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

A patient with acromegaly is described with a relatively small eosinophilic adenoma of the hypophysis, the cardiopathy standing out on the foreground of the clinical pictrire, due to which it has for a long time been interpreted as a primary cardiac ailment. The cardiac disorder proceeds with cardiomegaly, conductivity disturbances and left, quickly progressing into complete and resistant to treatment cardiac insufficiency. The problem of the origination of the so called primary cardiac insufficiency is discussed, resulting from the direct effect of STH upon myocardium.
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PMID:[Acromegalic cardiopathy]. 14 29

Unexplained cardiomegaly with cardiac failure was observed in a 42-year-old woman in whom a pituitary tumour had been treated by radiotherapy five years previously. She had been amenorrhoeic for 10 years. Thyroid and adrenal function was normal. Despite treatment with digitalis and diuretic, her cardiac disease progressed until she died suddenly at the age of 45. Hyperprolactinaemia was evident some weeks before death, her serum concentration of 68 ng/ml being well above both the reported normal range (2--20 ng/ml) and the concentrations in eight female controls being treated for severe cardiac failure (5--25 ng/ml). Although the association of these two disorders might merely represent coincidence, heart disease with similar features is common in acromegaly and does not correlate with plasma growth hormone concentration. Since prolactin is known to exert metabolic growth hormone-like effects in animals and in man, the possibility should be considered that prolactin hypersecretion might induce or maintain cardiac disease in some patients with pituitary tumours. A preliminary survey of 35 subjects with hyperprolactinaemia has shown five with raised blood pressure and four, two of whom were normotensive, with cardiomegaly on chest radiography.
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PMID:Cardiomegaly and heart failure in a patient with prolactin-secreting pituitary tumour. 15 31

Examination of the cardiovascular apparatus (cv) of 25 acromegalic patients revealed an increased incidence of cardiovascular pathology as against normal individuals. Acromegalic patients with arterial hypertension (AH) show a twice higher incidence of ischemic cardiopathy, cardiomegaly with obvious or latent cardiac failure, arrhythmias, which frequently lead to death. The uncertain pathogeny of cardiomyopathy implied: hypoxia due to heart hypertrophy (over 500 g and increased cross-section of the fibre to over 26/mu), adrenergic deficiency resulting from increased protein synthesis and decrease in thyrosine, a precursor of myocardic cathecolamines. The increased incidence of coronary pathology is favoured in acromegalic patients by diabetes, hyperlipoproteinemia, low endogenous heparin, increased ureic acid and platelet adhesivity. Hypophysectomy by hypophysolysis (20 cases) brings relief and cures cardiovascular pathology, reduces AH, corrects the coronary risk factors, cures hypophyseal diabetes. The existence of AH and cardiovascular pathology is an indication for surgical treatment in evolutive acromegaly.
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PMID:Cardiovascular pathology in acromegaly and some effects of the 90 yttrium implant in the hypophysis. 69 1

Heart disease frequently occurs in advanced acromegaly. In order to investigate cardiac mass and function in acromegaly in the absence of obvious cardiac disease, we performed Doppler echocardiography in 15 asymptomatic acromegalic patients (six of them had systemic hypertension). The data were compared with those of a group of 10 age-matched controls. Left ventricular mass index (LVMI) was increased in acromegaly (110 +/- 32 vs 32 +/- 12 g m-2, P = 0.02), but shortening fraction and systolic time intervals did not differ. Mitral EF slope was decreased (80 +/- 21 vs 101 +/- 30 mms-1, P less than 0.02), while the duration of the isovolumic relaxation period (IRP) was increased (92 +/- 13 vs 69 +/- 16 ms, P less than 0.01). Hypertensive acromegalic patients (n = 6) had a higher LVMI than normotensive acromegalic patients (n = 9) (133 +/- 27 vs 94 +/- 24 g m-2, P = 0.02) and this was confirmed by a meta-analysis of data in the literature: the prevalence of hypertrophy was 76% in the presence of hypertension vs 50% in its absence, P less than 0.002. IRP was prolonged in normotensive acromegalic patients vs normal controls (90 +/- 11 vs 69 +/- 16 ms, P less than 0.01). In conclusion, subclinical cardiac abnormalities occur frequently in acromegaly in the absence of obvious heart disease, and hypertrophy is observed in asymptomatic hypertensive acromegaly. Moreover, diastolic abnormalities are found in asymptomatic acromegaly and could be caused by several heart-related factors.
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PMID:Cardiac hypertrophy and function in asymptomatic acromegaly. 183 May 50

The aim of this study was to assess the effects a long-acting somatostatin analogue (octreotide) had on the heart function of acromegalic patients. Five patients fulfilling clinical criteria of active acromegaly without symptoms of heart dysfunction, were treated with increased doses of octreotide (300, 600, 900, 1,200 and 1,500 micrograms/daily) over a period of six months. Growth hormone (GH) profiles were carried out during each different dose of octreotide. M-Mode, two dimensional and Doppler echocardiographic evaluation were performed both before and after treatment. Although the GH levels of all patients dropped after each increment of the octreotide, the responses were not homogeneous. Six months after the onset of treatment, echocardiographic studies revealed a significant reduction in the interventricular septum thickness (IVST) (p less than 0.05) and Doppler analyses showed an increase in the early diastolic transmitral flow velocity (p less than 0.05). Our results indicate that octreotide is capable of reversing acromegalic cardiopathy, since it not only reduces GH levels to within normal limits but improves left ventricular hypertrophy and distensibility without modifying contractility.
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PMID:Acromegalic cardiopathy improves after treatment with increasing doses of octreotide. 204 21

