Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heart muscle disease in acromegaly manifests usually as cardiac hypertrophy. Based on a retrospective analysis, it was suggested that cardiac hypertrophy is slowly reversible after normalization of plasma growth hormone levels. The reversibility of acromegalic heart muscle disease during and after treatment of acromegaly was studied prospectively. A cohort of 78 patients was examined echocardiographically in 1981, and 38 survivors of this group were reexamined 10 years later. Patients were classified according to original hormonal activity in 1981, and change in hormonal activity during follow-up into the following 4 groups: group I--hormonally inactive for entire follow-up (n = 10); group II--hormonally active for entire follow-up (n = 11); group III--initially hormonally inactive with later resurgence (n = 6); and group IV--initially hormonally active with later normalization of growth hormone levels (n = 11). No significant echocardiographic changes occurred during follow-up in group I. Left ventricular posterior wall and septal diastolic thickness, and left ventricular mass increased significantly (all p < 0.05) in group II. Left ventricular posterior wall thickness, mass and diastolic volume increased significantly (p < 0.05, < 0.01 and < 0.001, respectively) in group III. On the contrary, there were significant decreases in left ventricular mass, and both diastolic and systolic left ventricular volumes (p < 0.01, < 0.05 and < 0.05, respectively) in group IV. It is concluded that both hypertrophy and dilatation of the left ventricle in acromegaly are slowly reversible after successful treatment. On the contrary, continuing or relapsed hyperproduction of growth hormone causes further deterioration of acromegalic heart disease.
 ...
PMID:Long-term echocardiographic follow-up of acromegalic heart disease. 832 85

The aim of this study was to investigate the effects of a 6-month octreotide treatment on cardiac mass and function by means of Doppler echocardiography in 11 normotensive patients affected with active acromegaly. The GH and insulin-like growth factor-I levels were normalized during octreotide therapy from 34 +/- 6.5 and 767.4 +/- 72.4 micrograms/L to 4.6 +/- 0.9 and 235 +/- 10.3 micrograms/L, respectively (P < 0.001; mean +/- SEM). After the 6-month treatment, we observed a significant decrease in the left ventricular mass index from 138 +/- 11 to 116 +/- 13 g/m2 (P < 0.001) and in the mean wall thickness/internal end-diastolic radius ratio from 0.47 +/- 0.1 to 0.44 +/- 0.1 (P < 0.001). No significant differences were found in systolic function indices, whereas diastolic filling indices improved over the course of the therapy; the isovolumic relaxation time decreased from 115 +/- 6 to 100 +/- 6 ms (P < 0.05), tricuspid late diastolic filling velocities decreased from 41 +/- 3 to 36 +/- 2 cm/s (P < 0.03), and tricuspid deceleration time decreased from 280 +/- 28 to 198 +/- 15 ms (P < 0.005); the ratio of early to late peak velocity of the right ventricular filling significantly increased from 1 +/- 0.01 to 1.3 +/- 0.1 (P < 0.03). A significant correlation was detected between left ventricular mass regression and increase in the early to late peak velocity ratio of the left ventricular filling (r = 0.62; P < 0.05). The results of this study show an improvement in cardiac structural and functional abnormalities during chronic treatment with octreotide, thus supporting the hypothesis of a specific heart disease secondary to high circulating GH levels.
 ...
PMID:Chronic treatment with the somatostatin analog octreotide improves cardiac abnormalities in acromegaly. 837 Jul

Dilated cardiomyopathy associated with acromegaly is rare, but may improve with octreotide, a somatostatin analogue. The authors give the first description here of paradoxical worsening in cardiac function during such treatment, with the onset of episodes of acute decompensation following each attempt at starting treatment. Thus worsening was confirmed objectively by a challenge test with octreotide: increased dyspnea, fall in shortening fraction and in echocardiographic cardiac output (of 17 to 14% and 4 to 3 l/min respectively), a decrease in isotopic ejection fraction from 15 to 6% and this in parallel with efficacy regarding hormone levels of GH and IGF1 and a reduction in tumour size by CT scan. No further episode of decompensation occurred after treatment was stopped permanently. The patient underwent a transplant 3 months later. Suppression of the positive inotropic effect of GH by octreotide, associated with an increase in peripheral resistance is suggested. A negative inotropic effect of this hormonal analogue on too advanced a case of heart disease is also a possibility.
 ...
PMID:[Dilated cardiomyopathy in acromegaly worsening under octreotide treatment. Apropos of a case]. 849 2

