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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Classic high-output thyrotoxic heart disease is generally considered a direct effect of thyroid hormone. In contrast, the cause of the less common low-output heart failure is generally unknown. The aim of this study was to retrospectively evaluate available endomyocardial biopsy tissue from patients with coexistent Graves' disease and idiopathic low-output heart failure and determine whether the biopsy features were consistent with an autoimmune process. The study group consisted of 11 patients whose mean age was 47 years when they were diagnosed with hyperthyroidism and 52 years when diagnosed with cardiac dysfunction. Right ventricular endomyocardial biopsy tissue revealed severe lymphocytic myocarditis in a patient with severe ophthalmopathy and showed borderline myocarditis in a patient without ophthalmopathy. Biopsy tissues from 6 other patients showed appreciable myocyte hypertrophy and interstitial fibrosis, consistent with dilated cardiomyopathy. Two patients had nondiagnostic biopsy specimens, and 1 patient had features suggestive of arrhythmogenic right ventricular dysplasia. In conclusion, for the 11 patients with Graves' disease and unexplained systolic dysfunction, only 2 (18%) had lymphocytic infiltrates consistent with an autoimmune process. Thus, among patients with Graves' disease, most cases of low-output cardiac dysfunction appear to be due to causes other than an active autoimmune inflammatory process.
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PMID:Graves' disease and low-output cardiac dysfunction: implications for autoimmune disease in endomyocardial biopsy tissue from eleven patients. 1095 13

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

The complications (thromboembolism and jaundice), averse effects (metabolic disorders, hypertension and bleeding) and the risks (cancer and teratologic effects) of oral contraceptives are summarized and compared to those of other methods. Venous thrombosis is more frequent than arterial thrombosis; both are rare but can be severe; risk is decreased with minidose pills. Cholostatic jaundice is likely only in those with history of such jaundice in pregnancy. Decreased oral glucose tolerance similar to diabetes of pregnancy, similarly, is more common with high dose pills. Triglycerides, pre-beta lipoproteins and t otal cholesterol levels are increased to the upper limit of normal, but stabilize after 3 months of pill intake in normal women. Mixed hyperlipidemia in some women can be detected by the cholesterol to triglycerides ratio after 8 and 12 hours of fasting. Other possible side effects are hypertension, elevated thyroid hormone, depression due to abnormal tryptophan metabolism, acne, cholasma, varices, spotting, amenorrhea. The risk of cancer is still unknown, but that of chromosomal defects in unfounded. To avoid these complications, the physician must observe the contraindications of history of thromboembolism, heart disease, jaundice, hypertension and cancer, and follow patients regularly by gynecologic exam, glucose tolerance and blood lipid tests and take blood pressure. In comparison, diaphragms give 15% failure rates, and copper IUDs less than 1%, but about 10% expulsions and 10% removals for bleeding.
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PMID:[Complications of contraception]. 1225 11

Using noninvasive imaging, we have previously demonstrated that myocardial efficiency is impaired in hypothyroidism and improves after establishing euthyroid conditions. Little is known about the effects of abnormally elevated thyroid hormone exposure on cardiac metabolic performance. We studied 10 patients without evidence of heart disease in mild hyperthyroidism, and after therapy under euthyroid conditions. Cardiac oxidative metabolism was quantified by positron emission tomography with [(11)C]acetate. Left ventricular geometry was determined by cine magnetic resonance imaging. Myocardial efficiency, defined by the relation between work and oxygen consumption, was estimated using the work metabolic index [WMI = stroke volume * systolic blood pressure * heart rate/(oxidative metabolism * ventricular mass)]. In hyperthyroidism, heart rate and cardiac output were expectedly higher. Peripheral vascular resistance was reduced. Differences of blood pressure, stroke volume, and ventricular mass were not observed. Oxidative metabolism was significantly higher, but WMI was not different from the euthyroid state. In summary, while improvement of efficiency through thyroid hormone substitution was observed previously in hypothyroidism, our data in mild hyperthyroidism suggest an increase of oxygen consumption, paralleled by an increase of work. Thus, moderately elevated thyroid hormone levels neither result in further increase nor in reduction of cardiac metabolic performance.
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PMID:Cardiac oxidative metabolism, function, and metabolic performance in mild hyperthyroidism: a noninvasive study using positron emission tomography and magnetic resonance imaging. 1285 14

