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

We describe a female newborn infant with McCune-Albright syndrome. In addition to the cutaneous pigmentation, she had apparent manifestations of hyperthyroidism and Cushing syndrome since birth. X-ray examinations showed many scattered lucencies in multiple bones. Endocrinological findings were as follows: serum T 4 276 nmol/l; free T 4 125 pmol/l; TSH less than 1 mU/l; serum cortisol greater than 2210 nmol/l; plasma ACTH less than 10 pg/ml; urinary free cortisol 865 nmol/day; estradiol 0.36 nmol/l. Regardless of treatment with antithyroid drugs and an inhibitor of 3 beta-hydroxysteroid dehydrogenase, the patient died of cardiac failure at the age of 4 months. Autopsy findings included a follicle cyst in the right ovary and multinodular hyperplasia in the thyroid and both adrenals. To our knowledge such a severe neonatal form of McCune-Albright syndrome has not been described in the literature.
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PMID:A case of neonatal McCune-Albright syndrome with Cushing syndrome and hyperthyroidism. 175 13

Withdrawal of captopril therapy for cardiac failure results in increments in plasma cortisol, noradrenaline and heart rate. To determine whether these changes related to the concomitant rise in circulating angiotensin II, we infused angiotensin II at 0.5, 2, 4 and 8 ng/kg/minute, each infusion lasting for 1 hour, in 4 patients during maintenance captopril therapy for heart failure. A control solution of 5% dextrose was infused over a similar time interval on a separate day. The study was performed under metabolic balance conditions, with constant body posture and continuous haemodynamic monitoring. Angiotensin II induced the expected rise in arterial pressure and in plasma aldosterone. In contrast the diurnal decline in plasma ACTH and cortisol was not altered, and no changes in noradrenaline or heart rate were observed. Plasma angiotensin II appears to have little or no effect on ACTH, cortisol, noradrenaline and heart rate under the conditions of this study.
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PMID:Hormone and haemodynamic effects of angiotensin II infusion during captopril treatment for heart failure. 298 94

Relationships between clinical status, haemodynamic measurements, hormone and biochemical indices, and maintenance diuretic dose in patients with chronic cardiac failure, are not clear. This study assessed such relationships and their stability under standardized conditions in 21 hospitalized patients. The daily maintenance dose of frusemide correlated closely and in a positive fashion with plasma levels of renin activity, angiotensin II and aldosterone (P less than 0.001), and to a lesser extent with plasma noradrenaline. Although there was some overlap, patients most incapacitated by their heart failure had the highest circulating levels of renin activity, angiotensin II, aldosterone and noradrenaline. Plasma aldosterone correlated closely with concomitant angiotensin II levels (r = 0.70, P less than 0.001) but not with its other secretagogues ACTH (as reflected by plasma cortisol) or plasma potassium. Close positive correlations between angiotensin II and plasma levels of urea and creatinine (P less than 0.01) were observed. Both renin and angiotensin II showed positive relationships with right heart pressures, but were inversely related to cardiac index and arterial pressure. These results show close relationships between clinical and haemodynamic indices on one hand, and hormones on the other. The renin-angiotensin system appears to be the primary regulator of aldosterone under these conditions, and its activity relates closely to haemodynamic measurements and to the degree of azotaemia.
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PMID:Stability and inter-relationships of hormone, haemodynamic and electrolyte levels in heart failure in man. 389 Nov 72

The apparatus "Artificial Beta-Cell" or "Biostator" was used in treatment of 115 patients with diabetes mellitus and concomitant ischemia of the heart. At the same time 30 patients with diabetes mellitus and ischemia of the heart were treated for diabetes mellitus with the routine methods. Hormones such as ACTH, STH, hydrocortisone, immunoreactive insulin and S-peptide, lipid metabolism and glycosylated hemoglobin were investigated in the time course of the treatment. It was shown that adequate correction of glycemia with the "Biostator" promoted renormalization of the levels of ACTH and hydrocortisone. The results were especially favourable in the group of patients with myocardial infarction and chronic ischemia of the heart with the signs of cardiac insufficiency. Moreover, in the patients of the main group there was a tendency for normalization of lipid metabolism and glycosylated hemoglobin. The results of carbohydrate metabolism compensation in patients of the control group were not always satisfactory and the periods of compensation were longer. The clinico-biochemical indices reflected the favourable effect of the use of the "Biostator" and its advantages over the routine methods in treatment of diabetes mellitus.
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PMID:[Control and correction of the blood sugar in diabetes with concomitant ischemic heart disease using the artificial beta-cell apparatus employing glucose oxidase as the enzyme]. 396 92

