Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report here a case of a 53-year-old woman with mitochondrial 3243 (A-->G) mutation diabetes. Diabetes mellitus was diagnosed at 39 years of age. At 50 years of age, cardiomyopathy and hypothyroidism were noted. At 53 years of age, the patient was admitted to our hospital for treatment of necrotic ulceration of toes. However, she died of massive heart failure. Pathological examination at autopsy showed a decrease in size, number, and acidophilicity of islets in the pancreas. Immunohistochemical stain revealed a decrease in the beta-cell population to 20.5+/-9.2% and a relative increase in alpha-cell population to 48.6+/-11.5%.
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PMID:Decrease of beta-cells and increase of alpha-cells in a diabetic patient with mitochondrial DNA 3243 (A-->G) mutation. 1471 57

The aim of this study is to clarify the specificities of atrial fibrillation in hyperthyroidism. It's a retrospective study of 6 years, about 14 patients hospitalized for hyperthyroidism with atrial fibrillation. There were 9 Women and 5 men, 55.7 +/- 11.5 years old. Arryhthmia was discovered especially with palpitation and dyspnea. Cardiac echography diagnosed valvular disease in 83.3% of cases. Cardiovascular complications concerned 5 patients and consisted in cardiac insufficiency and cardiomyopathy in one case. Treatment of hyperthyroid consisted in radio-iodine administered to 7 patients at the dose of 9.8 +/- 3.9 mCi. Two patients had total thyroidectomy. Arryhthmia was treated with propranolol, 98.3 +/- 70 mg daily and anticoagulant treatment was given. From the group of nine hyperthyroid recovered patients, arryhthmia was reduced in 3 cases. In this group, age was higher and arryhthmia history was longer. We conclude that chances to treat arryhthmia associated to hyperthyroid are higher when euthyroidism or even hypothyroidism is rapidly obtained, during of atrial evolution is short and some factors aren't present, like aging, existence of valvular disease or left auricular dilatation.
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PMID:[Therapeutic specifics in atrial fibrillation in hyperthyroidism. Study of 14 cases]. 1498 28

Hypothyroidism is common, potentially serious, often clinically overlooked, readily diagnosed by laboratory testing, and eminently treatable. The condition is particularly prevalent in older women, in whom autoimmune thyroiditis is common. Other important causes include congenital thyroid disorders, previous thyroid surgery and irradiation, drugs such as lithium carbonate and amiodarone, and pituitary and hypothalamic disorders. Worldwide, dietary iodine deficiency remains an important cause. Hypothyroidism can present with nonspecific constitutional and neuropsychiatric complaints, or with hypercholesterolaemia, hyponatraemia, hyperprolactinaemia, or hyperhomocysteinaemia. Severe untreated hypothyroidism can lead to heart failure, psychosis, and coma. Although these manifestations are neither specific nor sensitive, the diagnosis is confirmed or excluded by measurements of serum thyrotropin and free thyroxine. Thyroxine replacement therapy is highly effective and safe, but suboptimal dosing is common in clinical practice. Patient noncompliance, drug interactions, and pregnancy can lead to inadequate treatment. Iatrogenic thyrotoxicosis can cause symptoms, and, even when mild, provoke atrial fibrillation and osteoporosis. We summarise present understanding of the history, epidemiology, pathophysiology, and clinical diagnosis and management of hypothyroidism.
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PMID:Hypothyroidism. 1513 22

The abundance of published data on the neonatal effects of maternal Graves' disease (GD) contrasts with the paucity of information on fetal effects. In our yet unpublished study, we prospectively studied 72 pregnant women with a history of Graves' disease. Fetal ultrasonography was done at 22 and 32 weeks of gestational age. Fetal goiter was found at 32 weeks in 11 of the fetuses of the 41 mothers with positive TSH-receptor antibodies and/or antithyroid treatment and in none of the fetuses of the 31 other mothers. In the 11 fetuses with goiter, ultrasound findings (thyroid Doppler and bone maturation), fetal heart rate, and maternal antibody and antithyroid drug status effectively discriminated between hypothyroidism (n=7) and hyperthyroidism (n=4). One fetus with hyperthyroidism died in utero at 35 weeks from heart failure. Treatment was successful in the ten other fetuses. One fetus without goiter had moderate hypothyroidism at birth. This study showed that it is of the utmost importance to have the fetal thyroid scrutinized by an expert ultrasonographist and to have team work with obstetricians and paediatric endocrinologists in pregnant mothers with GD. This allowed us to accurately determine fetal thyroid status and to adapt the treatment in mothers successfully. Fetal hyperthyroidism does exist and needs an appropriate aggressive treatment.
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PMID:Fetal and neonatal thyroid function in relation to maternal Graves' disease. 1515 41

Most patients with dilated cardiomyopathy have a poor prognosis due to progressive and irreversible myocardial dysfunction. Rarely, is a metabolic etiology responsive to specific therapy identified. Although many studies have confirmed that thyroid hormone deficiency is associated with a reversible decrease in myocardial contractility, it has remained controversial whether hypothyroidism alone can cause a dilated cardiomyopathy and clinical heart failure. In this study, we report the case of a patient with severe hypothyroidism and a dilated cardiomyopathy complicated by heart failure, which has receded after recovery to euthyroidism with L-thyroxin therapy. This case suggests that hypothyroidism should be evoked systematically when a dilated cardiomyopathy is diagnosed.
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PMID:[Hypothyroid dilated cardiomyopathy]. 1536 18

