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Query: UMLS:C0018799 (heart disease)
34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biondi, Fazio, and colleagues recently reported that long term T4 treatment to suppress serum TSH markedly affects cardiac function. T4-treated patients had more symptoms [12.2 +/- 3.9 (+/-SD) vs. 4.2 +/- 2.3 by quantitative questionnaire], higher mean heart rate, increased incidence of atrial extrasystoles, increased interventricular septal thickness and left ventricular mass index (LVMi), and significant diastolic dysfunction. The severity of cardiac abnormalities was highly correlated with scores of a rating scale used for assessing symptoms of thyrotoxicosis. We have duplicated their studies in 17 athyreotic patients (mean age, 45 +/- 10 yr; range, 27-63 yr) without heart disease or hypertension whose dose of T4 was titrated to suppress serum TSH to less than 0.01 microU/mL. The mean duration of T4 treatment was 9.2 +/- 5.4 yr. Controls were healthy volunteers matched for sex and age (+/-3 yr). The mean T4 dose was 2.8 +/- 0.9 micrograms/kg (0.192 +/- 0.058 mg/day). By questionnaire, patients had minimal symptoms, although their symptom score was significantly greater than the control value (4 +/- 3 vs. 2 +/- 1; P < 0.05; maximum score, 36). No differences in mean heart rate or in atrial or ventricular extrasystoles were noted. In patients, indexes of systolic and diastolic function and interventricular septal thickness were similar to control values. The mean LVMi was normal in both groups. However, the mean LVMi in patients (117 +/- 35 g/m2) was higher than that in controls (92 +/- 31; P < 0.05). In conclusion, patients were minimally affected by TSH-suppressive doses of T4. They had few symptoms and no increase in extrasystoles or basal heart rate. Based on current knowledge, the increase in LVMi observed in patients without associated significant systolic or diastolic abnormalities does not have clinical or prognostic importance. Therefore, in the absence of symptoms of thyrotoxicosis, patients treated with TSH-suppressive doses of L-T4 may be followed clinically without specific cardiac laboratory studies.
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PMID:Minimal cardiac effects in asymptomatic athyreotic patients chronically treated with thyrotropin-suppressive doses of L-thyroxine. 966 56

The adverse health effects of thyrotoxicosis have been carefully documented and most practitioners are familiar with the clinical consequences for the patient. Until recently, many patients experienced the adverse effects of excessive thyroxine dosages. Which can now be avoided by the application of highly sensitive immunometric assays for monitoring serum thyrotrophin (thyroid-stimulating hormone; TSH) levels. However, sensitive monitoring of serum thyrotrophin levels has led to the frequent recognition of biochemical subclinical hyperthyroidism (isolated suppression of thyrotrophin). Because of the increased recognition of this condition, the adverse effects of thyroxine therapy can be divided into those associated with subclinical hyperthyroidism and those associated with the euthyroid state. Investigation of the potential clinical consequences of thyrotrophin-suppressing dosages of thyroxine has dominated studies over the last decade, with less attention being given to euthyroid patients. It appears that the adverse effects of thyroxine are considerably more common when serum thyrotrophin has been suppressed. They are usually manifested in older patients as increased bone mineral loss in postmenopausal women and as cardiac effects in patients with intrinsic heart disease. These patients may have subtle behavioural alterations and other clinically silent organ effects that occur infrequently. Children who are euthyroid while taking thyroxine occasionally develop pseudotumour cerebri shortly after starting hormone replacement for hypothyroidism. Otherwise, thyroxine dosages that render patients euthyroid, as evidenced by thyrotrophin values that are within the normal range, rarely cause adverse effects. Thus, avoidance of dosages that cause thyrotrophin suppression, when not clinically indicated, is the primary approach to the management of these adverse effects.
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PMID:Adverse effects of thyroid hormones. 941 3

We have critically reviewed the available information on iodine-induced hyperthyroidism (IIH) from published sources and other reports as well as the experience of the authors in Tasmania, Zaire, Zimbabwe, and Brazil. Administration of iodine in almost any chemical form may induce an episode of thyrotoxicosis (IIH). This has been observed in epidemic incidence in several countries when iodine has been given as prophylaxis in a variety of vehicles, but the attack rate as recorded has been low. IIH is most commonly encountered in older persons with long standing nodular goiter and in regions of chronic iodine deficiency, but instances in the young have been recorded. It customarily occurs after an incremental rise in mean iodine intake in the course of programs for the prevention of iodine deficiency, or when iodine-containing drugs such as radiocontrast media or amiodarone are administered. The biological basis for IIH appears most often to be mutational events in thyroid cells that lead to autonomy of function. When the mass of cells with such an event becomes sufficient and iodine supply is increased, the subject may become thyrotoxic. These changes may occur in localized foci within the gland or in the process of nodule formation. IIH may also occur with an increase in iodine intake in those whose hyperthyroidism (Graves' disease) is not expressed because of iodine deficiency. The risks of IIH are principally to the elderly who may have heart disease, and to those who live in regions where there is limited access to medical care. More information is needed on the long-term health impact of IIH or "subclinical" IIH, especially in the course of prophylaxis programs with iodized salt or iodinated oil in regions where access to health care is limited.
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PMID:Iodine-induced hyperthyroidism: occurrence and epidemiology. 949 58

