Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amiodarone has been used in cardiology for more than 20 years as an anti-angina and anti-arrhythmia agent. In the seventies, variations in thyroid hormone and TSH concentrations were described in treated patients. Only recently, however the pathogenic mechanisms leading to dysthyroidism in long-term treatment have been described. Today, the gravity of amiodarone-induced hyperthyroidism has been greatly reduced due to a better understanding of the underlying mechanisms and better surveillance of thyroid function. In clinical practice, the following attitude can be proposed. Thyroid exploration should be completed before prescribing amiodarone: clinical examination should emphasize personal or familial history in search of dysthyroidism or goitre; hormone assays (TSH, free T4) are needed to eliminate any latent thyroid dysfunction, particularly hyperthyroidism with little or no clinical manifestation but sometimes the causal factor in cardiac symptomatology; search for a significant level of anti-thyroperoxidase antibodies can reveal underlying chronic thyroiditis. After prescription, clinical surveillance and TSH assay should be performed at 3 months then every 6 months during treatment. After withdrawal, surveillance should be continued with check-ups at 6 and 12 months.
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PMID:[Effects of amiodarone on thyroid function]. 854 16

A 65-year-old woman with aortic stenosis, ischemic heart disease, and Graves' disease had complained of effort angina. She then suffered from liver dysfunction due to treatment with antithyroid drugs. One year after the start of radioiodine administration, she demonstrated unstable angina with palpitation and sweating. Laboratory studies revealed a recurrent hyperthyroid state, and a second coronary angiogram revealed progressive ischemic heart disease. Combined coronary artery bypass grafting, aortic valve replacement, and total thyroidectomy were performed. The postoperative course was uneventful without any problems associated with hyperthyroidism or hypothyroidism. Combined cardiac surgery and total thyroidectomy can be performed safely if the perioperative levels of thyroid hormone are maintained at euthyroid or hypothyroid levels.
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PMID:Combined cardiac surgery and total thyroidectomy: a case report. 1061 50

Three patients with angina pectoris and hypopituitarism underwent coronary artery bypass grafting. The patients received perioperative replacement steroid and thyroid hormone therapy, and there were no complications. Careful perioperative hormonal management is necessary for patients with hypopituitarism.
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PMID:Coronary artery bypass grafting in patients with hypopituitarism. 1073 53

A 49-year-old woman with bronchial asthma was followed up at our hospital. After 3 years, she experienced an attack of chest pain with ST elevation in the precordal leads of electrocardiography. After admission, the chest pain and ST elevation disappeared, but the chest pain recurred after 6 days. Coronary angiography revealed no significant stenosis in the coronary arteries. After discharge, she had the chest pain repeatedly. ST elevation in the II, III, aVF leads was recorded. The diagnosis was coronary multispasm. The chest pain was refractory to medical therapy. Hypereosinophilia developed and bronchial asthma worsened. After steroid administration, the angina and bronchial asthma ceased. She has lost about 15 kg during 1 year. Laboratory data revealed low thyroid-stimulating hormone, high thyroid hormone, positive thyroglobulin antibody, and negative thyroid-stimulating hormone receptor antibody. The diagnosis was chronic thyroiditis. The multi-vasospastic angina refractory to medical therapy was caused by the hyperthyroid stage of chronic thyroiditis and hypereosinophilia.
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PMID:[Multi-vasospastic angina refractory to medical therapy caused by hyperthyroid stage of chronic thyroiditis and hypereosinophilia: a case report]. 1080 26

