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)

Myocardial infarction occurs rarely with thyrotoxicosis. A 34-year-old woman with thyrotoxicosis sustained a transmural myocardial infarction and subsequently on cardiac catheterization studies had no significant coronary arterial disease but only residual apical wall akinesia. Thyroid hormone may directly influence myocardial oxygen supply and demand and, by some unknown mechanism exclusive of major coronary arterial blood supply, cause a critical imbalance resulting in angina pectoris and myocardial infarction.
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PMID:Myocardial infarction associated with thyrotoxicosis. 87 41

Management of patients with chest pain and hypothyroidism is a clinical dilemma. Thyroid replacement therapy may exacerbate angina pectoris. Administration of a beta blocker such as propranolol (Inderal) concomitantly with thyroid replacement therapy is useful in treatment of angina. However, beta blockers can induce variant angina owing to increased norepinephrine secretion and enhanced alpha-mediated responsiveness in the hypothyroid state. Hypotension and syncopal episodes may develop in the hypothyroid patient after administration of nitrates. Cardiac catheterization and revascularization are well tolerated by myxedematous patients with angina. After surgery, full thyroid replacement therapy should be initiated gradually and with caution.
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PMID:Hypothyroidism with angina pectoris. A clinical dilemma. 308 77

Amiodarone, an iodine-containing drug used frequently in the treatment of cardiac arrhythmias and angina pectoris, has many effects on thyroid hormone metabolism, including decreasing the production of triiodothyronine (T3) and decreasing the clearance of thyroxine and reverse T3. These effects result in elevated serum thyroxine and reverse T3 concentrations and decreased serum T3 concentrations. In addition, iodine-induced hyperthyroidism or hypothyroidism may occur in patients chronically treated with amiodarone. This study is a retrospective analysis of the incidence of thyroid dysfunction in Lucca and Pisa, West Tuscany, Italy, and in Worcester, Massachusetts. Hyperthyroidism was a more frequent (9.6%) complication of amiodarone therapy in West Tuscany, where iodine intake is moderately low; hypothyroidism was more frequent (22%) in Worcester, where iodine intake is sufficient. In patients receiving chronic amiodarone therapy, clinically suspected hyperthyroidism is best confirmed by showing elevations in serum T3 or free T3 concentrations; hypothyroidism is best diagnosed by showing an elevated serum thyrotrophin concentration. Thyroid function should be carefully monitored in patients receiving amiodarone chronically, especially if they have goiter or Hashimoto's thyroiditis.
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PMID:Environmental iodine intake and thyroid dysfunction during chronic amiodarone therapy. 642 91

Amiodarone is an antiarrhythmic agent with high iodine content. Ten patients treated with amiodarone developed thyrotoxicosis. I131 uptakes were negligible, and TT3 levels low in relation to TT4 levels, and sometimes even normal. Cessation of amiodarone caused thyroid functions to return to normal in one to five months, unrelated to propylthiouracil treatment. Eight of the patients had normal thyroid glands on radioscan or palpation. All patients tested had normal TRH tests. Thyrotoxicosis is a relatively common complication of amiodarone treatment, probably caused by its high iodine content. It is possible in apparently normal thyroid glands, suggesting failure of the homeostatic mechanisms controlling thyroid synthesis and release in these patients. Amiodarone is very efficient in controlling tachyarrhythmias and angina pectoris, situations in which thyrotoxicosis is dangerous. Thyroid function tests should therefore be drawn periodically, and the complication considered whenever tachyarrhythmias worsen on treatment with amiodarone.
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PMID:Thyrotoxicosis induced by amiodarone, a new efficient antiarrhythmic drug with high iodine content. 646 85

Thyroid replacement therapy in patients with myxoedema associated with coronary atherosclerosis often exacerbates angina or occasionally precipitates myocardial infarction. Coronary revascularization has been proposed for these patients. In an attempt to evaluate the risks of anesthesia and surgery in hypothyroidism against the possible occurrence of a coronary event during preoperative thyroid replacement therapy, we reviewed the literature and report an additional five hypothyroid patients undergoing coronary bypass grafting without operative complications. It seems recommendable not delay thyroid replacement therapy in hypothyroid patients, who need coronary artery surgery, until a few days after the intervention.
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PMID:Coronary artery surgery in patients with myxoedema. 661 Feb 71

