…36 There have also been reports of abnormalities in glucose metabolism and in haemostatic parameters, the latter being mainly indicated by the increased activity of factor VII 37 and plasminogen activator inhibitor-1, suggesting that a hypofibrinolytic and hypercoagulable state may play a significant role in the development of atherosclerosis in patients with SCH. 38 A recent report in patients with a post-non-ST elevation acute coronary syndrome found a higher thrombus burden in the subclinically hypothyroid 39 However, this association was not detectable when the analysis was limited to patients with serum TSH within the reference range, since neither serum FT4 nor FT3 had any significant association with the thrombus area. 39 Serum TSH levels, particularly in the SCH range, were associated with a higher thrombus burden despite optimal recommended secondary prevention therapy, this possibly accounting for the higher CV risk seen in SCH patients.…”

Section: Hypercoagulation and Insulin Resistancementioning

confidence: 94%

“…38 A recent report in patients with a post-non-ST elevation acute coronary syndrome found a higher thrombus burden in the subclinically hypothyroid 39 However, this association was not detectable when the analysis was limited to patients with serum TSH within the reference range, since neither serum FT4 nor FT3 had any significant association with the thrombus area. 39 Serum TSH levels, particularly in the SCH range, were associated with a higher thrombus burden despite optimal recommended secondary prevention therapy, this possibly accounting for the higher CV risk seen in SCH patients.…”

Section: Hypercoagulation and Insulin Resistancementioning

confidence: 94%

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Cardiovascular Risk in Patients with Subclinical Hypothyroidism

Duntas¹,

Chiovato²

2014

European Endocrinology

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Subclinical hypothyroidism (SCH) has been associated with increased cardiovascular mortality due to adverse effects mainly on lipids and blood pressure (BP). There is evidence that SCH, especially in patients with thyroid-stimulating hormone (TSH) >10mU/l, may increase cardiovascular risk. Some uncertainty exists regarding the association of SCH with BP; however, that the coexistence of SCH with BP and hypercholesterolaemia has a negative cardiovascular impact is beyond doubt. Insulin resistance, by modulating various risk factors including coagulation, may potentially increase cardiovascular risk. Periodic health examinations including screening has been advised in patients >35 years of age, while treatment with thyroxine should be tailored to each patient. KeywordsSubclinical hypothyroidism, cardiovascular risk, thyroid-stimulating hormone, lipids, blood pressure, the metabolic syndrome Hypothyroidism is usually a progressive disease that impacts the entirety of bodily functions. As the heart is the main target of thyroid hormone activity, hypothyroidism may precipitate or aggravate heart failure, influencing heart rate and blood pressure (BP) while increasing cardiovascular (CV) stiffness and also cardiomegaly.1,2 Overt hypothyroidism (OH) is therefore associated with heightened CV morbidity and mortality. 3 Subclinical hypothyroidism (SCH) is defined as a condition characterised by elevated serum thyroid-stimulating hormone (TSH) concentrations (TSH: >4.5 mu/l), while circulating thyroxine (T4) and tri-iodothyronine (T3) levels remain within the population reference range. 4 The incidence of SCH varies between 4 and 20 % depending upon the gender (females are more prone), age (older than 65) and population studied. 5,6 The consequences of SCH are variable at several levels and may depend on the duration and the degree of elevation of serum TSH. Hence, a number of important questions arise relating to SCH, including whether it raises CV risk and therefore mortality, whether it negatively influences metabolic parameters and whether it should be treated with L-thyroxine. 4,7 Besides the classic risk factors for CV disease (CVD), i.e. hypercholesterolaemia and diastolic hypertension, some newer risk factors such as a disrupted coagulability and insulin resistance have recently been evaluated. 8 This review aims to update and discuss the available data regarding CV risk in patients with SCH. Subclinical Hypothyroidism and LipidsClinical hypothyroidism has been associated with elevated levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (ApoB), all of which contribute substantially to heightened risk of coronary artery disease.9-11 Thyroid hormone controls the generation of cholesterol by regulating the activity of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) enzyme and its degradation rate by regulating the expression of the SREBP-2 gene, the transcription factor that positively regulates the activity of LDL receptor.12,13 Thus, thyroid hormone action ...

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Section: Hypercoagulation and Insulin Resistancementioning

confidence: 94%

Section: Hypercoagulation and Insulin Resistancementioning

confidence: 94%

Cardiovascular Risk in Patients with Subclinical Hypothyroidism

Duntas¹,

Chiovato²

2014

European Endocrinology

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“…15 A recent study using the Badimon chamber, a model which simulates ex vivo coronary artery blood fl ow through a diseased artery, has shown that thrombus area in patients with SCH 7-10 days post non-ST elevation myocardial infarction is larger than in euthyroid patients, despite the use of aspirin and clopidogrel. 16 This may help explain the higher cardiovascular risk seen in patients with SCH, as such a state is likely to be thrombogenic.…”

