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

The courses of two neonates treated with intravenous amiodarone for supraventricular tachyarrhythmia, both of whom developed significant adverse effects, are reported. A 13-day-old term newborn developed hypothyroidism after 27 days of mostly intravenous amiodarone for atrioventricular reciprocating tachycardia and severe heart failure. A one-day-old, 36 weeks' gestation newborn developed electromechanical dissociation after receiving an intravenous bolus of amiodarone for rapid atrial flutter. Judicious use of amiodarone is recommended.
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PMID:Risks of intravenous amiodarone in neonates. 967 71

Primary pulmonary hypertension (PPH) is a pulmonary vascular disease characterized by an elevation in mean pulmonary artery pressure and pulmonary vascular resistance. Recently, PPH gained national attention because of its association with appetite suppressants. PPH may also be associated with pregnancy, hypothyroidism, autoimmune disorders, human immunodeficiency virus infection, and the use of drugs such as oral contraceptives and cocaine. Patients with PPH may report dyspnea on exertion and fatigue. Early diagnosis is crucial. New therapeutic regimens have dramatically reduced mortality rates and improved quality of life by halting the progression of pulmonary vascular remodeling and averting right-sided heart failure. These therapies include high-dose calcium channel antagonists, anticoagulants, and continuous intravenous prostacyclin. Lung or heart-lung transplantation remains a viable therapeutic option for patients who are treated late in the disease process, who are not responsive to medical management, or who remain symptomatic and continue to deteriorate.
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PMID:Diagnosing and treating primary pulmonary hypertension. 1050 69

Thyroid hormone deficiency has profound effects on the cardiovascular system, resulting in decreased cardiac contractility, adrenergic responsiveness, and vascular volume and increased peripheral vascular resistance. To determine the importance of direct cardiac effects in the genesis of hypothyroid cardiac dysfunction, the cardiac myocyte was specifically targeted with a mutant thyroid hormone receptor (TR)-beta (Delta337T-TR-beta(1)) driven by the alpha-myosin heavy chain (alpha-MHC) gene promoter. As a control in these experiments, a wild-type (Wt) TR-beta(1) was also targeted to the heart by using the same promoter. Transgenic mice expressing the mutant TR displayed an mRNA expression pattern consistent with cardiac hypothyroidism, even though their peripheral thyroid hormone levels were normal. When these animals were rendered hypothyroid or thyrotoxic, mRNA expression of MHC isoforms remained unchanged in the hearts of the Delta337T transgenic animals, in contrast to Wt controls or transgenic animals expressing Wt TR-beta(1), which exhibited the expected changes in steady-state MHC mRNA levels. Studies in Langendorff heart preparations from mutant TR-beta(1) transgenic animals revealed evidence of heart failure with a significant reduction in +dP/dT, -dP/dT, and force-frequency responses compared with values in Wt controls and transgenic mice overexpressing the Wt TR-beta(1). In contrast, in vivo measures of cardiac performance were similar between Wt and mutant animals, indicating that the diminished performance of the mutant transgenic heart in vitro was compensated for by other mechanisms in vivo. This is the first demonstration indicating that isolated cardiac hypothyroidism causes cardiac dysfunction in the absence of changes in the adrenergic or peripheral vascular system.
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PMID:Cardiac dysfunction caused by myocardium-specific expression of a mutant thyroid hormone receptor. 1074 7

Thyroid hormones influence cardiac performance directly and indirectly via changes in peripheral circulation. Little, however, is known about the effect on myocardial oxidative metabolism and its relation to cardiac function and geometry. Patients with a history of thyroidectomy for thyroid cancer present a unique model to investigate the cardiac effects of hypothyroidism. Ten patients without heart disease were investigated in the hypothyroid state and again 4-6 weeks later under euthyroid conditions. Myocardial oxidative metabolism was measured by positron emission tomography with [11C]acetate and the clearance constant k(mono). Cine magnetic resonance imaging was applied to determine left ventricular geometry. A stroke work index (SWI = stroke volume x systolic blood pressure/ventricular mass) was calculated. Then, to estimate myocardial efficiency, a work metabolic index [WMI = SWI x heart rate/k(mono)] was obtained. Compared to hormone replacement, systemic vascular resistance and left ventricular mass were significantly higher in hypothyroidism. Ejection fraction and SWI were significantly lower. Despite an additional reduction of k(mono), the WMI was significantly lower, too. In summary, cardiac oxygen consumption is reduced in hypothyroidism. This reduction is associated with increased peripheral resistance and reduced contractility. Estimates of cardiac work are more severely suppressed than those of oxidative metabolism, suggesting decreased efficiency. These findings may provide an explanation for development or worsening of heart failure in hypothyroid patients with preexisting heart disease.
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PMID:Effect of thyroid hormones on cardiac function, geometry, and oxidative metabolism assessed noninvasively by positron emission tomography and magnetic resonance imaging. 1084 59

