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Query: UMLS:C0018801 (heart failure)
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We describe three cases of thyroid storm who developed sudden cardiorespiratory arrest soon after the administration of propranolol orally. CASE 1: A 43 years old Chinese lady presented with complaints of fever and chills. She had a urinary tract infection and also had signs of overt thyrotoxicosis. She was diagnosed to have thyroid storm and was started on oral propranolol, carbimazole and intravenous hydrocortisone and ceftriaxone. Soon after propranolol was given orally she developed an asystolic cardiorespiratory arrest. CASE 2: A 72 years old Chinese gentleman presented with confusion, fever and rapid atrial fibrillation. He was diagnosed to have thyroid storm and was started on oral propranolol, carbimazole and intravenous hydrocortisone and ceftriaxone. He developed a cardiorespiratory arrest about 6 hours after commencement of therapy. CASE 3: A 48-year-old Chinese gentleman presented with complains of dyspnoea and palpitations. He was diagnosed to have thyroid storm and was started on oral propranolol, carbimazole, intravenous hydrocortisone and antibiotics. About 12 hours after admission, he developed a cardiorespiratory arrest. All three patients developed cardiorespiratory arrest soon after the administration of propranolol orally. We conclude that in selective patients who have low output cardiac failure in association with severe thyrotoxicosis, it maybe advisable to avoid use of a beta blocker. A safer alternative is the use of ultra short-acting beta-blockers, such as intravenous esmolol, with extreme caution.
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PMID:Cardiovascular collapse associated with beta blockade in thyroid storm. 1770 86

Thyroid hormones are essential to maintain normal function of many systems including the cardiovascular system. Their excess or deficiency may upset human body homeostasis. Hyperthyroidism leads to cardiovascular system's hyperdynamic status which is characterized by tachycardia, increased difference between systolic and diastolic arterial pressure, significant increase of the stroke volume and improvement of the left ventricular diastolic function. Long-lasting thyrotoxicosis in patient with heart disease may result in atrial fibrillation, deterioration of angina pectoris or congestive heart failure. Hypothyroidism leads to hemodynamic disturbances which are quite different than those observed in hyperthyroidism, but cardiac symptoms are scant in clinical practice. Hypothyroidism's clinical significance is limited to atherosclerosis progression and intensification of ischaemic heart disease symptoms. Both leads to symptomatic cardiovascular system failure or its deterioration. We should emphasize that cardiovascular system dysfunction associated with thyrometabolic disturbances subsides when euthyreosis is restored. It sounds promising that there are reports suggesting a potential advantage of thyroxin treatment in patients with acute or chronic cardiovascular system diseases. These hypotheses result from the observations that heart dysfunction in hypothyroidism is similar to that observed in heart failure.
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PMID:[Thyrometabolic disorders and heart failure]. 1794 Sep 89

We report the treatment of four thyrotoxic patients. Two were cases of type I amiodarone-induced thyrotoxicosis (AIT) treated with methimazole. The third Graves' disease patient, who became hypothyroid 25 years after subtotal thyroidectomy, developed type II AIT. Furthermore, one case with heart failure and ventricular tachycardia, who developed an adverse reaction to antithyroid agents and was prescribed amiodarone, underwent total thyroidectomy. The clinical course was uneventful, and the patient is doing well. Since amiodarone contains a large amount of iodine, it is frequently difficult to make a differential diagnosis. Surgical treatment of Graves' disease patients is recommended when immediate control of hyperthyroidism and heart failure is required.
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PMID:Differential diagnosis and appropriate treatment of four thyrotoxic patients with Graves' disease required to take amiodarone due to life-threatening arrhythmia. 1842 Nov 94

Thyroid hormone has many effects on the heart and cardiovascular system. Thyrotoxicosis is associated with increased cardiovascular morbidity and mortality, primarily due to heart failure and thromboembolism. However, the relationship between thyroid hormone excess and the cardiac complications of angina pectoris and myocardial infarction remains largely speculative. Moreover, few studies have been reported on the effect of thyroid hormone levels within normal range on coronary artery disease (CAD). Therefore we examined the association of thyroid function with coronary artery diseases in euthyroid angina patients. Total 192 subjects (mean age; 60.8 yrs) were enrolled in which coronary angiograms were performed due to chest pain. We measured free thyroxine (FT(4)), thyroid stimulating hormone (TSH), serum lipid levels and high-sensitivity C-reactive protein (hsCRP) levels and analyzed their association with the presence of CAD. Serum FT(4) levels were higher in patients with CAD compared with the patients without CAD (1.31 +/- 0.30 vs 1.20 +/- 0.23, p = 0.006), and high FT(4) level was associated with the presence of multi-vessel disease. Multivariate analysis showed that age (odds ratio (OR) 1.04; 95% confidence interval (CI) 1.01-1.07, p = 0.007), hypertension (OR 2.04; 95% CI 1.06-3.90, p = 0.036) and FT(4) (OR 4.23; 95% CI 1.12-15.99, p = 0.033), were the determinants for CAD. The relative risk (RR) for CAD in highest tertile of FT(4) showed increased risk compared with the lowest tertile (RR 1.98; 95% CI 0.98-3.99, p<0.001). Our study showed that FT(4) levels were associated with the presence and the severity of CAD. Also, this study suggests that elevated serum FT(4) levels even within normal range could be a risk factor for CAD. Further studies will be necessary to confirm the relationship of thyroid function and CAD.
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PMID:Higher serum free thyroxine levels are associated with coronary artery disease. 1849 53