The importance of cardiovascular system involvement in hyperthyroidism has been recognized for many years. In the elderly patient, often with mild but prolonged elevation of plasma thyroid hormones, symptoms and signs of heart failure and complicating atrial fibrillation (AF) may dominate the clinical picture and mask the more classic endocrine manifestations of the disease. Impaired cardiopulmonary function and exercise capacity, significantly more marked in older patients, is observed in hyperthyroidism. Thyrotoxicosis can aggravate pre-existing heart disease and can also lead to AF, congestive heart failure, or worsening of angina pectoris. Regarding the high incidence of AF in older patients with hyperthyroidism, it is also important to detect subclinical hyperthyroidism in older patients with AF, thus warranting the measurement of the serum thyrotropin (TSH) concentration for early recognition and treatment. Most cardiac abnormalities return to normal once a euthyroid state has been achieved, although AF may persist in a minority. Optimal treatment requires rapid and definitive antithyroid therapy. Furthermore, anticoagulation is recommended for thyrotoxic patients with AF older than 50 years, those who have histories of previous emboli, hypertension, or with echocardiographic evidence of left atrial enlargement and/or myxomatous valves.
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PMID:Cardiac risks of hyperthyroidism in the elderly. 992 Mar 73

Authors report about a left ventricular thrombus as a complication of thyrotoxic heart disease, on a 45 years old woman. Clinical state featured signs of thyrotoxicosis, global cardiac failure and hypertension. The electrocardiogram showed a left axis deviation, the chest X-ray a cardiac enlargement (cardio-thoracic index = 0.55) on behalf of left movement of heart walls and severe left ventricule dysfunction (Ejection fraction about 18%). This exam also found a big thrombus at he left ventricule apex. The treatment disappearance of the thrombosis and improvement of cardiac failure signs and echographic parameters. Authors discuss circumstances leading to thrombosis in thyrotoxic heart disease, and the usefulness of anticoagulant drug therapy.
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PMID:[Cardiac thyrotoxicosis and left ventricular thrombosis, a case report]. 1079 74

We report a case of reversible, dilated cardiomyopathy due to thyrotoxicosis, which occurred in a young male without any underlying heart disease. The patient presented a clinical picture of cardiogenic shock related to severe left ventricular dilation and dysfunction and with new-onset atrial fibrillation and very high ventricular rate. In spite of vigorous medical therapy, there was only a mild improvement of clinical and hemodynamic status and ventricular rate persisted inappropriately elevated. Subsequently, laboratory test results allowed for recognition of thyrotoxicosis (secondary to Graves's disease) and then specific thyrostatic treatment was added. There was a prompt clinical improvement and parallel, progressive reversal of left ventricular dysfunction. The patient could be converted to normal sinus rhythm and one week later was discharged in good condition. We discuss the pathophysiological mechanism for the induction of this rare form of thyrotoxic cardiomyopathy and emphasize that awareness of this possible presentation of hyperthyroidism is essential to identify patients with potentially reversible dilated cardiomyopathy.
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PMID:[Dilated thyrotoxic cardiomyopathy]. 1093 39

The RTH syndrome is an instructive example of a receptor resistance syndrome. A typical case history is reported here. The patient had had symptoms for many years and was first diagnosed as having inappropriate secretion of TSH. Pituitary tumour was excluded. The primary symptom was palpitations and the patient was partially thyroidectomized many years ago on suspicion of thyrotoxicosis. She was then given substitutional Eltroxin, but, because of palpitations, the dose was reduced to almost zero, after which the patient contracted symptoms suggesting myxoedema. The thyroid values could not be used for clinical assessment, however the symptoms of myxoedema disappeared when the Eltroxin dose was increased to 75 micrograms/day. When the dose was increased further the heart symptoms became too troublesome. The patient had no signs of underlying heart disease.
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PMID:[RTH syndrome--resistance to thyroid hormone syndrome]. 1157 81