The TRAP220 component of the TRAP/SMCC complex, a mammalian homologof the yeast Mediator that shows diverse coactivation functions, interacts directly with nuclear receptors. Ablation of the murine Trap220 gene revealed that null mutants die during an early gestational stage with heart failure and exhibit impaired neuronal development with extensive apoptosis. Primary embryonic fibroblasts derived from null mutants show an impaired cell cycle regulation and a prominent decrease of thyroid hormone receptor function that is restored by ectopic TRAP220 but no defect in activation by Gal4-RARalpha/RXRalpha, p53, or VP16. Moreover, haploinsufficient animals show growth retardation, pituitary hypothyroidism, and widely impaired transcription in certain organs. These results indicate that TRAP220 is essential for a wide range of physiological processes but also that it has gene- and activator-selective functions.
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PMID:Involvement of the TRAP220 component of the TRAP/SMCC coactivator complex in embryonic development and thyroid hormone action. 1088 4

Clinical complications of transfusional iron overload are still common in patients with thalassaemia major (TM) and it is not clear how best to monitor body iron stores during long-term follow-up to anticipate tissue damage. In this study, we have reviewed a group of 32 patients who underwent liver biopsy between 1984 and 1986. We developed a method of assessing the trend in serum ferritin (TSF) during long-term monitoring and compared this with mean serum ferritin (MSF) and initial liver iron (LI) concentration to determine whether, individually or in combination, they were accurate in predicting clinical outcome. LI levels were low (< 7 mg/g), medium (7-15 mg/g) and high (> 15 mg/g dry weight) in 15, 7 and 10 patients respectively. MSF was low (< 1500 microg/l), medium (1500-2500 microg/l) and high (> 2500 microg/l) in 10, 14 and 8 patients. TSF was low, medium and high risk in 9, 9 and 11 out of 29 evaluable patients. During a median follow-up of 13.6 years (range 2.3-14.8 years) after biopsy, nine patients died and an additional three patients developed heart failure. Hypothyroidism developed in five, hypoparathyroidism in four, and diabetes mellitus in seven patients. Cirrhosis developed in four of 10 evaluable patients. The clinical end-point of death or cardiac failure was significantly associated with increasing iron load using all three means of assessment. Although numbers were insufficient for statistical analysis, MSF or TSF were more closely associated with complications of iron overload than LI. There was no clear additional value in combining LI with MSF or TSF. The data show that quantitation of liver iron from a single liver biopsy has little value in long-term monitoring of iron stores. Most complications can be avoided if ferritin levels can be brought down to <1500 microg/l.
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PMID:Hepatic iron concentration combined with long-term monitoring of serum ferritin to predict complications of iron overload in thalassaemia major. 1105 91

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

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

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

The similarities between the changes in cardiac gene expression in pathological ventricular hypertrophy and hypothyroidism suggest a role of impaired cardiac thyroid hormone (TH) action in the development of contractile dysfunction during chronic cardiac pressure overload. Here we studied the possible involvement of altered cardiac TH metabolism using a rat model of right-ventricular (RV) hypertrophy induced by pressure-overload. Pathological RV hypertrophy was indicated by decreased mRNA levels of sarcoplasmic reticulum(SR) Ca2-ATPase type 2a (SERCA2a) and myosin heavy chain a (MHCalpha), and increased levels of MHCbeta mRNA. Enzyme activity of type HI deiodinase (D3), which converts T4 and T3 to the inactive compounds rT3 and 3,3'-T2, respectively, was identified in ventricular tissue. This activity was stimulated up to five fold in hypertrophic RV, but remained unaltered in the non-hypertrophic left ventricle (LV). A low level of type Ideiodinase activity was also detected, which decreased significantly in both RV and LV. Stimulation of RV D3 activity was significantly higher in those animals in which hypertrophy progressed to heart failure, compared to animals that developed compensatory hypertrophy. The induction of a cardiac TR-degrading deiodinase maybe expected to result in reduced cellular levels of T3 and thereby contribute to a local hypothyroid state in the hypertrophic and, particularly, in the failing ventricle.
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PMID:Induction of thyroid hormone-degrading deiodinase in cardiac hypertrophy and failure. 1207 17


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