Atrial fibrilliation (AF) is often combined with advanced age and structural heart disease, conditions known to invite serious proarrhythmic complications of antiarrhythmic drug therapy. Recent controlled trials comparing two AF treatment strategies-rhythm control requiring atrial defibrilliation and antiarrhythmic drugs to prevent AF and ventiricular rate control obviating sinus rhythm maintenance with such drugs-showed equal or superior results with rate control. AF is associated with derepressions of "fetospecific" expression patterns that may profoundly alter the responsiveness of atrial muscle to antiarrhythmic drugs. Therefore, effects of drugs predicted according to pharmacological classifications evaluating drug actions in intact myocardium only should be interpreted cautiously. The classification proposed by Vaughan Williams fails to distinguish between acute and chronic drug efficacy and toxicity as recommended in classical pharmacology. There is, however, overwhelming evidence that acute and chronic drug effects often differ fundamentally. For instance, amiodarone acts acutely as a sodium channel blocker, whereas chronic effects may be mediated by a downregulation of thyroid hormone receptors. Meaningful direct effects of amiodarone on atrial potassium channels is questionable, since the main candidate target-current (IKr) may not be expressed in human atrial muscle. Multiple biophysical factors contribute to the lack of ion channel-selective actions of antiarrhythmic agents. Nonselectivity becomes particularly important in the context of mechanisms of action of Vaughan Williams Class I and III agents on human atrial muscle. Preclinical studies indicate that Class I agents such as flecainide and propafenone may act in AF predominantly as Class III agents. Meta-analyses of antiarrhythmic agents for the prevention of AF have failed to reveal superior drugs or drug classes. Superiority of amiodarone over other agents may depend on arbitrary amiodarone-favoring loading protocols producing significant differential effects exclusively during the acute phase of treatment. In conclusion, the classification of current antiarrhythmic agents into Class I and III may not be a useful simplification when applied to the pharmacotherapy of AF.
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PMID:Class I or class III agents for atrial fibrillation: are asking the right question? 1291 11

Selenium is an essential trace element. It is, however toxic at concentration little above which is required for health. Selenium is incorporated into proteins as selenocysteine, the 21(st) amino acid. Selenoproteins are found in bacteria, archaea and eukaryotes. Biochemical and physicochemical properties of selenium result in the unique redox characteristics of selenocysteine and its use in antioxidant enzymes. In this context of a redox reaction is the reduction of reactive oxygen metabolites by glutathione peroxidases, helping to maintain membrane integrity, reduces the oxidative damage to lipids, lipoproteins, and DNA. Selenium has structural and enzymatic roles. Selenium influences a number of endocrine processes, most notably, those involved in thyroid hormone synthesis and metabolism. Se is needed for the proper functioning of the immune system, a role in viral suppression, AIDS, and also is implicated in delaying the aging process. Its deficiency has been linked to a number of disorders such as heart disease, diabetes, and diseases of the liver, and it is required for sperm motility and may reduce the risk of miscarriage. Se supplementation has recently moved from the realm of correcting nutritional deficiencies to one of pharmacological intervention, especially in the clinical domain of cancer chemoprevention. During the last few years, a tremendous effort has been directed toward the synthesis of stable organoselenium compounds that could be used as antioxidants, enzyme modulators, antitumor, antimicrobials, antihypertensive agents, antivirals and cytokine inducers. The biochemistry and pharmacology of selenium-based compounds are subjects of intense current interest, especially from the point of view of public heath. The purpose of this review is to discuss the recent pharmacological applications of organoselenium compounds as therapeutic agents in the treatment of several diseases.
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PMID:Organoselenium compounds as potential therapeutic and chemopreventive agents: a review. 1518 May 70

Thyrotoxicosis is associated with increased cardiovascular morbidity and mortality, primarily due to heart failure and thromboembolism. Palpitations, caused by sinus tachycardia and occasionally by atrial fibrillation, are the most frequent cardiovascular symptom. As atrial fibrillation may be the only manifestation of thyrotoxicosis, thyroid hormone excess should routinely be excluded in patients with this rhythm disturbance. Heart failure occurs mostly in the presence of underlying heart disease or tachycardia-induced cardiomyopathy in patients with long-standing atrial fibrillation. On occasion, long-standing hyperthyroidism may lead to heart failure even in the absence of concomitant cardiac conditions. Beta-blockers offer symptomatic relief and at the same time slow the ventricular response in patients with atrial fibrillation. Amiodarone, and occasionally iodinated contrast agents, may cause iodine-induced thyrotoxicosis. Clinical suspicion is essential in the diagnosis of amiodarone-induced thyrotoxicosis (AIT), because the antiadrenergic effect of the drug may conceal symptoms. AIT should be considered in any patient on amiodarone in the presence of new-onset or recurrent atrial arrhythmias or unexplained weight loss. Beyond discontinuation of amiodarone, treatment options include propylthiouracil or methimazole, potassium perchlorate, steroids, lithium and, if pharmacological treatment fails, surgery. Amiodarone may potentially be used less frequently in the future since recent studies have shown that this drug is inferior to implantable cardioverter defibrillators in prevention of sudden cardiac death in patients with severe heart failure. In addition, non-iodinated amiodarone analogues are currently in advanced phase of clinical testing.
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PMID:Thyrotoxicosis and the cardiovascular system. 1598 1

