UMLS:C0151744 - FACTA Search

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Query: UMLS:C0151744 (myocardial ischemia)
31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this paper the authors have evaluated the incidence and the clinical implications of sick euthyroid syndrome (SES) in a group of 144 patients in a department of internal medicine. SES is an alteration of thyroid hormone values in the absence of a thyroid disease, which is seen in patients suffering from serious diseases. Having classified SES into 3 subgroups according to the different alterations seen in the values of T3, T4, FT3, FT4, TSH, rT3 and TBG, they show the hypotheses that explain the biochemical mechanisms which are at the basis of these hormonal alterations. Fourteen of the 144 patients under observation were excluded as they were suffering from ascertained or subclinical thyroid disease. Thirty (23% of cases) of the remaining 130 patients had alterations of the thyroid hormones in accordance with SES diagnosis. Of these 30 patients, 19 had hormone values found in SES type I (63%), 2 in SES type II (6.5%) and 9 in SES type III (30.5%). In SES type I the diseases seen, in order of frequency, were: obstructive chronic bronchopneumopathy with acute respiratory failure, diabetic ketoacidosis, neoplasms, ischemic heart disease, cardiac failure, chronic renal failure, liver diseases, acute cerebral vasculopathies, sepsis and collagenopathies. The disease seen in the 2 cases of SES type II was obstructive chronic bronchopneumopathy with acute respiratory failure. In SES type III the diseases seen were, in order of frequency: diabetic ketoacidosis, lung diseases, ischemic heart disease, cardiac failure, peripheral arteriopathies, acute cerebral vasculopathies, neoplasms, liver diseases, acute renal failure. The incidence of SES in 23% of the admitted to hospital patients was found to be slightly higher than in other studies; this could be explained by a stricter selection of inpatients: in fact self-sufficient patients or those not needing urgent admission, were sent to an efficient out patient clinic where necessary examinations were quickly carried out, hospitalization being reserved for patients with more serious illnesses. We would like to underline how the incidence of SES is much greater than that of what is known as thyroid disease (23% compared to 5%), thereby confirming that it is the most frequent cause of alterations of thyroid hormones. With regard to the pathogenetical hypotheses, it is confirmed that in SES, the reduction of T3 values is accompanied by an increase in the values of rT3 as for reduced activity of 5-desiodinasis enzyme. In SES type III the increase of T4 values is due to the increase of TBG resulting in an increase in the link for T4 and therefore a reduced peripheral hormone activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The euthyroid sick syndrome. Its incidence and clinical significance in an internal medicine department]. 802 42

Reversible silent myocardial ischemia associated with treatment of long-standing hypothyroidism has recently been reported using thallium-201 (201Tl) myocardial single photon emission tomography (SPET). The aim of the present study was to evaluate whether patients with short-term hypothyroidism (serum thyrotropin [TSH] levels above 30 mU/L) have an increased risk of silent myocardial ischemia. We studied 20 patients with differentiated thyroid carcinoma that had undergone thyroidectomy and ablative (131)I therapy. None of the patients had a known history of atherosclerotic cardiovascular disease. In the course of a planned follow-up examination, suppressive levothyroxine (LT4) therapy was discontinued 7 weeks prior to scintigraphy and replaced by triiodothyronine (T3) therapy for 4 weeks. No thyroid hormone medication was given during the 3 weeks preceding the diagnostic procedures. All patients were hypothyroid (TSH 87.2 +/- 30.8 mU/L, mean +/- SD) at the time of the examination. 20lTl-SPET was performed immediately after bicycle exercise stress test and again after a delay of 4 hours. In case of abnormal results, (n = 3) the examination was repeated after patients were euthyroid. Two patients showed effects of soft-tissue attenuation (breast attenuation in a female and diaphragmatic attenuation in a male subject). Myocardial ischemia was revealed in 1 patient but was seen in both hypothyroid and euthyroid examinations. The results of the present study show that short-term severe hypothyroidism as encountered in athyreotic patients after cessation of thyroxine medication for several weeks, is not associated with an impairment of myocardial perfusion.
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PMID:Severe short-term hypothyroidism is not associated with an increased incidence of myocardial ischemia as assessed by thallium-201 stress/rest myocardial scintigraphy. 1009 Mar 15