Amiodarone and dronedarone are two clinically important benzofuran derivatives. Amiodarone has been used widely for treating resistant tachyarrhythmias in the past three decades. However amiodarone and its main metabolically active metabolite desethylamiodarone can adversely affect many organs, including the thyroid gland. Amiodarone-induced thyroid disorders are common and often present as a management challenge for endocrinologists. The pathogenesis of amiodarone-induced thyroid dysfunction is complex but the inherent effects of the drug itself as well as its high iodine content appear to play a central role. The non-iodinated dronedarone also exhibits anti-arrhythmic properties but appears to be less toxic to the thyroid. This review describes the biochemistry of benzofuran derivatives, including their pharmacology and the physiology necessary for understanding the cellular mechanisms involved in their actions. The known effects of these compounds on thyroid action are described. Recommendations for management of amiodarone-induced hypothyroidism and thyrotoxicosis are suggested. Dronedarone appears to be an alternative but less-effective anti-arrhythmic agent and it does not have adverse effects on thyroid function. It may have a future role as an alternative agent in patients being considered for amiodarone therapy especially those at high risk of developing thyroid dysfunction but not in severe heart failure.
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PMID:Benzofuran derivatives and the thyroid. 1872 7

The most recognizable features of hyperthyroidism are those that result from the effects of triiodothyronine (T3) on the heart and cardiovascular system: decreased systemic vascular resistance and increased resting heart rate, left ventricular contractility, blood volume, and cardiac output. Although these measures of cardiac performance are enhanced in hyperthyroidism, the finding of clinical cardiac failure can be somewhat paradoxical. About 6% of thyrotoxic individuals develop symptoms of heart failure, but less than 1% develop dilated -cardiomyopathy with impaired left ventricular systolic function. Heart failure resulting from thyrotoxicosis is due to a tachycardia-mediated mechanism leading to an increased level of cytosolic calcium during diastole with reduced ventricular contractility and diastolic dysfunction, often with tricuspid regurgitation. Pulmonary artery hypertension in thyrotoxicosis is gaining awareness as a cause of isolated right-sided heart failure. In both cases, older individuals are more likely to be affected. Treatment needs to be directed at management of the acute cardiovascular complications, control of the heart rate, and thyroid-specific therapy to restore a euthyroid state that will lead to resolution of the signs and symptoms of heart failure.
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PMID:Thyrotoxic cardiac disease. 1875 67

Serum BNP (brain naturiuretic peptide) and ANP (atrial natriuretic peptide) levels are reportedly elevated in patients with thyrotoxicosis. The increases may not be due to thyrotoxicosis itself but to secondary cardiovascular changes such as chronic heart failure (HF) or atrial fibrillation (AF) which frequently accompany thyrotoxicosis. We measured serum ANP and BNP levels in 130 patients with thyrotoxicosis and correlated them with HF severity and thyroid function. Thirty-seven normal subjects served as controls. Serum BNP levels in thyrotoxic patients were significantly higher than those in control subjects and significantly correlated with serum free T4, free T3 and ANP levels. In untreated Graves' disease serum BNP level was significantly elevated in patients with HF or AF. Multiple regression analysis revealed that HF, free T4, female gender and AF are independent contributing factors to the elevated BNP level, and that these four factors contributed about 40%. On the other hand, HF and AF were contributing variables for ANP level but the overall contribution of these factors was only 10%. After normalization of thyroid function, serum BNP levels were normalized in 70.5% of Graves' patients. BNP level in euthyroid state was dependent on the presence of HF and the BNP value before therapy, but not on thyroid hormone levels or AF. These data suggest that the cardiovascular condition is the major factor responsible for the elevated serum BNP and ANP levels in thyrotoxic patients, while thyrotoxicosis itself is an independent but minor contributing factor. Thus, the determination of serum BNP levels in thyrotoxic patients is useful for monitoring cardiovascular conditions of HF.
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PMID:Serum concentrations of BNP and ANP in patients with thyrotoxicosis. 1882 6