Thyroid hormone metabolic disarray has been identified as a risk factor for the progression of heart disease and the development of heart failure (HF). Both hyper- and hypothyroidism have been associated with a failing myocardium. Poor cardiac contractility and low cardiac output due to hyperthyroidism is a rare occurrence and is mostly seen in patients with preexisting heart disease. Referred to as a "rate related" phenomenon, hyperthyroid-induced sustained sinus tachycardia or atrial fibrillation may further reduce ventricular contractility. Increasingly, the hypothyroid state, and in particular a low triiodothyronine level, has been associated with a reduced cardiac performance and poor prognosis in HF, even in the presence of normal thyroid-stimulating hormone levels. Low thyroid hormone levels alter cardiac gene expression and increase systemic vascular resistance, both resulting in a reduction of cardiac contractility and cardiac output. This review summarizes current data on thyroid dysfunction and HF as well as the emerging implications of the "low triiodothyronine state."
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PMID:Thyroid hormone and heart failure. 1691 3

Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors (NRs) that control many cellular and metabolic processes. These proteins are ligand-activated transcription factors and three isotypes called PPARalpha, PPARbeta/delta and PPARgamma have been identified in lower vertebrates and mammals. They display differential tissue distribution and each of the three subtypes fulfills specific functions; however, all three PPARs affect energy homoeostasis and inflammatory responses. In addition, their activity can be modulated by drugs such as the hypolipidemic fibrates and the insulin sensitizing thiazolidinediones. Thus, understanding the biology and identifying small molecule modulators of the PPARs is an active area of research and may impact chronic diseases such as diabetes, obesity, heart disease and atherosclerosis. The PPAR Resource Page (http://ppar.cas.psu.edu) is a website devoting to keeping scientists up-to-date with the latest research on these proteins and provides links to a variety of public databases. The site was launched in 1998 to disseminate information about PPAR including cDNA sequences, protein alignments, DNA response elements (PPREs), and sources of cDNAs, proteins and antibodies. Recent additions include bioinformatics support such as gene expression microarray and pathway analysis links. As part of the Nuclear Receptor Resource (NRR, http://nrr.georgetown.edu/NRR/nrrhome.htm) some tools are shared with other constituents of this larger project. These include electronic publication, and a listing of scientists interested in the steroid and thyroid hormone superfamily. Receiving greater than 300 unique visits per week, the PPAR resource page has become a useful tool for researchers of these important NRs.
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PMID:The PPAR resource page. 1749 68

MicroRNAs act as negative regulators of gene expression by inhibiting the translation or promoting the degradation of target mRNAs. Because individual microRNAs often regulate the expression of multiple target genes with related functions, modulating the expression of a single microRNA can, in principle, influence an entire gene network and thereby modify complex disease phenotypes. Recent studies have identified signature expression patterns of microRNAs associated with pathological cardiac hypertrophy, heart failure, and myocardial infarction in humans and mouse models of heart disease. Gain- and loss-of-function studies in mice have revealed profound and unexpected functions for these microRNAs in numerous facets of cardiac biology, including the control of myocyte growth, contractility, fibrosis, and angiogenesis, providing glimpses of new regulatory mechanisms and potential therapeutic targets for heart disease. Especially intriguing is the discovery of a network of muscle-specific microRNAs embedded within myosin heavy chain genes, which control myosin expression and the response of the heart to stress and thyroid hormone signaling. Disease-inducing cardiac microRNAs can be persistently silenced in vivo through systemic delivery of antimiRs, allowing for the direct therapeutic modulation of disease mechanisms. Here, we summarize current knowledge of the roles of miRNAs in heart disease and consider the advantages and potential challenges of microRNA-based approaches compared to conventional drug-based therapies.
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PMID:Toward microRNA-based therapeutics for heart disease: the sense in antisense. 1894 30


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