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

Hyperthyroidism and hypothyroidism are common disorders in the elderly and may remain unrecognised until a patient presents with an apparently unrelated problem. The finding of an elevated level of thyroid stimulating hormone (TSH) with a normal serum thyroxine (T4) level represents "subclinical hypothyroidism", which does not necessarily require treatment. Iodine can precipitate hyperthyroidism in patients with autonomous thyroid tissue and the iodine-rich antiarrhythmic agent, amiodarone, may cause either hyperthyroidism or hypothyroidism. The metabolism and clearance of numerous therapeutic agents is altered when thyroid status is abnormal, so that dose adjustment may be necessary. In cardiac failure secondary to hyperthyroidism, great care must be taken in prescribing beta-blockers and diuretics; dosage of digitalis preparations may need to be increased. Thyroid replacement therapy can aggravate myocardial ischaemia and it may be appropriate to consider coronary artery bypass grafting before hypothyroidism is fully corrected. Antithyroid drugs, surgery and radioactive iodine all have a place in the treatment of hyperthyroidism in the elderly, depending on factors such as disease severity and the characteristics of the goitre. T4 may be given together with an antithyroid drug in a "block-replace" regimen.
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PMID:Thyroid disease. 834 Nov 92

Screening for congenital hypothyroidism was carried out by measuring thyroid stimulating hormone (TSH) on dried blood spots (mean + 2SD cut off value 12 microU/ml) by fluoroimmunoassay using DELFIA kits. A total of 20,021 infants were screened, and seven cases with congenital hypothyroidism were detected, giving an incidence of congenital hypothyroidism of 1:2860 (female:male ratio 6:1). In four of seven infants with congenital hypothyroidism (57%) the mother also had thyroid disease, supporting the importance of genetic factors as a cause of congenital hypothyroidism. Transient hyperthyrotropinaemia occurred in 654 infants (recall rate 3.3%). There was a significant association of transient hyperthyrotropinaemia only with cardiac failure at birth or caesarean section (p < 0.01). Family studies showed no predisposition to thyroid diseases associated with a transient increase of TSH.
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PMID:Neonatal screening for congenital hypothyroidism in Estonia. 957 54

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

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

A case of fetal goitrous hypothyroidism associated with high-output cardiac failure is presented. At 32 weeks of gestation, the antenatal diagnosis of goiter was made based on ultrasound examination, and the fetal thyroid function was examined by amniocentesis and cordocentesis. Color and pulsed Doppler examinations demonstrated a high vascular flow pattern in the goiter and marked elevation of the maximum velocity in the common carotid artery at the level of the neck. It was suspected that arteriovenous shunting through the large goiter resulted in high-output cardiac failure with cardiomegaly and pleural effusion. The fetus was treated by injection of levothyroxine sodium into the amniotic fluid at 33 weeks of gestation and the goiter thereafter decreased in size, with subsequent improvement of the high-output cardiac failure. The maximum velocity in the common carotid artery fell rapidly before the shrinkage of the fetal goiter and in parallel with the fetal level of thyroid stimulating hormone.
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PMID:Antenatal diagnosis and treatment of a case of fetal goitrous hypothyroidism associated with high-output cardiac failure. 1198 87

Brain natriuretic peptide (BNP) is a powerful neurohormonal marker of left ventricular function and prognosis. Amiodarone either has no effect or improves the haemodynamics in patients with left ventricular dysfunction, but its effect on BNP is unknown. This study evaluated the effect of amiodarone on plasma BNP level in patients with heart failure and ventricular tachyarrhythmia. Plasma BNP level was studied in 46 patients with heart failure ventricular tachyarrhythmia, before (baseline) and at week 2 and months 1, 3 and 6 of amiodarone treatment. In addition, 21 patients with heart failure and ventricular tachyarrhythmia, who received an implantable cardioverter defibrillator, but not amiodarone, were studied on the same schedule. All patients had previously received potent vasodilator and beta-blocker therapy. Echocardiography and Holter monitoring were also performed. Amiodarone significantly decreased plasma BNP levels at week 2 to month 6 during therapy. Heart rates and frequencies of premature ventricular complexes were markedly reduced by amiodarone. Echocardiographic findings did not show a change in left ventricular end-diastolic dimensions, despite a slight increase in fraction shortening at month 6 during amiodarone therapy. The above parameters showed no change in patients without amiodarone. The effect of heart rate, premature ventricular complexes, fraction shortening, serum creatinine or thyroid stimulating hormone level was not significantly associated with decrease in BNP level during amiodarone therapy by a multivariate analysis. Among amiodarone-treated patients, mortality was higher in 24 with BNP levels >/=100 pg/ml at month 6 than in 22 with BNP levels <100 pg/ml during a mean follow-up period of 31 months. Amiodarone appears to have a decreasing effect on plasma BNP level, as well as an antiarrhythmic effect, in patients with heart failure and ventricular tachyarrhythmia.
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PMID:Amiodarone decreases plasma brain natriuretic peptide level in patients with heart failure and ventricular tachyarrhythmia. 1461 94

