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

Thyroid hormone plays an important role on myocardial development and function. The local effects of thyroid hormone are mediated by the receptor isoforms ultimately driving the expression of cardiac-specific genes. Although overt and subclinical thyroid dysfunction causes well-known changes in the cardiovascular system, little is known about local thyroid hormone action in normal and failing human myocardium. With a newly developed multiplex competitive RT-PCR method, we evaluated the expression of thyroid hormone receptor (TR) isoforms alpha-1, alpha-2, and beta-1 in normal human hearts and in end-stage congestive heart failure. A statistically significant difference in the expression of all three TR isoforms was observed among samples from normal subjects, ischemic heart disease (IHD), and dilated cardiomyopathy (DCM). In DCM, compared with normal, the studied TR isoforms were significantly increased. In IHD, the increased expression was found significant only for alpha-1 and alpha-2 isoforms. No differences were observed between the pathologic groups. In conclusion, a coordinated increment in the expression of the TR isoforms was observed in both DCM and IHD by multiplex competitive RT-PCR. The observed changes could represent a compensatory mechanism to myocardial failure or to locally altered thyroid hormone action.
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PMID:Increased expression of thyroid hormone receptor isoforms in end-stage human congestive heart failure. 1160 May 94

We report a 49-year-old man with primary hyperthyroidism who presented with pancytopenia. The patient presented with leg edema, sinus tachycardia, cardiomegaly, and pleural effusions, all from congestive heart failure. Laboratory data showed pancytopenia and primary hyperthyroidism; echocardiogram showed diffuse hyperkinesis of the left ventricular wall and right ventricular overloading. The bone marrow was moderately hypercellular and compatible with arrested hematopoiesis. Pancytopenia and heart failure improved after administration of methimazole and diuretics. However, high levels of thyroid hormone recurred with pancytopenia 4 months after admission. Therefore, subtotal thyroidectomy was performed, and the levels of thyroid hormones and peripheral blood cell counts have remained normal. Pancytopenia may be caused by hyperthyroidism.
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PMID:A case of thyrotoxicosis with pancytopenia. 1152 11

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

Amiodarone has been used as an anti-arrhythmic drug since the 1970s and has an established role in the treatment of ventricular tachyarrhythmias. Although considered to be a class III anti-arrhythmic, amiodarone also has class I, II and IV actions, which gives it a unique pharmacological and anti-arrhythmic profile. Amiodarone is a structural analogue of thyroid hormone and some of its anti-arrhythmic properties and toxicity may be attributable to interactions with nuclear thyroid hormone receptors. The lipid solubility of amiodarone gives it an exceptionally long half-life. Oral amiodarone takes days to work in ventricular tachyarrhythmias, but iv. amiodarone has immediate effect and can be used in life threatening ventricular arrhythmias. Intravenous amiodarone administered after out-of-hospital cardiac arrest due to ventricular fibrillation improves survival to hospital admission. Many survivors of myocardial infarction (MI) die during the subsequent year, probably due to ventricular arrhythmia. Amiodarone reduces sudden death after MI and this benefit is predominantly observed in patients with preserved cardiac function. Sudden cardiac death, predominantly due to ventricular arrhythmias, is also commonly seen in patients with heart failure. The Grupo de Estudio de la Sobrevida en lsuficiencia Cardiaca en Argentina (GESICA) and Estudio Piloto Argentino de Muerte Subita y Amiodarona (EPAMSA) trials showed survival benefit of amiodarone in heart failure, whereas Congestive Heart Failure-Survival Trial of Anti-arrhythmic Therapy (CHF-STAT) did not. Subsequent meta-analysis established a survival benefit of amiodarone in heart failure. Implanted Cardioverter Def ibrillators (ICDs) also give survival benefit to patients at risk of sudden death. In patients with a history of ventricular fibrillation or haemodynamically-compromising ventricular tachycardia, ICDs have been shown to be superior to anti-arrhythmic drugs, principally amiodarone. Further analysis has been undertaken to ascertain which patients are most likely to benefit from ICDs, as these are more expensive than treatment with amiodarone. Patients with severely depressed ejection fractions should be the first to be considered for ICDs. A new indication for amiodarone is atrial fibrillation or flutter. Amiodarone is effective in chronic and recent onset atrial fibrillation and orally or iv. for atrial fibrillation after heart surgery. In atrial fibrillation amiodarone is more than or equi-effective with flecainide, quinidine, racemic sotalol, propafenone and diltiazem and therefore should be considered for first line therapy. Amiodarone is also safe and effective in controlling refractory tachyarrhythmias in infants and is safe after cardiac surgery.
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PMID:Amiodarone -- waxed and waned and waxed again. 1182 23

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

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

The effects of hypothyroidism on the cardiovascular system have been the subject of much research over the last several decades. The hypothyroid cardiac phenotype includes impaired contractile function, decreased cardiac output, and alterations in myocyte gene expression. In the setting of cardiac disease, as in other acute illnesses, alterations in thyroid hormone metabolism occur that result in decreased serum triiodothyronine (T(3)) levels. This is referred to as low T(3) syndrome. Similarities between the heart failure phenotype and the hypothyroid cardiac phenotype are numerous including changes in the expression of thyroid hormone regulated myocyte specific genes. The heart responds in a very sensitive manner to reduced circulating levels of T(3) with decreased expression of positively regulated genes and increased expression of negatively regulated genes. In the present paper we review data on thyroid hormone mediated cardiac specific gene transcriptional regulation. T(3) replacement therapy for hypothyroidism restores normal expression of these T(3) regulated genes and recent experiments suggest that the diseased human heart in congestive failure would benefit from similar T(3) replacement therapy.
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PMID:Thyroid hormone-regulated cardiac gene expression and cardiovascular disease. 1216 8

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 hormone has multiple effects on the cardiovascular system, ranging from molecular and cellular effects to the consequent hemodynamic alterations. Consequently, thyroid function has been evaluated in small cohorts of patients with advanced heart failure that indicate a significant prevalence of morphologic or functional thyroid disorders. We sought to determine the prevalence of altered thyroid hormone metabolism in a broad spectrum of ambulatory heart failure patients. Thyroid function tests were evaluated in 132 ambulatory patients (98 males, 32 females, mean age, 67 years) with left ventricular systolic dysfunction (EF < 35%) and New York Heart Association (NYHA) class I-IV symptoms. Hypothyroidism was defined as serum thyroid-stimulating hormone (TSH) > 4.25 U/mL and low triiodothyronine (T3) state was defined as T3 levels < 80 ng/dL, with normal thyroxine (T4) and TSH level. Seven percent of patients were found to have primary hypothyroidism and 34% have a low T3 state. Of patients receiving amiodarone, 21% had elevated TSH levels and 76% had low T3 levels. The prevalence of abnormal thyroid function correlated with NYHA class. There is an unexpectedly high risk of hypothyroidism and low T3 syndrome in patients regardless of treatment with amiodarone, which appears to correlate with disease severity that requires further investigation.
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PMID:Thyroid hormone metabolism in patients with congestive heart failure: the low triiodothyronine state. 1216 15


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