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

Iodine-131 (I-131) ablation of thyroid remnant and/or persistent, recurrent or metastatic tumour is part of the initial and subsequent management of well-differentiated thyroid carcinoma. Key to optimizing the safety and efficacy of radioablation is maximizing the selective uptake of radioiodine by normal or neoplastic thyroid tissue. This is achieved by ensuring adequate serum concentrations of thyroid-stimulating hormone (TSH). Exogenous TSH administration obviates the thyroid hormone suppression therapy withdrawal that is necessary for endogenous TSH elevation. It also avoids the marked morbidity, discomfort, and impairment in professional and educational pursuits and quality of life that often result from such withdrawal. Multicentre clinical studies have documented the safety and efficacy of recombinant human TSH (rhTSH) in promoting radioiodine uptake in the diagnostic scanning of well-differentiated thyroid cancer. Study of the use of rhTSH to facilitate radioablation of remnant and malignant thyroid tissue is at an earlier stage, with formal clinical investigation underway. Since April 1995, however, rhTSH has been employed as a radioablative adjunct in over 100 patients in the manufacturer's Compassionate Use Program. Twelve of these cases, reported or reviewed in the present paper, provide preliminary evidence that rhTSH is safe and effective in the radioablation setting. More data are needed to confirm these observations and to provide guidelines for optimal radioiodine dosing, and should be furnished by ongoing clinical investigation. rhTSH is the only acceptable treatment option in a subgroup of patients with well-differentiated thyroid cancer, including those with hypopituitarism, ischaemic heart disease, a history of "myxoedema madness," debilitation due to very advanced disease or inability to produce TSH due to continued production of thyroxine by thyroid remnant or metastatic tumour. Therapeutic use of rhTSH may be considered in an increasing number of other cases.
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PMID:Recombinant human thyroid-stimulating hormone (rhTSH) in the radioablation of well-differentiated thyroid cancer: preliminary therapeutic experience. 1072 3

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

Amiodarone is a benzofuranic-derivative iodine-rich drug widely used for the treatment of tachyarrhythmias and, to a lesser extent, of ischemic heart disease. It often causes changes in thyroid function tests (typically an increase in serum T(4) and rT(3), and a decrease in serum T(3), concentrations), mainly related to the inhibition of 5'-deiodinase activity, resulting in a decrease in the generation of T(3) from T(4) and a decrease in the clearance of rT(3). In 14-18% of amiodarone-treated patients, there is overt thyroid dysfunction, either amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH). Both AIT and AIH may develop either in apparently normal thyroid glands or in glands with preexisting, clinically silent abnormalities. Preexisting Hashimoto's thyroiditis is a definite risk factor for the occurrence of AIH. The pathogenesis of iodine-induced AIH is related to a failure to escape from the acute Wolff-Chaikoff effect due to defects in thyroid hormonogenesis, and, in patients with positive thyroid autoantibody tests, to concomitant Hashimoto's thyroiditis. AIT is primarily related to excess iodine-induced thyroid hormone synthesis in an abnormal thyroid gland (type I AIT) or to amiodarone-related destructive thyroiditis (type II AIT), but mixed forms frequently exist. Treatment of AIH consists of L-T(4) replacement while continuing amiodarone therapy; alternatively, if feasible, amiodarone can be discontinued, especially in the absence of thyroid abnormalities, and the natural course toward euthyroidism can be accelerated by a short course of potassium perchlorate treatment. In type I AIT the main medical treatment consists of the simultaneous administration of thionamides and potassium perchlorate, while in type II AIT, glucocorticoids are the most useful therapeutic option. Mixed forms are best treated with a combination of thionamides, potassium perchlorate, and glucocorticoids. Radioiodine therapy is usually not feasible due to the low thyroidal radioiodine uptake, while thyroidectomy can be performed in cases resistant to medical therapy, with a slightly increased surgical risk.
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PMID:The effects of amiodarone on the thyroid. 1129 26

Thyroid hormone plays an important role on myocardial development and function. The local effects of thyroid hormone are mediated by the receptor isoforms ultimately driving the expression of cardiac-specific genes. Although overt and subclinical thyroid dysfunction causes well-known changes in the cardiovascular system, little is known about local thyroid hormone action in normal and failing human myocardium. With a newly developed multiplex competitive RT-PCR method, we evaluated the expression of thyroid hormone receptor (TR) isoforms alpha-1, alpha-2, and beta-1 in normal human hearts and in end-stage congestive heart failure. A statistically significant difference in the expression of all three TR isoforms was observed among samples from normal subjects, ischemic heart disease (IHD), and dilated cardiomyopathy (DCM). In DCM, compared with normal, the studied TR isoforms were significantly increased. In IHD, the increased expression was found significant only for alpha-1 and alpha-2 isoforms. No differences were observed between the pathologic groups. In conclusion, a coordinated increment in the expression of the TR isoforms was observed in both DCM and IHD by multiplex competitive RT-PCR. The observed changes could represent a compensatory mechanism to myocardial failure or to locally altered thyroid hormone action.
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PMID:Increased expression of thyroid hormone receptor isoforms in end-stage human congestive heart failure. 1160 May 94