We report on two infants (two and six month old) with infantile myoclonic seizures, who developed signs of hypertrophic cardiomyopathy (HCM), while receiving ACTH treatment (Tetracosactid=Synacthen Depot). The diagnosis of HCM was established by echocardiography. The first patient (R.M. female). showed signs of cardiac insufficiency and was treated with a beta-blocking agent (Propranolol=Dociton). This led to resolution of the clinical symptoms and reversal of myocardial muscle thickness as determined by echocardiography. The second patient (R.S. female) did not develop cardiac symptoms. A correlation between cardiomyopathy and ACTH treatment is discussed. Based on the various biological effects of ACTH different hypothetical explanations for this correlation are proposed: increased deposition of glycogen, enhanced protein synthesis, oedema of the myocardial tissue and systemic hypertension. Because of the correlation observed between ACTH treatment and the development of cardiomyopathy we recommend regular physical and echocardiographic examinations to detect cardiac involvement during treatment with ACTH.
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PMID:[Hypertrophic cardiomyopathy during ACTH treatment]. 630 97

1. Since important interrelationships between haemodynamic and hormone indices are possible in cardiac failure, measurements of cardiac output, mean pulmonary artery pressure, plasma renin activity, angiotensin II and aldosterone were carried out before and during acute and chronic frusemide therapy in patients with oedematous heart failure who had been given digoxin. 2. Cardiac output fell significantly 90 min after acute frusemide infection, then returned to baseline. Mean pulmonary artery pressure declined steadily throughout the 4 h of observation. 3. These haemodynamic changes occurred in the absence of major hormonal fluctuations and related presumably to direct vascular and diuretic actions of frusemide. 4. With more chronic (8-10 days) oral frusemide therapy, reciprocal changes between haemodynamic and hormone indices were observed. As the diuretic response to frusemide diminished, cardiac output and pulmonary artery pressure declined whereas the renin-angiotensin system was activated. Statistically significant inverse correlations were observed between these haemodynamic and hormone indices. 5. In both acute and chronic phases of the study, fluctuations in aldosterone levels were regulated by the renin-angiotensin system whereas ACTH, plasma potassium and plasma sodium played, at best, supportive roles.
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PMID:Haemodynamic and hormone responses to acute and chronic frusemide therapy in congestive heart failure. 700 35

The aim of this study was to evaluate changes of pituitary and adrenal cortex hormones in patients with congestive heart failure according to NYHA functional classes and to detect possible prognostic effects of these changes. We studied 101 patients: 60 with congestive heart failure, in absence of clinical, anamnestic signs of endocrine diseases (Group I, 37 males, 23 females; mean age 62 +/- 7.2 years) and 41 patients with cardiac diseases without signs of congestive heart failure, homogeneous for age and sex (Group II, 23 males, 18 females; mean age 61 +/- 8.5 years). All patients were submitted to a 12 month follow-up in order to evaluate hormonal changes. Hormonal study was performed through radioimmunoassay technique. Plasma levels of insulin, growth hormone (GH), adrenocorticotropine (ACTH), cortisol and prolactin (PRL) were evaluated. We observed in Group I a significant increase of cortisol and GH with respect to Group II. No significant difference occurred in plasma levels of insulin, PRL and ACTH. Subdividing Group I patients on the basis of NYHA classification, significant increase (p < 0.05) in cortisol and GH was observed in IV NYHA functional class with respect to II and III NYHA ones. Moreover a significant reduction (p < 0.02) of ACTH in IV NYHA functional class was also detected. Plasma levels of cortisol and GH were also significantly higher in patients dead during the follow-up with respect to survivors. Statistical analysis showed a linear negative correlation between cortisol and ACTH in III NYHA functional class (p < 0.03), a negative correlation between cortisol and radius/thickness ratio (p < 0.03) and between cortisol and serum glutamic oxalacetic transaminase (p < 0.05). In IV NYHA functional class a significant negative correlation between cortisol and shortening fraction (p < 0.05) also occurred. Plasma levels of cortisol and GH were significantly higher (p < 0.05) in IV NYHA functional class with respect to II and III classes, with associated significant reduction of shortening fraction (p < 0.05). Our data confirm that, besides catecholamines and renin-angiotensin-aldosterone system, in the presence of severe congestive heart failure (IV NYHA functional class), a significant activation of pituitary and adrenal cortex hormones occurs. It is still an open question whether this activation plays a pathogenetic role in the evolution of heart failure, but the significant increase of these hormones (GH and cortisol) seems to be significant negative prognostic markers.
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PMID:[The prognostic value of activation of the hypophyseal and adrenal cortical systems in severe heart failure]. 911 59