Myxoedema has been considered a major anaesthetic risk which could be increased by concurrent heart disease. Thyroid ablation with the production of myxoedema has, in the past, been used to control intractable angina. Eight ablated patients (Group I) and five patients with heart disease and incidental hypothyroidism (Group II) presented for open heart surgery. Management included diazepam-narcotic anaesthesia in generally reduced doses, careful monitoring and the use of digoxin, steroids and I-thyroxin given during or after operation. All patients survived. A number of the anaesthetic considerations and potential problems with myxoedema are discussed.
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PMID:Myxoedema and open heart surgery: anaesthesia and intensive care unit experience. 713 93

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

Thyroid hormones may exert cardiovascular actions by direct effects on the myocardium, by interacting with the sympathetic nervous system and through alterations of the peripheral circulation. Then, thyroid hormones increase myocardial contractility and relaxation, sensitise the myocardium to sympathetic nervous system and decrease arterial resistance. Hyperthyroidism results in an enhanced myocardial contractility, an increased cardiac output and a fall in systemic vascular resistance. Nevertheless "high output" cardiac decompensation may occur. Thyrotoxicosis may trigger arrythmia and disease seems to be associated with an increase in the frequency of mitral valve prolapse. Even in mild or subclinical hyperthyroidism complication may occur. Sympathetic blocking agents are the treatment of choice in addition to aetiologic treatment. Hypothyroidism is associated with bradycardia, a decreased cardiac output, increased vascular resistance and perhaps a decreased sensitivity of the sympathoadrenal system. An increase in cholesterolemia leads to an additional risk for the development of atherosclerosis. Main cardiovascular complications of hypothyroidism are angina pectoris, diastolic hypertension, atrio-ventricular blocks or pericarditis. Mild hypothyroidism might also be correlated with an increase in adverse effects.
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PMID:[Heart and thyroid]. 859 89

In some patients with severe hypothyroidism thyroxine replacement therapy precipitates or aggravates angina pectoris, whereas in other patients angina pectoris is ameliorated or even disappears. The reason for this paradox is unknown. It has been attributed either to reversible endocrine cardiomyopathy in the form of asymmetric septal hypertrophy (ASH) or reversible anatomical narrowing of the coronary arteries. The results of a recent investigation, in which myocardial performance was surveyed by radionuclide ventriculography throughout early thyroxine replacement therapy in severe hypothyroidism, were compatible with the presence of reversible coronary dysfunction rather than of ASH. The aim of the present investigation was to confirm these findings. In six severely hypothyroid patients, without echocardiographic evidence of ASH or evidence of concomitant coronary artery disease (CAD), exercise and redistribution tomographic myocardial thallium-201 imaging (SPECT) was performed before thyroxine replacement therapy and repeated after 10 days and again after 2 months during therapy. In four patients substantial regional perfusion defects were demonstrated after exercise that were normalized at rest both before, and in one subject also after 10 days, on thyroxine. With restoration of euthyroidism, exercise and redistribution SPECT were normal in every patient. Determination of exact confidence limits reveals that the proportional incidence of myocardial perfusion defects in hypothyroidism, indicating myocardial ischemia, will at least be 22% with 95% probability. Despite the relatively low specificity of SPECT it seems pertinent to conclude that impaired myocardial perfusion as assessed by SPECT probably is due to reversible coronary dysfunction inherent in the hypothyroid state, and that this is not an infrequent manifestation of severe hypothyroidism.
Thyroid 1995 Dec
PMID:Silent myocardial ischemia in hypothyroidism. 880 93

We report here a patient with recurrent Graves' disease on hemodialysis. She also suffered from angina pectoris, which was probably a manifestation of Graves' disease due to the increased oxygen demands in the presence of fixed coronary lesions. Although antithyroid drugs induced mild granulocytopenia, propylthiouracil (PTU) or methimazole (MMI) was not discontinued during the administration of granulocyte colony-stimulating factor (G-CSF). The patient received sodium iodine-131 therapy, and became euthyroid with no chest pain. To our knowledge, this is the first case that illustrated the usefulness of G-CSF for antithyroid drug-induced granulocytopenia prior to thyroid ablation for Graves' disease complicated with chronic renal failure and angina pectoris.
Thyroid 1997 Aug
PMID:Successful treatment of a patient with Graves' disease on hemodialysis complicated by antithyroid drug-induced granulocytopenia and angina pectoris. 929 52


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