The derangement of neuro-endocrine control of circulation influences both disease evolution and response to treatment in patients with heart failure, but little data are available about the complex relationships between the degree of neuro-hormonal activation and clinical severity. We studied the relationships between cardiac natriuretic hormones (CNHs) and several neuro-hormones and immunological markers in a prospective cohort of 105 consecutive patients with cardiomyopathy (77 men and 28 women, mean age 66.7+/-12.4 years, range 33-89 years). We assayed the circulating levels of CNHs (atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)), plasma renin activity (PRA), aldosterone, cortisol, adrenaline, noradrenaline, thyroid hormones and thyroid stimulating hormone (TSH), tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). The concentrations of all CNHs and neurohormones were higher in patients with heart failure compared to normal subjects, except for free triiodothyronine (FT3), which was below normal values. ANP was positively related to NYHA class, IL-6, adrenaline, noradrenaline and cortisol, while negatively with ejection fraction and FT3. BNP was positively related to age, NYHA class, IL-6, TNF-alpha, adrenaline, noradrenaline and cortisol, while negatively with ejection fraction and FT3. A stepwise multiple linear regression indicated that plasma ANP depended only on ejection fraction, adrenaline and noradrenaline values, while for plasma BNP variation NYHA class contributed too. Our data confirm a progressive activation of hormonal and immunological systems in patients with heart failure. Furthermore, CNH circulating levels in heart failure are affected not only by cardiac function and disease severity, but also by activation of neuro-hormonal and stress-related cytokine systems, as well as by the thyroid hormones, even on usual medical treatment.
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PMID:Cardiac natriuretic hormones, neuro-hormones, thyroid hormones and cytokines in normal subjects and patients with heart failure. 1525 79

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

A 60-year-old woman was admitted to a hospital complaining of dizziness and general fatigue in October, 2004. Because of heart failure and severe anemia, she was referred to our hospital. Based on a positive direct Coombs test and an elevated level of platelet-associated IgG (PAIgG), the patient was diagnosed as having autoimmune hemolytic anemia (AIHA) associated with idiopathic thrombocytopenic purpura (ITP), i.e., Evans syndrome. Basedow disease was also diagnosed due to hyperthyroidism with an elevation of anti-thyroid stimulating hormone (TSH) receptor antibodies. Both the Evans syndrome and Basedow disease were considerably ameliorated with plasma exchange, corticosteroid and thiamazole therapy. Although Basedow disease is known to be associated with hematological disorders such as AIHA or ITP, the combination of Basedow disease and Evans syndrome is rare. We report here a case of Basedow disease associated with Evans syndrome.
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PMID:[Basedow disease associated with Evans syndrome]. 1644 Jul 74

Hyperthyroidism occurs in approximately 1 in every 1000 to 2000 pregnancies. Although the signs and symptoms of the disease are similar in the pregnant and nonpregnant patient, the complications of hyperthyroidism can have even more profound consequences for the mother and fetus during gestation. These include maternal heart failure, preeclampsia, miscarriage, and preterm labor; as well as fetal loss and low birth weight. Furthermore, thyroid function and laboratory testing for hyperthyroidism are altered in pregnancy. The gestational increase in thyroid size, increased thyroid-binding globulin levels, increased serum total T4 and total T3 levels, and decreased thyroid stimulating hormone levels often confuses the evaluation of the thyroid status in pregnancy. Worldwide, the thionamides-propylthiouracil, methimazole, and carbimazole-have been used in pregnancy for the treatment of hyperthyroidism. However, propylthiouracil has been the drug of choice in the United States because it is believed to have less potential to induce fetal/neonatal hypothyrodism, to cross the placenta and into breast milk to a lesser degree, and to be less teratogenic than methimazole or carbimazole. None of the above have been substantiated in more recent studies. The pharmacokinetics of the thionamides in the pregnant and nonpregnant states, as well as the pharmacotherapeutic recommendation for hyperthyroidism will be reviewed.
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PMID:Pharmacokinetics and pharmacotherapy of thionamides in pregnancy. 1688 14


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