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

Intrahepatic cholestasis has rarely been observed in patients with thyrotoxicosis and generally occurs in association with coexistent congestive heart failure. We report the case of a 63-year-old man who was referred to our Institution because of jaundice and hyperthyroidism. During his hospital stay, his plasma bilirubin level reached 27.41 mg/dL. Clinical, biohumoral, and instrumental examinations excluded heart failure and autoimmune or viral hepatitis. After the start of therapy with methimazole, thyroid hormone and plasma bilirubin levels decreased progressively and simultaneously, eventually returning to normal. Plasma bilirubin values as high as the ones we recorded, in the absence of congestive heart failure or autoimmune chronic hepatitis, have not, to our knowledge, been previously reported.
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PMID:[Hyperthyroidism and cholestasis: a case report]. 1034 8

A woman with congestive heart failure and reduced left ventricular ejection fraction associated with hyperthyroidism is reported. Congestive heart failure resolved and left ventricular ejection fraction normalized within three weeks of treatment of her hyperthyroidism. The literature on previously reported cases of reversible systolic heart failure associated with hyperthyroidism is reviewed and the possible mechanisms leading to systolic dysfunction and congestive heart failure in thyrotoxicosis are discussed. One such mechanism may be the action of thyroid hormone on altering gene expression in cardiac cells; another could be the chronic tachycardia associated with thyrotoxicosis. Although it is a not a common cause of systolic heart failure, thyrotoxicosis should be considered in the differential diagnosis of cardiomyopathies because it is a potentially reversible cause.
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PMID:A case of thyrotoxicosis and reversible systolic cardiac dysfunction. 1041 19

Fetal and neonatal hyperthyroidism are usually produced by transplacental passage of thyroid-stimulating immunoglobulins. Most commonly, the thyroid-stimulating immunoglobulins are a component of active maternal Graves' disease. However, such antibodies may continue to be produced after ablation of the thyroid by surgery, radioiodine, or by the immune mechanisms of Hashimoto's thyroiditis. Other mechanisms that have produced fetal and neonatal hyperthyroidism include activating mutations of the stimulatory G protein in McCune-Albright syndrome and activating mutations of the thyrotropin (TSH) receptor. Fetal hyperthyroidism may be associated with intrauterine growth retardation, nonimmune fetal hydrops, craniosynostosis, and intrauterine death. Features of this condition in the neonate include hyperkinesis, diarrhea, poor weight gain, vomiting, ophthalmopathy, cardiac failure and arrhythmias, systemic and pulmonary hypertension, hepatosplenomegaly, jaundice, hyperviscosity syndrome, thrombocytopenia, and craniosynostosis. The time course of thyrotoxicosis depends on etiology. Remission by 20 weeks is most common in neonatal Graves' disease; remission by 48 weeks is nearly always seen. A subset of these patients may have persistent disease when there is a strong family history of Graves' diseases. Disease persistence is characteristic of patients with activating mutations of the TSH receptor. Treatment of fetal hyperthyroidism comprises administration of antithyroid drugs to the mother. Fetal heart rate and fetal growth should be monitored. Ultrasonography may reveal changes in thyroid size. At times, cordocentesis may be useful for monitoring fetal thyroid function. Hyperthyroid neonates may be treated with antithyroid drugs, beta-adrenergic receptor blocking agents, iodine, or iodinated contrast agents, and at times, with glucocorticoids and digoxin. Nonremitting causes of neonatal hyperthyroidism require ablative treatments such as thyroidectomy.
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PMID:Fetal and neonatal hyperthyroidism. 1044 21

The cases of two patients with hyperthyroidism and acute left ventricular (LV) dysfunction with segmental wall motion abnormalities resulting in heart failure are reported. Both had electrocardiographic changes mimicking ischemic coronary artery disease. Treatment with antithyroid medications, beta blockers, and angiotensin-converting enzyme inhibitors rapidly restored LV function. The rapid reversibility suggests a role for myocardial stunning, an important entity to recognize in hyperthyroidism since this form of LV dysfunction can be reversed with appropriate treatment.
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PMID:Myocardial stunning in hyperthyroidism. 1076 82