Thyroid hormones influence all major metabolic pathways. Their most obvious and well-known action is an increase in basal energy expenditure obtained acting on protein, carbohydrate and lipid metabolism. With specific regard to lipid metabolism, thyroid hormones affect synthesis, mobilization and degradation of lipids, although degradation is influenced more than synthesis. The main and best-known effects on lipid metabolism include: (a) enhanced utilization of lipid substrates; (b) increase in the synthesis and mobilization of triglycerides stored in adipose tissue; (c) increase in the concentration of non-esterified fatty acids (NEFA); and (d) increase of lipoprotein-lipase activity. While severe hypothyroidism is usually associated with an increased serum concentration of total cholesterol and atherogenic lipoproteins, the occurrence of acute myocardial infarction (AMI) in hypothyroid patients is not frequent. However, hypothyroid patients appear to have an increased incidence of residual myocardial ischemia following AMI. Even in subclinical hypothyroidism, which is characterized by raised serum TSH levels with normal serum thyroid hormone concentrations, mild hyperlipidemia is present and may contribute to an increased risk of atherogenesis. Prudent substitution therapy with L-thyroxine is indicated in patients with both overt and subclinical hypothyroidism, with or without angina, to counteract the cardiovascular risk resulting from hyper-dyslipidemia.
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PMID:Thyroid and lipid metabolism. 1099 23

This review discusses the clinically relevant effects of thyroid hormone excess on the heart. Tachycardia and atrial fibrillation are usually reversible after euthyroidism is restored. Atrial fibrillation may, however, take several months to return to sinus rhythm. The increase in contractility leads to an increase of cardiac output. The development of a relative myocardial hypertrophy following long-term high-dose therapy with thyroid hormones is controversial. Cardiac failure at stress in spite of an increased cardiac output at rest is a phenomenon typical for thyrotoxicosis. Reports of dilated cardiomyopathy associated with Graves' disease and evidence for TSH-receptors in the human myocardium suggest a relationship between these two diseases. Endomyocardial biopsy studies have, however, failed to prove this hypothesis. Mitral valve prolapse is more frequent in hyperthyroid patients than in normals. Thyroid hormone excess as well as the autoimmune origin of the disease are suggested as etiology for this phenomenon. The frequently observed angina pectoris seems to be a consequence of the increase in consumption of oxygen in the presence of an unchanged oxygen supply rather than of obstruction of coronary circulation. Well documented cases of myocardial infarction patients with thyroid hormone excess and normal coronary arteries in angiography substantiate this theory. Finally diagnostic and therapeutic options of the two forms of thyrotoxicosis induced by the antiarrhythmic drug amiodarone are presented.
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PMID:[Hyperthyroidism and heart]. 1129 43

Hypothyroidism is a common disorder affecting the cardiovascular, respiratory, hematopoietic, and renal organ systems--each of which is particularly germane in the management of the surgical patient. In general, treatment of recognized hypothyroidism is recommended before any surgical procedure whenever possible and euthyroidism should be documented by measurement of serum TSH as part of the preoperative evaluation. Such a strategy is likely to result in better surgical outcomes with improved morbidity and mortality. One exception to treating first with thyroid hormone is the patient with angina or coronary artery disease requiring bypass grafting, angioplasty or stenting. In this setting, preoperative thyroid hormone therapy could tax the ischemic myocardium. The coronary blood flow should be addressed first, and thyroid hormone therapy initiated afterwards. The authors have emphasized the need for caution in the interpretation of low serum thyroid hormones in sick or surgical patients because of the importance of distinguishing between hypothyroidism and the "euthyroid sick syndrome." There is no clear evidence at this point to support thyroid hormone replacement in the latter patients, and it may be potentially harmful. Rather, we hold that T3 treatment of various surgical and other patients with nonthyroidal illness should be deferred until proof of its therapeutic efficacy is demonstrated.
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PMID:Perioperative management of patients with hypothyroidism. 1280 May 43