Cardiovascular problems have long been recognized as responsible for an increased morbidity and mortality in patients with acromegaly. The aim of the present study was to evaluate echocardiographically the prevalence of cardiomyopathy in a cohort of acromegalic patients and to analyze the results in relation to demographic, clinical and hormonal data. This study, a retrospective controlled clinical trial, was performed in 25 acromegalic patients, 12 men and 13 women aged 26-66 years (mean: 52.6). Fifteen patients had an active disease, 10 were cured by previous pituitary surgery. The same echocardiographic parameters were analyzed in 50 healthy subjects aged 30-70 years (mean: 51.4). Serum GH was determined on at least 4 samples drawn over 24 hours and plasma IGF-I on a single point. Standardized parameters of diastolic and systolic function were evaluated by real-time Doppler echocardiography. Twelve patients with active acromegaly underwent also 48-hour ECG registering. Left ventricular (LV) hypertrophy was found in 14/25 patients (56%). No difference was found between patients with active disease (53%) and patients with cured acromegaly (60%). LV mass index was significantly increased in acromegalics in comparison with healthy subjects (137 +/- 43 g/m2 vs 96 +/- 16 g/m2, p < 0.01) and also the indices of LV diastolic function were significantly impaired. Asymmetric septal hypertrophy was found only in one patient. Hypertension was detected in 9/25 patients (36%) without difference between patients with active or cured disease (40% vs 30%, NS). No significant correlation was found between hormonal or clinical data and echocardiographic findings. During Holter monitoring, heart rate of acromegalics was not significantly different from that of controls (78 +/- 12 bpm vs 72 +/- 10 bpm, NS) and only isolated supraventricular or ventricular premature complexes (Lown class 1) were detected. In conclusion, this study provides evidence of subclinical LV dysfunction in acromegaly in the absence of other known causes of heart disease and no significant difference in echocardiographic pattern was apparent between active or cured acromegalics.
 ...
PMID:Doppler echocardiographic patterns in patients with acromegaly. 865 20

Evidence has accumulated regarding acromegalic heart muscle disease which existence now appears to be unequivocal. We took an advantage of a large group of acromegalic patients being followed-up at our institution for a long time and have studied pattern, nature and reversibility of acromegalic heart disease. Its major manifestation is cardiac hypertrophy expressed especially as left ventricular hypertrophy. The cardiac hypertrophy is slowly reversible after normalization of plasma growth hormone levels due to successful treatment. This we have first suggested on the basis of a retrospective analysis of clinical and echocardiographic data in 78 patients with acromegaly and subsequently confirmed by a 10-year prospective follow-up of the original patient cohort. We have also showed that effective treatment of acromegaly with a new slow release somatostatine analogue lanreotide leads to regression of cardiac hypertrophy.
 ...
PMID:Heart disease in acromegaly. 871 97

Patients with acromegaly have significant morbidity and mortality, associated with cardiovascular disease. Acromegaly is often complicated by other diseases such as diabetes mellitus, hypertension, and coronary artery disease, so the existence of acromegalic cardiomyopathy remains uncertain. Cardiac performance was investigated in patients with uncomplicated acromegaly. A subgroup of hypertensive acromegalics was also studied. In addition, the effects of chronic octreotide therapy or surgery on cardiac structure and function in acromegaly were studied. Twenty-six patients and 15 healthy controls underwent gated blood-pool cardiac scintigraphy and echocardiography at rest and during exercise. Echocardiography was repeated after 6 months of octreotide therapy (n = 11). Cardiac scintigraphy was repeated after 12 and 24 months of octreotide therapy (n = 10) or 12 to 24 months after surgery (n = 8). ECG, blood pressure, and heart rate were monitored during cardiac scintigraphy. Left ventricular mass (LVM) was calculated from the findings of the echocardiography. Serum growth hormone (GH) levels and plasma insulin-like growth factor-1 (IGF-1) levels were monitored. LVM index was significantly higher (P < .003) in acromegalics than controls and in hypertensive acromegalics than normotensives, but all other indices of cardiac function were similar. Chronic octreotide decreased GH and IGF-1 levels and improved the structural abnormalities as measured by echocardiography. Chronic octreotide or surgery did not alter cardiac function parameters. Thus, important changes in cardiac structure and function occur in uncomplicated acromegaly, and improvements can be demonstrated after chronic octreotide therapy. Heart disease in acromegaly appears to be secondary to high circulating GH levels.
 ...
PMID:Cardiovascular aspects in acromegaly: effects of treatment. 876 83

