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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute heart failure in adults is the unfolding of heart failure in minutes, hours or a few days. Low output heart failure describes a form of heart failure in which the heart pumps blood at a rate at rest or with exertion that is below the physiological range and the metabolizing tissues extract their required oxygen from blood at a lower rate, causing a proportionately smaller oxygen amount remaining in the blood. Therefore, a widened arterial-venous oxygen difference occurs. High output heart failure is characterized by pumping blood with a rate above the physiological range at rest or during exertion, resulting in an arterial-venous oxygen difference, which is normal or low. This may be caused by peripheral vasodilatation during sepsis or thyrotoxicosis, blood shunting, or reduced blood oxygen content/viscosity (Fig. 1). The differentiation between low output heart failure versus high output heart failure is of highest importance for the choice of therapy and therefore the information and the monitoring of the systemic vascular resistance. Patients who present with acute heart failure suffer from a severe complication of different cardiac disorders. Most often they have an acute injury that affects their myocardial performance (eg, myocardial infarction) or valvular/chamber integrity (mitral regurgitation, ventricular septal rupture), which leads to an acute rise in left-ventricular filling pressures resulting in pulmonary edema.
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PMID:New strategies for the management of acute decompensated heart failure. 1135 11

Abnormal liver function in thyroid disorders may be secondary to thyrotoxicosis or to autoimmune injury to the liver. We report the case of a 36-year-old female who developed jaundice and pruritus with mild cholestasis and moderately elevated transaminase levels. The diagnosis of Graves' disease was made shortly thereafter. Laboratory findings were: alanine and aspartate aminotransferase 219 (IU/I (N: 9-50) and 102 IU/I (N: 10-15) respectively, alkaline phosphatase 336 IU/I (N: 40-135), bilirubin 24 micromol/I (N: 2-23), and gamma-glutamyl transpeptidase 232 IU/I (N: 9-43). Abdominal ultrasonography showed normal bile ducts; echocardiography ruled out heart failure; viral and autoimmune markers for hepatitis and cirrhosis were negative. Percutaneous liver biopsy showed moderate intrahepatic steatosis, anisokaryosis, lymphocyte infiltration in the portal areas, and Kupffer cell hyperplasia. Outcome was favorable after seven months of iodine therapy, confirming the diagnosis of thyrotoxicosis hepatitis.
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PMID:[Thyrotoxicosis hepatitis: a case report]. 1145 76

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

In the treatment of the thyrotoxic heart a radical, early thyroeliminating procedure should have preference. As the method of first choice a single administration of a whole calculated dose of I131 is recommended without previous medicamentous preparation up to 25-30 mCie which can be administered also in the out-patient department, with subsequent immediate treatment with thyrostatics and beta-blockers till remission of thyrotoxicosis is achieved (6-12 weeks). Total strumectomy after medicamentous preparation in remission of thyrotoxicosis is preferred in large multinodular, iodinated patients and in solitary toxic adenoma where however also partial STE (lobectomy) is possible and radioiodine is equivalent. Its dosage in toxic adenoma and nodular goitre is however in general higher than in diffuse goitre but the incidence of late postadministration hypothyroidism is lower. Fibrillation arrhythmia usually (in ca 60%) recedes spontaneously with the assistance of beta-blockers in remission of thyrotoxicosis. If this does not occur, pharmacological or electric cardioversion is necessary after anticoagulation preparation, because persistence of FA is an important risk factor of cardiac failure and thromboembolic complications. Eurhythmia then usually lasts as long as remission of thyrotoxicosis persists or there is no overdosage of substitution doses of T4 during treatment of hypothyroidism which develops after thyroelimination treatment. Amiodarone is unsuitable, even contraindicated, for treatment of fibrillation arrhythmia in thyrotoxic heart.
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PMID:[Thyrotoxic heart disease. Part II--aspects of treatment of thyrotoxicosis with cardiac involvement]. 1194 22