In this study three problems concerning interactions between thyroid and cardiovascular system are discussed. Cardiac arrhythmias, congestive heart failure, pleural effusion, hyperlipidaemia, arterial hypertension may be consequences of thyroid disorders leading to inappropriate hormone secretion. During such illnesses as heart failure, myocardial infarction and in patients undergoing coronary artery bypass surgery profound changes may occur in thyroid hormone metabolism known as sick euthyroid syndrome. Treatment with amiodarone may lead to changes in thyroid tests results and to development of hypothyroidism or thyrotoxicosis.
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PMID:[Thyroid and cardiovascular disorders]. 1551 16

Cardiovascular manifestations of thyrotoxicosis and thyroid dysfunction caused by amiodarone. The cardiovascular symptoms of thyrotoxicosis were described more than two hundred years ago and remained the basis of diagnosis in modern medicine. Myocardium, peripheral circulation and sympathetic nerve system, all affecting cardiovascular hemodynamics, are influenced by thyroid hormones in many ways. Sub-clinical hyperthyroidism is characterized by suppressed thyroid stimulating hormone and normal free triiodothyronine and free thyroxine levels. Cardiovascular symptoms: elevation of heart rate, myocardial contractility, stroke volume, myocardial oxygen consumption, systolic blood pressure and reduction in systemic vascular resistance and diastolic blood pressure can be often seen even in case of subclinical hyperthyroidism. Thyrotoxicosis exacerbates the symptoms of a preexisting heart disease, but it can also cause complaints in case of a structurally normal heart. The most common cardiac complications are arrhythmias (mainly atrial fibrillation), heart failure and hypertension. Amiodarone is used for the treatment and prevention of several arrhythmias. It is safely applicable even in case of left ventricular dysfunction. The more common application is limited by its side effects that can develop even at low doses and may involve several organs (thyroid gland, lungs, liver, heart, nerve system among others). The complex effect of amiodarone on thyroid function ranges from mild abnormalities of thyroid function tests to overt thyrotoxicosis or hypothyroidism.
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PMID:[Cardiovascular manifestations of thyrotoxicosis and thyroid dysfunction caused by amiodarone]. 1563 34

Edema develops as one of symptoms and signs in several endocrine disorders, and sometimes can be important clue in detecting the basal endocrine disorder. In patients with long-standing hypothyroidism, characteristic edematous skin changes develop and be called myxedema. In hyperthyroid patients with Graves' disease, peripheral edema sometimes develop with or without heart failure. Severe eyelid puffiness composing Graves' ophthalmopathy and 'circumscribing myxedema', mostly in the pretibial regions, are also highly disease-specific disorders. In Cushing's syndrome, both adrenal and ACTH-dependent, peripheral edema is sometimes important sign leading suspicion of this syndrome. In diabetic patients, attention should be paid to edema constantly especially with nephropathy and hypertension. In diabetic nephropathy stage 3B, aggravation of renal function is often progressive. Recently the range of therapeutic options of glycemic controls has been extended with introduction of thiazolidinediones (TZDs). Weight gain and peripheral edema are recognized side effects of these drugs, particularly when used in combination with insulin. The potential risk of worsened heart failure should be taken into consideration when TZDs are used in patients with diabetes and heart diseases.
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PMID:[Edema in endocrine and metabolic diseases]. 1567 23

Growing evidence suggests that thyroid dysfunction may contribute to progression of cardiac disease to heart failure. We investigated the effects of a therapeutic dose of thyroid hormones (TH) on cardiomyopathic (CM) hamsters from 4 to 6 mo of age. CM hamsters had subclinical hypothyroidism (normal thyroxine, elevated TSH). Left ventricular (LV) function was determined by echocardiography and hemodynamics. Whole tissue pathology and isolated myocyte size and number were assessed. TH treatment prevented the decline in heart rate and rate of LV pressure increase and improved LV ejection fraction. The percentage of fibrosis/necrosis in untreated 4-mo-old CM (4CM; 15.5 +/- 2.2%) and 6-mo-old CM (6CM; 21.5 +/- 2.4%) hamsters was pronounced and was reversed in treated CM (TCM; 11.9 +/- 0.9%) hamsters. Total ventricular myocyte number was the same between 4- and 6-mo-old controls but was reduced by 30% in 4CM and 43% in 6CM hamsters. TH treatment completely prevented further loss of myocytes in TCM hamsters. Compared with age-matched controls, resting and maximum coronary blood flow was impaired in 4CM and 6CM hamsters. Blood flow was completely normalized by TH treatment. We conclude that TH treatment of CM hamsters with subclinical hypothyroidism normalized impaired coronary blood flow, which prevented the decline in LV function and loss of myocytes.
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PMID:Treatment of subclinical hypothyroidism reverses ischemia and prevents myocyte loss and progressive LV dysfunction in hamsters with dilated cardiomyopathy. 1602 68

Cholesterol pericarditis is an uncommon form of pericardial disease, of unknown pathophysiology, that is characterized by chronic relapsing, usually large, pericardial effusions that are distinctive due to a high level of cholesterol. Usually it is idiopathic, but it can be associated with various systemic diseases such as hypothyroidism, rheumatoid arthritis and tuberculosis, among others. Its clinical course is usually indolent and complications such as cardiac tamponade and chronic constrictive pericarditis are relatively rare. However, the need for surgery for complete treatment has been reported in at least 10 % of cases. When rheumatoid arthritis is the underlying cause, this outcome is more frequent among those with an acute episode of pericarditis during the course of the disease. We report the case of a 61-year-old female rheumatoid arthritis patient, who presented with heart failure due to a large pericardial effusion and was successfully treated by a surgical approach.
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PMID:Cholesterol pericarditis--relapsing pericardial effusion in a patient with rheumatoid arthritis. 1604 69


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