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

A young man with previously unrecognized Graves' disease presented with atrial fibrillation and severe low-output heart failure due to dilated cardiomyopathy. The patient's cardiomyopathy resolved and cardiac function recovered shortly after hyperthyroidism and tachycardia were treated during hospitalization. The temporal relationship between heart rate and cardiac function during the recovery period suggests that chronic tachycardia may have been an important cause of his cardiac dysfunction. Thyrotoxicosis seemed to be directly responsible for the development of sustained supraventricular tachycardia in this patient, which then led to tachycardia-induced cardiomyopathy causing severe low-output heart failure. Although relatively infrequent, this etiology should not be overlooked in patients thyrotoxicosis and heart failure. This is the first case in which the time course and the temporal relationship between the control of heart rate and the recovery of cardiac function are illustrated in a thyrotoxic patient.
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PMID:Tachycardia-induced cardiomyopathy secondary to thyrotoxicosis: a young man with previously unrecognized Graves' disease. 1108 Dec 59

A 45-year-old woman was referred to our hospital because of hyperthyroidism complicated by atrial fibrillation and heart failure. Laboratory data revealed pancytopenia, with a white blood cell count of 2,600/microliter, red blood cell count of 330 x 10(4)/microliter, and platelet count of 6.2 x 10(4)/microliter. The patient had normal transaminase levels, but tests for hepaplastin and cholinesterase showed values of 34% and 1.4 U/ml, respectively, indicating liver dysfunction. There was also decreased excretion of indocyanine green. After initiation of treatment with 30 mg thiamazole and 20 mg propranolol daily, the patient's thyroid function normalized and the other abnormal laboratory findings such as pancytopenia and liver dysfunction also disappeared. Pancytopenia is a rare complication of hyperthyroidism. In this case, various laboratory abnormalities were normalized by antithyroid therapy alone, indicating that the hyperthyroidism itself was closely related to the pathogenesis of pancytopenia and liver dysfunction.
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PMID:[Recovery from pancytopenia and liver dysfunction after administration of thiamazole for hyperthyroidism]. 1119 44

More than 200 years ago, Caleb Parry described cardiological manifestations of hyperthyroidism. Interaction of thyroid hormones and sympathoadrenal system (responsible for rhythm disorders) and direct effect of thyroid hormones on the cardiac muscle (responsible for occurrence of hypertrophy and cardiac insufficiency) have been recognized as the pathophysiological basis of cardiovascular disorders of patients with hyperthyroidism. The aim of the study was to retrospectively analyze surgically treated patients with different types of hyperthyreosis, and establish the incidence and clinical significance of the left ventricular dysfunction related to duration and treatment of hyperthyreosis. Evaluation of left ventricular function was based on the ejection fraction during exercise. Signs of hypertrophy were echocardiographically, radiographically and electrocardiographicaly recorded. Over the period 1993-1997 at the Surgical Department of the institute of Endocrinology in Belgrade 423 patients with hyperthyreosis were operated: 293 (69.26%) patients had Graves-Basedow's disease, 74 (17.49%) toxic adenoma, and 58 (13.28%) toxic polynodal struma. The average duration of the disease in patients with Graves-Basedow's hyperthyreosis was 5 yrs, and the average age of patients was 29 yrs; the average duration of hyperthyreosis in patients with toxic adenoma was 1.2 yrs, and in cases of toxic polynodal struma 17 yrs. Pathological response of ejection fraction during exercise was recorded in 60% of patients. Signs of hypertrophy of the left chamber were recorded in 17% of subjects, and insufficiency of the left chamber with congestive stasis in the lungs in 4.6% of patients. The most common ECG changes were: synus tachycardia, higher voltage of P and T waves, elevated amplitude of QRS complex, prolonged P-Q and shortened Q-T intervals. In 20% of cases atrial fibrillation was evidenced. One patient had ECG signs of myocardial infarction. Clinical features of left ventricular dysfunction in hyperthyroidism include: occurrence in younger patients with history of hyperthyroidism, progressive course and occurrence of congestive cardiac failure as well as reversible nature of all cardiac changes after radical therapy of hyperthyreosis which can be medical, surgical or irradiation.
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PMID:[Cardiovascular manifestations of hyperthyroidism. Clinical significance and preoperative preparation]. 1133 17

We report a 18 years old woman that was admitted with a history of four days of cardiac failure with acute pulmonary edema, high blood pressure, left ventricular dilatation and moderate to severe systolic dysfunction. Twenty four hours after admission she had a miscarriage, expelling a mole. The diagnosis of hyperthyroidism caused by a mole and early pre eclampsia was confirmed and the patient was managed with diuretics and dopamine. Symptoms abated, thyroid function tests, cardiac function and size returned to normal values and the patient was discharged asymptomatic, ten days after admission.
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PMID:[Gestational hyperthyroidism: a case associated to molar pregnancy]. 1137 99

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


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