Thyroid hormones have been shown to be absolutely necessary for early brain development. During pregnancy, both maternal and foetal thyroid hormones contribute to foetal brain development and maternal supply explains why most of the athyreotic newborns usually do not show any signs of hypothyroidism at birth. Foetal and/or neonatal hypothyroidism is a rare disorder. Its incidence, as indicated by neonatal screening, is about 1:4000. Abnormal thyroid development (i.e. agenesia, ectopic gland, hypoplasia) or inborn errors in thyroid hormone biosynthesis are the most common causes of permanent congenital hypothyroidism. Recent studies reported that mutations involving Thyroid Transcriptor Factors (TTF) such as TTF-1, TTF-2, PAX-8 play an important role in altered foetal thyroid development. Deficiency of transcriptor factor (Pit-1, Prop-1, LHX-3) both in mother and in the foetus represents another rare cause of foetal hypothyroidism. At birth clinical picture may be not always so obvious and typical signs appear only after several weeks but a delayed diagnosis could have severe consequences consisting of delayed physical and mental development. Even if substitutive therapy is promptly started some learning difficulties might still arise suggesting that intrauterine adequate levels of thyroid hormones are absolutely necessary for a normal neurological development. Placental transfer of maternal antithyroid antibodies inhibiting fetal thyroid function can cause transient hypothyroidism at birth. If the mother with thyroid autoimmune disease is also hypothyroid during pregnancy and she doesn't receive substitutive therapy, a worse neurological outcome may be expected for her foetus. Foetal and/or neonatal hyperthyroidism is a rare condition and its incidence has been estimated around 1:4000-40000, according to various authors. The most common causes are maternal thyroid autoimmune disorders, such as Graves' disease and Hashimoto's thyroiditis. Rarer non autoimmune causes recently identified are represented by TSH receptor mutations leading to constitutively activated TSH receptor. Infants born to mothers with Graves' history may develop neonatal thyrotoxicosis. Foetal/neonatal disease is due to transplacental thyrotrophin receptor stimulating antibodies (TRAb) passage. It's extremely important recognizing and treating Graves' disease in mothers as soon as possible, because a thyrotoxic state may have adverse effects on the outcome of pregnancy and both on the foetus and newborn. Thyrotoxic foetuses may develop goitre, tachycardia, hydrops associated with heart failure, growth retardation, craniosynostosis, increased foetal motility and accelerated bone maturation. Neonatal Graves' disease tends to resolve spontaneously within 3-12 weeks as maternal thyroid stimulating immunoglobulins are cleared from the circulation but subsequent development may be impaired by perceptual motor difficulties. Hashimoto's thyroiditis is a very common autoimmune thyroid disease. In presence of maternal Hashimoto's thyroiditis, there are usually no consequences on foetal thyroid, even if antiTPO and antiTg antibodies can be found in the newborn due to transplacental passage. However there are some literature reports describing foetal and neonatal hyperthyroidism in the affected mothers' offspring.
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PMID:Foetal and neonatal thyroid disorders. 1224 77

Thyrotoxicosis is associated with increased cardiovascular morbidity and mortality, primarily due to heart failure and thromboembolism. However, its signs and symptoms may be subtle and can easily be missed. Therefore, one should suspect thyrotoxicosis in patients with palpitations, exercise intolerance, dyspnea on exertion, and other cardiovascular signs.
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PMID:Thyrotoxicosis and the cardiovascular system: subtle but serious effects. 1254 27

The authors report a case of reduction of thyrotoxicosis-related atrial fibrillation by cibenzoline. The initial clinical features of heart failure rapidly resolved and the echocardiographic left ventricular shortening fraction returned to normal. Cibenzoline could be used as antiarrhythmic treatment in atrial fibrillation related to thyrotoxicosis.
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PMID:[Efficacy of cibenzoline in a case of atrial fibrillation due to cardiac thyrotoxicosis]. 1255 35

Amiodarone is an antiarhytmic drug used in many clinical situations for its probed effect; it is also preferred in particular groups of patients (heart failure, post-ischemical) for its safe and its prognostic benefits. However, a substantial proportion of amiodarone treated patients develop either hypothyroidism or thyrotoxicosis. Both abnormalities may occur in apparently normal glands or in glandes with pre-existed abnormalities. It may be difficult to recognize the dysfunction because of the many changes in thyroid function test results that occur in euthyroid patients who are receiving amiodarone. Hypothyroidism is a well defined clinical situation managable thanks to common guidelines. The occurrence of hypothyroidism does not necessitate withdrawing amiodarone while instituting L-T4 replacement therapy, although many cases are transient and will spontaneously remit after amiodarone withdrawal. At the opposite, hyperthyroidism needs more attention to be diagnosed and to be treated, in fact there is a "personal" clinical-therapeutical behave towards it, caused by the lack of big trials made on this clinical situation. Effective strategies exist for the management of thyroid dysfunction, these should be tailored to the needs of the individual patient.
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PMID:[Amiodarone and thyroid dysfunction: a pending problem]. 1465 Aug 17

Besides the typical and in this case severe signs of hyperthyroidism the thyrotoxic crisis is characterized by additional signs and symptoms such as fever, cardiac involvement (tachycardia, arrhythmia, heart failure) and central nervous impairment eventually leading to coma. Additional diseases and comorbidities impair the diagnostic process and may mask the symptoms of thyrotoxicosis. If undiagnosed, this situation harbors a mortality of approximately 90%. The precise knowledge of typical (and atypical) symptoms is mandatory in order to rapidly recognize this situation and to initiate pharmacological treatment and/or surgery. An experienced endocrinologist should always be involved in this decision process.
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PMID:[Thyrotoxic crisis]. 1468 83

A case of neonatal thyrotoxicosis secondary to maternal autoimmune hyperthyroidism is reported in an infant born at 34 weeks gestation who presented with tachycardia, jitteriness, diarrhea, and a small goiter. Propranolol and oxygen were used to treat high-output cardiac failure and transient persistent pulmonary hypertension. The infant's response to propylthiouracil therapy, gradual resolution of cardiac and systemic symptoms, and normaliziation of thyroid studies are described. Thyroid physiology and function and the special considerations in a premature infant are reviewed. An overview of maternal autoimmune hyperthyroidism and the implications for the developing fetus and neonate are presented. The risk factors for, and clinical presentation of, hyperthyroidism are outlined and treatment strategies highlighted. The nursing care of infants with hyperthyroidism is carefully described with an emphasis on the surveillance for and management of multisystem manifestations.
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PMID:A case report of neonatal thyrotoxicosis due to maternal autoimmune hyperthyroidism. 1469 99


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