Thyroid hormone has effects on both the peripheral circulation and the myocardium. These include a decline in the systemic vascular resistance and an increase in cardiac output and cardiac contractility. Exposure to excess thyroid hormone, as occurs in thyrotoxicosis, can not only aggravate preexisting cardiac disease but also by itself lead to cardiac disease. More patients are being reported with thyrotoxicosis in Nigeria while the facilities for diagnosis and treatment are improving and becoming more available. There should therefore be a greater awareness of the cardiac problems associated with thyrotoxicosis, especially atrial fibrillation and cardiac failure. Initial management of heart disease in thyrotoxicosis should focus on the prompt alleviation of hyperthyroidism combined with judicious use of diuretics, digoxin and beta-blockers.
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PMID:Thyrotoxicosis and the heart--a review of the literature. 1170 57

Atrial fibrillation (AF) is a common clinical problem, particularly in the elderly, and in patients with organic heart disease. A small percentage of patients, have a potentially reversible cause. Atrial fibrillation is in most patients (approximately 70%) associated with chronic organic heart disease including valvular heart disease, coronary artery disease, hypertension, particularly if left ventricular hypertrophy is present, hypertrophic cardiomyopathy, dilated cardiomyopathy and congenital heart disease and most commonly in adults, atrial septal defect. As in many chronic conditions, determining whether AF is the result or is unrelated to the underlying heart disease, remains unclear. The list of possible etiologies also include cardiac amyloidosis, hemochromatosis and endomyocardial fibrosis. Other heart diseases, such as mitral valve prolapse (with or without mitral regurgitation), calcification of the mitral annulus, atrial myxoma, pheochomocytoma and idiopathic dilated right atrium, present a higher incidence of AF. The relationship between these findings and the arrhythmia are still unclear. Atrial fibrillation may occur in the absence of detectable organic heart disease, the so-called "lone AF", in about 30% of cases. The term "lone AF" or "idiopathic AF" implies the absence of any detectable etiology including hyperthyroidism, chronic obstructive lung disease, overt sinus node dysfunction, and overt or concealed preexcitation (Wolf-Parkinson-White syndrome), only to mention a few of other rare causes of AF. In every instance of recently discovered AF, thyrotoxicosis should be ruled out. The autonomous nervous system may contribute to the occurrence of AF in some patients. Atrial fibrillation occurs commonly in patients with valvular heart disease, particularly when it involves the mitral valve. The occurrence of AF is unrelated to the severity of mitral stenosis but is more common in patients with enlarged left atrium and congestive heart failure. In patients with coronary artery disease, Af occurs predominantly in older patients, males and patients with left ventricular dysfunction. Important predictive factors of AF include hypertension, left ventricular hypertrophy and diabetes. However, the relation between AF and hypertension remains unclear. The risk of the development of AF, in an individual patient, is often difficult to assess but increasing age, presence of valvular heart disease and congestive heart failure, increase the risk of AF.
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PMID:Atrial fibrillation, the arrhythmia of the elderly, causes and associated conditions. 1210 96

This is a descriptive and follow-up study of the efficacy of radioiodine (131I) in the treatment of hyperthyroidism in Nigerian patients, and is aimed at creating awareness about the therapy amongst medical practitioners in the West African sub-region. Twenty-two patients (13 female, 9 males) were seen with clinical and biochemical features of thyrotoxicosis, and were treated with 131I between 1991 and 1999. The age range was 31 to 60 years, with a mean age of 44.2 +/- 1.8 years. The indications for 131I therapy were diverse and included its use as a first-line treatment for Graves' disease, thyrotoxic heart disease, recurrent thyrotoxicosis and failed antithyroid drug therapy. An incremental fixed-dose regimen was used in successive years, for different batches of patients. The duration of follow-up ranged from two months to nine years with a mean duration of 3.6 +/- 0.5 years. Three patients achieved euthyroidism, two patients needed a re-treatment with 131I because of persistent Hyperthyroidism. Nine patients developed hypothyroidism between two to 30 months of receiving 131I therapy. While seven other patients defaulted soon after the treatment and one patient who also had type 1 diabetes mellitus suffered a sudden death after two months. In conclusion, our experience revealed similar outcomes as have been reported by other workers. Radioactive iodine was found to be a safe and an effective treatment for hyperthyroidism in Nigerian patients, but a high rate of default precludes adequate long-term follow-up.
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PMID:Experience in the use of radioactive iodine therapy for hyperthyroidism in Nigerian patients. A study of twenty-two patients. 1500 98


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