In experimental models where chronic inappropriate (relative to sodium intake and intravascular volume) elevations in circulating mineralocorticoids (aldosterone or deoxycorticosterone) are created, a reactive fibrosis with vascular remodeling is observed in systemic organs and the heart. Until recently, it was assumed that aldosterone was derived solely from adrenal glands via the circulation; however, there is now convincing evidence that cells of the heart and vasculature express genes responsible for the formation of both aldosterone and corticosterone and are capable of producing these steroids. Vascular endothelial and smooth muscle cells express CYP11B1 and CYP11B2, genes responsible for 11 beta -hydroxylase and aldosterone synthase, respectively. Furthermore, smooth muscle cells elaborate aldosterone. There is evidence that similar regulatory mechanisms operate in vascular cells as in adrenal cortex, since aldosterone synthase and 11 beta -hydroxylase expression are differentially modulated by low sodium/high potassium, angiotensin II and ACTH. It is likely that such localized corticosteroid production also occurs at sites of tissue repair, where populations of collagen-producing myofibroblasts, nourished by a neovasculature, predominate. Using a subcutaneous pouch model of granulation tissue we have obtained compelling data which would support such a notion. The mineralocorticoid receptor antagonist, spironolactone, severely attenuates pouch formation over a 2-week period and significantly reduces pouch wall hydroxyproline concentration. This effect is apparent even following adrenalectomy, when circulating corticosteroids are undetectable; however, with adrenalectomy alone, pouch formation is barely affected. This we took to be a possible indication of an effect of local, non-adrenal steroids in maintaining pouch tissue. Spironolactone inhibits angiogenesis. A recent clinical study demonstrates the efficacy of low-dose spironolactone in enhancing survival in patients with advanced chronic cardiac failure. Although it is not known how spironolactone brings about such an improvement in survival, we would propose that inhibition of fibrous tissue formation and/or angiogenesis might be important contributory factors. Further studies are required to address the relative contributions of circulating vs local aldosterone in promoting normal vs pathologic connective tissue formation.
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PMID:Extra-adrenal mineralocorticoids and cardiovascular tissue. 1037 93

Woman 75-year-old treated 30 years for syndrome of acromegaly refused pituitary surgery and irradiation. Five years and nine months before death she had a colon carcinoma successfully removed. Multinodular hyperfunctional goitre was treated with carbimazole. For six last years of life corticosteroids were given as a replacement therapy. Her cause of death was the heart failure due to acromegalic heart disease. In autopsy a large intrasellar and extrasellar pituitary adenoma without rests of nonneoplastic tissue was found. Nevertheless the target peripheral endocrine glands except ovaries, were not atrophic. A multinodular goitre and diffuse adrenocortical hyperplasia were revealed. Histology, and immunohistochemistry demonstrated that mot neoplastic cells were producing GH and ACTH, dispersly Prl, scattered cells were positive for beta-subunit of FSH, LH, TSH. Electron microscopy proved most of the cells to be densely granulated. We classify the adenoma according to the newly proposed WHO pituitary tumours classification (1) as plurihormonal, hyperfunctional, extrasellar, typical adenoma from densely granulated cells. We conclude that in plurihormonal adenomas with dominant (in the case referred acromegalic) symptomatology the additional hormonal production should be monitored as a possible source of important complications.
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PMID:[Multihormonal and multifunctional hypophyseal adenoma and the acromegaly syndrome]. 1104 8

An extremely ill patient, with Cushing's syndrome caused by an ACTH-secreting pituitary macroadenoma, experienced complications of end-stage cardiomyopathy, profound psychosis, and multiple metabolic disturbances. Initially treated unsuccessfully by a combination of conventional surgical, medical, and radiotherapeutic approaches, he responded dramatically to high-dose long-term mifepristone therapy (up to 25 mg/kg x d). Treatment efficacy was confirmed by the normalization of all biochemical glucocorticoid-sensitive measurements, as well as by the significant reversal of the patient's heart failure, the resolution of his psychotic depression, and the eventual unusual return of his adrenal axis to normal. His 18-month-long mifepristone treatment course was notable for development of severe hypokalemia that was attributed to excessive cortisol activation of the mineralocorticoid receptor, which responded to spironolactone administration. This case illustrates the efficacy of high-dose long-term treatment with mifepristone in refractory Cushing's syndrome. The case also demonstrates the potential need for concomitant mineralocorticoid receptor blockade in mifepristone-treated Cushing's disease, because cortisol levels may rise markedly, reflecting corticotroph disinhibition, to cause manifestations of mineralocorticoid excess.
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PMID:Successful long-term treatment of refractory Cushing's disease with high-dose mifepristone (RU 486). 1150 80


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