Section: Mechanisms Underlying the Increased Cardiovascular Risk In Schmentioning

confidence: 99%

Thyroid disease and vascular risk

Jabbar

Razvi

2014

Clinical Medicine

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Subclinical hypothyroidism (SCH) is a common condition seen in up to 10% of adults, mainly women and the elderly. Several prospective longitudinal cohort studies have shown a higher risk of cardiovascular disease in people with SCH but mainly in younger individuals. There are also a number of interventional trials that have shown that treatment of SCH with levo-thyroxine improves cardiovascular risk factors, but there is a dearth of level 1 evidence regarding cardiovascular events. In addition, there is increasing proof concerning the association of abnormal thyroid function at the time of an acute myocardial infarction with adverse cardiovascular outcomes. This review describes the literature dealing with thyroid function in relation to cardiovascular disease and also outlines the effect of treatment in addressing cardiovascular risk.

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“…Thus, even mild hypothyroidism following AMI could be an important marker for poor outcome, and one that is ripe for cost-effective intervention if level 1 evidence of efficacy can be shown. In a recent preliminary analysis, we have shown that thrombus area, as measured by a model that simulates ex vivo coronary artery blood flow, is higher in people with SCH 7 to 10 days post non-ST elevation AMI despite dual anti-platelet therapy (with aspirin and clopidogrel) [ 18 ]. In multivariate analysis, serum TSH concentrations were directly associated with thrombus area, with a strength of association similar to other established cardiac risk factors such as diabetes mellitus and hypertension [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

“…In a recent preliminary analysis, we have shown that thrombus area, as measured by a model that simulates ex vivo coronary artery blood flow, is higher in people with SCH 7 to 10 days post non-ST elevation AMI despite dual anti-platelet therapy (with aspirin and clopidogrel) [ 18 ]. In multivariate analysis, serum TSH concentrations were directly associated with thrombus area, with a strength of association similar to other established cardiac risk factors such as diabetes mellitus and hypertension [ 18 ]. It is currently unknown whether levothyroxine treatment in SCH patients after an AMI can improve ventricular function, improve endothelial function and improve blood coagulability and rheology.…”

Section: Introductionmentioning

confidence: 99%

Thyroxine in acute myocardial infarction (ThyrAMI) - levothyroxine in subclinical hypothyroidism post-acute myocardial infarction: study protocol for a randomised controlled trial

Jabbar

Ingoe

Pearce

et al. 2015

Trials

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BackgroundCardiac disease is the most common cause of morbidity and mortality in the United Kingdom. Even minor changes in thyroid hormone concentration may impact adversely on the cardiovascular system. Subclinical hypothyroidism (SCH) after admission for an acute cardiac problem has been associated with an increase in cardiac mortality and overall death. We have designed protocols for a prospective observational study to assess the association of thyroid function at the time of acute myocardial infarction (AMI) with cardiovascular outcomes, and a double-blinded randomised placebo-controlled trial of levothyroxine to evaluate its effect on LV function and vascular health.Methods/DesignThyrAMI 1: This will be a prospective longitudinal observational study of patients with AMI that will be followed for 24 months to study the association between thyroid status at the time of AMI (within 24 hours of diagnosis) with vascular outcomes.ThyrAMI 2: This will be a prospective double-blinded randomised placebo-controlled trial of levothyroxine of 12 months duration in patients with AMI and SCH.Setting: Patients will be recruited from five hospitals in the North East of England.Participants: One hundred patients with thyroid function tests within the subclinical hypothyroid range upon admission with an AMI and no previous history of thyroid disease.Intervention: Levothyroxine will be administered at a starting dose of 25 mcg once daily, which will be increased at intervals if needed to maintain a TSH level between 0.4 to 2.5 mU/L, versus a placebo.Randomisation: Participants will be randomized with a computerised randomisation algorithm, stratified by type of MI (NSTEMI versus STEMI), in a 1:1 ratio to levothyroxine therapy or placebo (as container or bottle numbers), starting within 21 (+/− 7) days of AMI.Blinding: Assignment to either the LT4 or placebo arm will be double-blinded.Outcomes: The outcome will be the effect of levothyroxine on ventricular function, endothelial function and blood coagulability and rheology.DiscussionThere is evidence to suggest that treatment of SCH can improve cardiovascular parameters. Therefore, ThyrAMI 1 and ThyrAMI 2 will be the first trials investigating SCH in AMI to give a better insight into whether thyroid hormone levels are a key target for improving cardiovascular outcomes.Trial registrationISRCTN number: ISRCTN52505169. Date of registration: 09/01/2015

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Blood Thrombogenicity Is Independently Associated With Serum TSH Levels in Post–Non-ST Elevation Acute Coronary Syndrome

Cited by 25 publications

References 21 publications

Cardiovascular Risk in Patients with Subclinical Hypothyroidism

Cardiovascular Risk in Patients with Subclinical Hypothyroidism

Thyroid disease and vascular risk

Thyroxine in acute myocardial infarction (ThyrAMI) - levothyroxine in subclinical hypothyroidism post-acute myocardial infarction: study protocol for a randomised controlled trial

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