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

Cardiovascular disorders in patients affected with hyperthyroidism are very common; the increase in the heart rate and in inotropism combines with a rise in the cardiac index towards which the reduction in peripheral resistances and an increase in the venous return to the heart contribute. The increase in myocardial excitabi1ity, caused above all by triiodothyronine, may be attended with atrial extrasystoles or even with atrial fibrillation. Congestive heart failure during hyperthyroidism, even if rare, may either reveal itself in association with pre-existent cardiopathy or to be precipitated by tachyar-rhythrmia, particu1arly, by paroxysmal atrial fibrillation. The case is described of a young woman affected with Graves' disease, presenting an ingravescent dyspnoea, in which sinusal tachycardia, the S1Q3 electrocardiographic figure and the echocardiographic reports of a right ventricu1ar overload with pulmonary hypertension and systemic venous congestion, suggest picture of acute pulmonary embolism. The isolated dysfunction of the right ventricle resolved quickly after an adequate antithyroid therapy. The oddness of presentation of Graves' disease in this case would suggest the execution of the thyroid profile for all patients with a primary diagnosis of heart failure, in order to single out hyperthyroid subjects with reversible myocardial dysfunction.
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PMID:[Right ventricular heart failure in hyperthyroidism]. 1153 53

A 42-year-old man and a 31-year-old man with congestive heart failure caused by the thyroid stimulating hormone(TSH) secreting pituitary adenoma were reported. Heart failure was improved after transsphenoidal resection of the pituitary adenoma in each patient. The syndrome of inappropriate secretion of TSH causes hyperthyroidism. Thyroid hormone acts directly on cardiac muscle to increase the stroke volume. Hyperthyroidism itself reduces the peripheral vascular resistance and an elevated basal metabolism which is the basic physiologic change in hyperthyroidism dilates small vessels and reduces vascular resistance. The reduced vascular resistance contributes to increase stroke volume. Thyroid hormone also acts directly on the cardiac pacemakers to be apt to cause tachycardiac atrial fibrillation. These mechanical changes in hyperthyroidism increase not only the cardiac output but also the venous return. The increased blood volume and the shortened ventricular filling time due to tachycardia result in congestive heart failure. TSH secreting pituitary adenoma is a rare tumor, however heart failure is common disease. TSH secreting pituitary adenoma should be taken into consideration in patients with heart failure. The presented cases were very enlightening to understand the relation between brain tumor and heart disease.
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PMID:[Congestive heart failure caused by the thyroid stimulating hormone(TSH) secreting pituitary adenoma: report of two cases]. 1157 21

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

FROM A CLINICAL POINT OF VIEW: Diagnosis of dysthyroidism in the elderly is particularly difficult because of the lack of sensitivity and specificity of classical symptoms and examinations. Neuro-mental and cardiovascular signs are frequent: dysthyroidism should always be searched for in the presence of dementia, depressive syndrome, heart failure or tachyarrhythmia. BIOLOGICAL DATA: Simple screening must therefore be widely proposed and relies on complete thyroid stimulating hormone (TSH) assay, further completed by free thyroid hormone assay. Biological diagnosis is easy in the healthy elderly patient, but interpretation of the assays is delicate in the case of intercurrent diseases or treatment with amiodarone. THE CAUSES TO BE LOOKED FOR: The detection of hypothyroidism does not require etiological exploration, other than the search for iodine overload. In cases of hyperthyroidism, scanning usually reveals a nodular goitre. THERAPEUTIC REGIMENS: In most cases treatment is simple. Replacement therapy is used for hypothyroidism. Patience and cardiovascular monitoring are essential. In the absence of iodine overload or compressive goitre, radioactive iodine is the treatment of choice. These simple treatments avoid the loss of physical and mental autonomy and cardiovascular complications. The importance of screening of these so-called "profitable" diseases in the elderly is obvious.
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PMID:[Dysthyroidism in elderly patients. Clinical characteristics]. 1181 26