Thyrotoxicosis is underdiagnosed because of its low occurrence in series from Africa. The aim of this study was to evaluate the frequency, the demographic data, and the etiological aspects of thyrotoxicosis among hyperthyroidy. Thirty-six patients with thyrotoxicosis (group I) gathered during a period of four years was analysed, as well as 180 hyperthyroidy cases (group II). Cardiothyrotoxicosis was observed with a frequency of 16.6%. The mean age was respectively of 44.5+/-13.3 versus 32.8+/-11.4 years (p<10(-6)). Cardiothyrotoxicosis was related to multinodular goitres (18 cases), a Basedow disease (14 cases), a toxic adenoma (four cases), while the principal cause of hyperthyroidy was toxic adenoma followed by the Basedow disease (72 cases, 40%). Different modes of presentation of cardiothyrotoxicosis were found: cardiac heart failure in 27 cases (75%), permanent atrial fibrillation in 22 cases (61.1%), atrial flutter in two cases, coronary insufficiency in four cases, ventricular extrasystoli (trigeminism) in two cases, second auriculoventricular block in two cases, dilated myocardiopathy in 10 cases (27.7%), ischemic myocardiopathy in four cases, severe mitral regurgitation in one case. This study confirms the relative frequency of cardiothyrotoxicosis, the proportionally weak place of Basedow disease among hyperthyroidy's causes, and role of associated cardiac disease to the hyperthyroid.
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PMID:[Cardiothyrotoxicosis in the young adult in Marrakech. A report of 36 cases]. 1893 25

A 65-year-old woman presented to the hospital with weight loss and diarrhea. A diagnosis of thyroid storm was established by the presence of fever, lethargy, tachycardia, heart failure (HF), and abnormal thyroid function tests. An acute coronary syndrome (ACS) was suspected because of anteroseptal ST-segment elevations on electrocardiogram and severe left ventricular (LV) dysfunction with apical dilation on echocardiogram. The ejection fraction (EF) was 25%. Treatment for ACS and HF was begun. Coronary arteriography revealed normal coronaries. Propylthiouracil and corticosteroids were added to treat thyrotoxicosis. On Day 4, repeat echocardiography confirmed an EF of 65% and complete resolution of LV dysfunction and cavity dilation. Reversible LV dysfunction and apical cavity dilation is consistent with Takotsubo cardiomyopathy. While commonly associated with psychological trauma, its association with thyroid storm has only been reported twice before. Knowledge of this possible association is of importance in establishing the diagnosis and instituting a proper treatment plan.
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PMID:An association between Takotsubo cardiomyopathy and thyroid storm. 1949 50

Thyroid hormone receptors (TRs) exert profound effects on development, metabolism, and multiple specific organ functions. Principally by regulating crucial genes in a variety of tissues, the thyroid hormones, 3,5,3'-triiodo-L-thyronine (L-T(3), 1) and 3,5,3',5'-tetraiodo-L-thyronine (L-T(4), 2), influence basal calorigenesis and oxygen consumption, cardiac rate and contractility, lipid metabolism, bone structure and strength, and central nervous system functions critical for normal mentation and mood. Elevated levels of circulating and tissue 1 and/or 2 result in the thyrotoxic clinical state, manifested by weight loss despite increased caloric intake; heat intolerance due to increased calorigenesis; cardiac tachyarrhythmias, systolic hypertension, and heart failure; skeletal muscle weakness; and a spectrum of neuropsychiatric symptoms ranging from anxiety to delirium and psychosis. The current standard treatments of endogenous hyperthyroidism causing thyrotoxicosis reduce the overproduction of thyroid hormones by pharmacologically inhibiting their synthesis or release (e.g., with thionamides or lithium, respectively), or by ablating thyroid tissue surgically or with radioiodine. TR-antagonists could hypothetically have significant clinical use in treating thyrotoxic states if they were capable of promptly and completely restoring euthyroid levels of thyroid-specific gene activity. No TRalpha-selective ligands have been prepared up to this date, ligands that potentially would further ameliorate the problem with cardiac disease connected with hyperthyroidism and maybe cardiac arrhythmia. Despite its significant potential use, no TR-antagonist has reached clinical application. Design of TR-antagonists ligands has been based on the attachment of a large extension group at the 5-prime position of 1 or other structurally related analogues. This extension is believed to distort folding of the C-terminal helix (helix 12) to the body of the ligand binding domain (LBD), which normally forms a coactivator site. Examples of synthetic TR antagonists based on this extension strategy are reviewed, as well as other strategies to achieve functional TR-antagonism.
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PMID:Thyroid hormone antagonists: potential medical applications and structure activity relationships. 1954 68


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