Recombinant TSH is effective in providing exogenous TSH stimulation for patients with differentiated thyroid cancer on thyroid hormone-suppressive therapy. It allows for detection of thyroid remnant and metastases by radioiodine scan and by serum thyroglobulin determination. The sensitivity and image quality of the WBS are similar after rTSH and after THSH withdrawal in the majority of patients. The equivalent 100% sensitivity of rTSH- and withdrawal-stimulated serum thyroglobulin measurement alone in identifying patients with radioiodine uptake outside the thyroid bed [38] may eventually lead to more extensive use of serum thyroglobulin testing after rTSH, with more selective application of radioiodine WBS [39]. Currently, a phase IV trial is in progress to evaluate the efficacy of rTSH-stimulated thyroglobulin levels as the primary modality for long-term follow-up of low risk thyroid cancer patients. The use of rTSH prevents the morbidity, metabolic impairment and the risk of tumor progression associated with THST withdrawal, because of shorter exposure time to elevated TSH [38]. Furthermore, it decreases the radiation exposure of healthy tissues due to faster iodine clearance in euthyroidism. rTSH is well tolerated, with transient nausea in 10.5% and headache in 7.3% of patients. No antibodies specific to rTSH were documented, even after multiple courses of the drug. Currently, rTSH is suggested for patients who do not respond to hormone withdrawal or cannot tolerate hypothyroidism. For patients with low risk of tumor recurrence, rTSH-stimulated testing may be used at 6-12 months after postoperative I-131 ablation and with a repeat cycle of rTSH one year later, followed by testing every 3-5 years. In high risk patients, one set of negative I-131 scan and thyroglobulin test results after hormone withdrawal are recommended before using rTSH testing, because of a greater sensitivity of the withdrawal scan and because rTSH is not currently approved for subsequent I-131 therapy often indicated in these patients [24]. Subsequently, two cycles of rTSH testing are recommended at 6-12 month intervals, followed by testing every 1-3 years for at least the first decade after initial diagnosis. The cost of this commercially available form of rTSH has been considered a major impediment to its common use; however, this should be weighed against the loss of productivity of working hours related to withdrawal [40]. In the therapeutic setting, rTSH is the only acceptable option in a subgroup of patients with hypopituitarism, ischemic heart disease, a history of "myxedema madness," debilitation due to advanced disease, or inability to elicit TSH elevation due to continued production of thyroxine by thyroid remnant or metastatic tumor [33,38]. In conclusion, recombinant TSH facilitates the management of patients with differentiated thyroid carcinoma. It increases the sensitivity of thyroglobulin testing during thyroid hormone suppression therapy and enables radioiodine uptake for whole-body scan and occasionally for radioiodine therapy, without the need for prolonged THST withdrawal and its associated hypothyroidism, reduced quality of life and risk of tumor progression.
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PMID:Recombinant thyroid-stimulating hormone in differentiated thyroid cancer. 1172 83

A silent, reversible myocardial ischemia with normal coronary angiography and reversible with thyroid hormone substitution, has been recently described in hypothyroid patients. We report a 49 years old male with an abnormal exercise electrocardiogram detected in a preventive medical examination. He had laboratory evidence of hypothyroidism and a history of two years of asthenia and progressive coarsening of the voice. The Thallium myocardial perfusion study, showed an alteration of coronary flow during exercise in the septum and lower wall of the left ventricle. Thyroid hormone substitution was started and three months later, a coronary angiography was normal. After six months a repeated Thallium perfusion study and exercise electrocardiogram were informed as normal.
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PMID:[Reversible myocardial ischemia in hypothyroidism: Case report]. 1183 86

The Na+/H+ exchanger is a pH regulatory protein with a ubiquitous distribution in eukaryotic cells. Several isoforms of the Na+/H+ exchanger are known. The first isoform to be characterized and cloned, NHE1, is present on the plasma membrane of cells and functions to remove one intracellular proton in exchange for one extracellular sodium ion. It is involved in pH regulation, cell growth, differentiation, and cell migration. NHE1 is also involved in the cycle of damage that occurs in the heart with ischemic heart disease. Recent studies have shown that the Na+/H+ exchanger is regulated in response to thyroid hormone. Reduction in circulating thyroid hormone levels reduces the amount of both protein and mRNA of NHE1. Conversely, an elevation of thyroid hormone levels has the opposite effects. Transcriptional regulation of NHE1 expression has been demonstrated. The NHE1 promoter contains a TR alpha(1) binding site located between -841 to -800 bp. This element responds positively to TR alpha(1). This regulation of the NHE1 promoter by thyroid hormone is proposed to be responsible for postnatal changes in expression of the Na+/H+ exchanger.
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PMID:Regulation of expression of the Na+/H+ exchanger by thyroid hormone. 1519 85

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