A perioperative anesthetic management of a 69 year old woman with acromegaly whose clinical course was characterized by severe heart failure is described. The patient showed symptoms of massive cardiomegaly. Endocrine studies indicated that her pituitary tumor was active with hyperproduction of growth hormone. There was no demonstrable evidence for other known causes of heart disease. Following hormonal therapy using continuous subcutaneous infusion of somatostatin for about two months, there was improvement in daily activity and reduction in heart size. After the improvement of cardiac function, transsphenoidal hypophysectomy was performed under general anesthesia and its perioperative course was quite uneventful. We conclude that because cardiac involvement such as left ventricular dilatation in acromegaly might be reversible with proper treatment, any surgical procedure, as long as the case is elective, should be considered after hormone therapy.
 ...
PMID:[A patient with acromegalic heart disease--a case report]. 925 11

Growth hormone (GH), probably acting indirectly through locally produced insulin-like growth factor I, stimulates myocardial hypertrophy and increases myocyte contractility. In experimental models insulin-like growth factor I appears to be a key regulator of ventricular hypertrophy. Many adults with growth hormone deficiency (GHD) have reduced left ventricular mass, a lower ejection fraction, and reduced exercise tolerance. Elevated serum lipid levels, increased visceral fat, and early atheroma formation may contribute to an increased mortality rate from cardiovascular disease in these persons, but GH replacement therapy appears to correct many of these abnormalities. GH excess (acromegaly) results in cardiac hypertrophy that can progress to cardiac failure. Treatment with octreotide at least partially reverses cardiac hypertrophy and dysfunction. GH treatment may induce beneficial cardiac hypertrophy in adults without GHD who have dilated cardiomyopathy. Significant cardiac dysfunction has not been reported in children with GHD who are treated with GH, nor have adverse cardiac effects been reported with GH in short children without GHD, including those with Turner syndrome. We now have extensive experience with the therapeutic use of GH in children with cardiac structural abnormalities (e.g., Turner and Noonan syndromes, congenital heart disease), and such use appears to be safe. Furthermore, cardiac complications of GH in children without cardiac disease are rare. Continued observation to ensure that GH therapy has no long-term effects on cardiac anatomy or function in children is necessary.
 ...
PMID:Is growth hormone good for the heart? 925 33

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.
 ...
PMID:[Multihormonal and multifunctional hypophyseal adenoma and the acromegaly syndrome]. 1104 8

Acromegaly is a consequence of chronic growth hormone (GH) excess, due in the majority of cases to a GH-secreting pituitary adenoma, and occurring with a population prevalence of 60 per million and an incidence of 3-4 per million per year. Males and females appear to be equally affected with an average age of presentation of 44 years. Younger patients may have more aggressive tumours and higher GH concentrations. There is co-existent hyperprolactinaemia in about one third of cases, and a variable proportion of [figure: see text] tumours appear to have activating mutations of the gsp gene or other genetic abnormalities. Acute complications such as carpal tunnel syndrome, sweating and obstructive sleep apnoea are usually readily reversible with treatment of the condition, but chronic complications such as hypertension, diabetes and heart disease are less readily corrected and post-treatment GH levels of < 2.5 ug/L (5 mU/L) are needed to achieve the prevalence found in the general community. Such 'curative' levels of GH are achieved in only about 50% of patients with current therapies, and as a result there is an ongoing excess of patients with chronic complications of acromegaly leading to increased morbidity and mortality from the disorder, with observed-to-expected mortality ratios ranging from 1.6-3.3 and only approaching unity in those with growth hormone levels < 2.5 ug/L following treatment. Prognostic factors include in some studies the presence of diabetes and [table: see text] hypertension prior to diagnosis as well as measures of exposure to excessive growth hormone derived from the product of preoperative serum GH and the time from first symptoms to treatment. Overall, however, the most important prognostic variable appears to be the serum GH concentration achieved by treatment, with an increasing consensus that this needs to be < 2.5 ug/L (5 mU/L) to achieve cure of the condition.
 ...
PMID:Epidemiology of acromegaly. 1108 Nov 70


<< Previous 1 2 3 Next >>