The purpose of this study was to investigate whether thyroid hormone levels have any predictive value for mortality in patients presenting to the emergency department with acute myocardial infarction (AMI). Three groups of patients admitted to the emergency department within the 11-month study period were considered eligible: 95 patients with chest pain and proven AMI, 26 patients with chest pain and no AMI, and 114 patients who served as controls with no evidence of any major disease. Cardiac enzymes and the following thyroid hormones were analyzed and compared between groups, regarding effects of historical and demographic factors: thyrotrophin, free triiodothyronine (FT3), total triiodothyronine (TT3), free thyroxine (FT4), and total thyroxine (TT4). Sixteen patients with AMI (16.8%) died within the study period. Troponin T and creatine kinase-B with an M-type subunit levels were significantly higher in the nonsurvivors when compared with survivors. Survivors in the AMI group had higher TT3, TT4, and lower FT4 levels, while the nonsurvivors in the AMI group had higher thyrotrophin and lower TT3, FT3 and FT4 levels than controls. In the AMI group, the nonsurvivors had lower TT3 and FT3 levels than the survivors. A history of diabetes mellitus and/or angina, TT3, or FT3 was an independent predictor of mortality. TT3 and FT3 appear to be independent prognostic factors in patients with AMI.
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PMID:Prognostic value of thyroid hormone levels in acute myocardial infarction: just an epiphenomenon? 1633 Sep 14

Thyroid hormone has many effects on the heart and cardiovascular system. Thyrotoxicosis is associated with increased cardiovascular morbidity and mortality, primarily due to heart failure and thromboembolism. However, the relationship between thyroid hormone excess and the cardiac complications of angina pectoris and myocardial infarction remains largely speculative. Moreover, few studies have been reported on the effect of thyroid hormone levels within normal range on coronary artery disease (CAD). Therefore we examined the association of thyroid function with coronary artery diseases in euthyroid angina patients. Total 192 subjects (mean age; 60.8 yrs) were enrolled in which coronary angiograms were performed due to chest pain. We measured free thyroxine (FT(4)), thyroid stimulating hormone (TSH), serum lipid levels and high-sensitivity C-reactive protein (hsCRP) levels and analyzed their association with the presence of CAD. Serum FT(4) levels were higher in patients with CAD compared with the patients without CAD (1.31 +/- 0.30 vs 1.20 +/- 0.23, p = 0.006), and high FT(4) level was associated with the presence of multi-vessel disease. Multivariate analysis showed that age (odds ratio (OR) 1.04; 95% confidence interval (CI) 1.01-1.07, p = 0.007), hypertension (OR 2.04; 95% CI 1.06-3.90, p = 0.036) and FT(4) (OR 4.23; 95% CI 1.12-15.99, p = 0.033), were the determinants for CAD. The relative risk (RR) for CAD in highest tertile of FT(4) showed increased risk compared with the lowest tertile (RR 1.98; 95% CI 0.98-3.99, p<0.001). Our study showed that FT(4) levels were associated with the presence and the severity of CAD. Also, this study suggests that elevated serum FT(4) levels even within normal range could be a risk factor for CAD. Further studies will be necessary to confirm the relationship of thyroid function and CAD.
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PMID:Higher serum free thyroxine levels are associated with coronary artery disease. 1849 53

Dyslipidemia is a common finding in patients with thyroid disease, explained by the adverse effects of thyroid hormones in almost all steps of lipid metabolism. Not only overt but also subclinical hypo- and hyperthyroidism, through different mechanisms, are associated with lipid alterations, mainly concerning total and LDL cholesterol and less often HDL cholesterol, triglycerides, lipoprotein (a), apolipoprotein A1, and apolipoprotein B. In addition to quantitative, qualitative alterations of lipids have been also reported, including atherogenic and oxidized LDL and HDL particles. In thyroid disease, dyslipidemia coexists with various metabolic abnormalities and induce insulin resistance and oxidative stress via a vice-vicious cycle. The above associations in combination with the thyroid hormone induced hemodynamic alterations, might explain the increased risk of coronary artery disease, cerebral ischemia risk, and angina pectoris in older, and possibly ischemic stroke in younger patients with overt or subclinical hyperthyroidism.
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PMID:Lipid abnormalities and cardiometabolic risk in patients with overt and subclinical thyroid disease. 2178 82


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