The most striking clinical effects of hyperthyroidism are on the heart. These effects concern both heart rate and function. The increased contractility is mainly based on the indirect inotropic effect of peripheral vasodilation as a consequence of hyperthyroidism. Although contractility at rest is enhanced in hyperthyroidism, cardiac reserve is decreased due to diminished chronotropic, inotropic and vasodilatory reserve. In hyperthyroid patients, the clinical impression is often that of a hyperadrenergic circulation. However, the sensitivity of the heart for catecholamines is not increased. The diminution of palpitations by beta-adrenergic blockers in hyperthyroid patients is due to both a decrease in heart rate and atrial extrasystoles, and is not the consequence of a normalisation of cardiac contractility. Heart failure is almost exclusively found in patients with pre-existing cardiac disease. In the case of serious heart failure a rapid reduction of circulating thyroid hormone by means of thyreostatics is important as well. There is no consensus as to whether patients with thyrotoxic atrial fibrillation should be treated with oral anticoagulants. However, most experts recommend oral anticoagulants for elderly patients (> 60 years) or patients with additional risk factors for embolism.
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PMID:[Cardiovascular effects of hyperthyroidism and their treatment]. 1213 47

Atrial fibrillation is often induced in patients with hyperthyroidism and may trigger heart failure. Its prevalence and outcome were examined to obtain up-to-date information. Persistent atrial fibrillation was observed in approximately 1.7% of new hyperthyroid patients. It occurs more frequently in males (2.86%) than in females (1.36%), even though the number of male hyperthyroid patients is only one fifth of female patients. The rate increased with age, being 8% in the patients older than 70 years old. The initial treatment is to control the heart rate with routine pharmacologic therapy and to start antithyroid therapy as quickly as possible. Attempted cardioversion should be deferred until approximately the fourth month of maintaining a euthyroid state, because more than 56% of atrial fibrillation spontaneously reverts to sinus rhythm when the thyroid hormone levels start to decline. Elective cardioversion for those whose atrial fibrillation persists is highly effective and sinus rhythm maintenance rates were 56.7% and 47.6% at the 10th and the 14th year, respectively, even though the duration of atrial fibrillation prior to cardioversion was extremely long (35.0 +/- 29.0 months).
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PMID:Hyperthyroidism and the management of atrial fibrillation. 1216 11

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

We report a case of a fifty year old woman with Graves' disease with positive AntiTPO antibodies and positive AntiTSH receptor antibodies, who was hospitalized with a right cardiac failure. A pulmonary hypertension was discovered on echocardiography. After adequate antithyroid therapy, the right cardiac failure regressed rapidly and pulmonary pressure normalised. An autoimmune process has often been proposed to explain the association between pulmonary hypertension and hyperthyroidism. We report the arguments supporting this autoimmune etiopathogenesis. We also discuss an other hypothesis based on a direct effect of thyroid hormones on the pulmonary circulation and the effects of high cardiac output associated with hyperthyroidism.
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PMID:[Primary pulmonary hypertension arterial and Basedow disease]. 1252 39

We report the case of a 48-year-old woman with a diagnosis of pulmonary hypertension and hyperthyroidism (Graves' disease) in whom pulmonary artery pressures became normal after treatment of thyroid disease. The possible pathogenic mechanisms involved in this association include the presence of hyperdynamic heart failure and/or the presence of immune alterations underlying both conditions.
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PMID:[Reference figures for pulmonary artery pressures after effective treatment of Graves' disease]. 1255 20

Spontaneously hypertensive heart failure (SHHF) rats develop hypertension and heart failure. We hypothesized that induction of hyperthyroidism should accelerate development of heart failure in male SHHF rats. Male and female SHHF rats received diets containing desiccated thyroid glands (DTG) or a control diet for 8 wk. Male and female Wistar-Kyoto rats were used as normotensive controls. DTG treatment reduced body weight in male, but not female, SHHF rats but increased body temperature and heart weight-to-body weight ratio in both genders. In DTG-treated male SHHF rats, serum triiodothyronine levels doubled relative to SHHF controls, whereas O2 consumption increased in DTG-treated SHHF rats. Frequency of breathing in air increased in DTG-treated female rats, and ventilation increased in DTG-treated male rats. Ventilatory equivalents exhibited gender differences in SHHF rats, were decreased in both genders by DTG treatment, and reached levels similar to those of Wistar-Kyoto rats. DTG increased heart rate, right ventricular pressure, and contractility in both genders and increased left ventricular pressure in SHHF male rats. These results refute our hypothesis and suggest that cardiopulmonary function of SHHF male rats may be improved by DTG treatment.
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PMID:Gender-specific effects of thyroid hormones on cardiopulmonary function in SHHF rats. 1290 10


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