Acromegaly is associated with an increased cardiac morbidity and mortality, but it is not clear whether this is the result of increased incidence of hypertension and coronary heart disease or of a specific disease of heart muscle. Thirty four acromegalic patients were studied by non-invasive techniques. Seven of these patients had raised plasma concentrations of growth hormone at the time of study; three were newly diagnosed and had not received any treatment. Hypertension was present in nine (26%) but only three (9%) had electrocardiographic left ventricular hypertrophy. Echocardiography showed ventricular hypertrophy in 12 (48%) and increased left ventricular mass in 17 (68%) patients. Holter monitoring detected important ventricular arrhythmias in 14 patients. Thallium-201 scanning showed evidence for coronary heart disease in eight patients. Systolic time intervals were normal except when there was coexistent ischaemic heart disease. A comparison between 19 acromegalic patients with no other detectable cause of heart disease and 22 age matched controls showed appreciably abnormal left ventricular diastolic function in the group with acromegaly. The abnormalities shown did not correlate with left ventricular mass or wall thickness. There was no difference in diastolic function between patients with active acromegaly and those with treated acromegaly. Hypertensive acromegalic patients had worse diastolic function than hypertensive controls, suggesting that hypertension may further impair the left ventricular diastolic abnormality in acromegaly. This is the first study to find evidence of subclinical cardiac diastolic dysfunction in acromegaly and it supports the suggestion that there is a specific disease of heart muscle in acromegaly.
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PMID:Subclinical cardiac dysfunction in acromegaly: evidence for a specific disease of heart muscle. 239 Mar 94

In a series of 256 patients with acromegaly, 10 had evidence of heart disease for which no explanation apart from the acromegaly could be found. Heart disease presented with effort dyspnoea, cardiac failure, palpitation, ECG changes or cardiomegaly. Initial chest radiographs showed cardiac enlargement in seven patients. Electrocardiograms were abnormal in nine patients with repolarisation disorders or intraventricular conduction defects. Rhythm disturbances were found in six. Echocardiograms were performed on six patients; all were abnormal showing left ventricular hypertrophy or impaired function. In five patients radionuclide ventriculography was also performed. Cardiac catheterisation was undertaken on seven patients; all showed either hypertrophy or dilatation of the left ventricle. Coronary arteries were widely dilated in two patients and in another there was dilation of the proximal segment only. In six of the 10 patients, acromegaly was cured by transsphenoidal surgery. This resulted in limited improvement of cardiac function in two patients only. Of the four patients who were not cured, three died and one was lost to the study. Four patients in total died and autopsies were obtained in two: one showed changes suggesting myocarditis and the other diffuse fibrosis. It is concluded that acromegaly may infrequently lead to heart disease, and that if recognised at an early stage progression may, in a proportion of patients, be arrested by successful treatment.
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PMID:Acromegalic heart disease: influence of treatment of the acromegaly on the heart. 296 20

Thirty eight acromegalic patients (A) and a control group (C) of subjects without heart disease, were studied with echocardiography. Acromegalies were divided in two groups, A1 and A2, who had increase or normal serum growth hormone (GH) levels respectively after treatment (pituitary adenectomy and/or bromocriptine), at the time of the study. In acromegalic patients (A) mean left ventricular (LV) dimensions were normal while LV wall and septal thickness, LV mass and left atrial (LA) dimension were increased compared to control subjects. LVH was present in 79% of acromegalic patients. Asymmetric septal hypertrophy (ASH) was found in 10,5% of our patients. In group A1, IVS, LVPW, LVMM/m2 were significantly increased as compared to group A2. Fractional shortening (FS), ejection fraction (EF), mean velocity of circumferential fibre shortening (Vcf), frequency-normalized Vcf (Vcfn), posterior left ventricular wall velocity (PWV), and normalized PWV (PWVn) were normal in both groups. In patients with active acromegaly (Al) IVS and LVMM/m2 correlated well with the total duration of the disease (r=0.550 p less than 0.01 for IVS; r=0.624 p less than 0.01 for LVMM/m2) and with the duration of acromegaly before treatment (r=0.568, p less than 0.01 for IVS; r=0.500 p less than 0.01 for LVMM/m2). Furthermore a positive correlation was found between IVS and GH levels (r=0,550 p less than 0.01). Concomitant coronary artery disease and or hypertension did not seem to play any role in causing the above mentioned echocardiographic changes. Echocardiography is useful in assessing the cardiac involvement in patients with acromegaly.
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PMID:[Acromegalic cardiomyopathy: an echocardiographic study]. 688 53

A 64-year-old woman with active acromegaly of 33 years' duration, severe carpal tunnel syndrome, and subclinical heart disease was treated with bromocriptine mesylate. Within eight months of therapy, basal growth hormone (GH) levels decreased from 90.0 to 7.0 ng/mL, and hand volume was reduced from 375 to 295 mL. Concomitantly, echocardiographic studies showed normal left ventricular size and function. Electromyographic studies demonstrated normal function in both median nerves. Bromocriptine may correct cardiac dysfunction and carpal tunnel syndrome in acromegaly either by reduction of GH oversecretion or by a direct effect of bromocriptine on dopamine receptors in the heart and peripheral nerve endings.
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PMID:Bromocriptine for an acromegalic patient. Improvement in cardiac function and carpal tunnel syndrome. 742 Jun 85

GH exerts direct effects on myocardial growth and function. Evidence from laboratory models shows that GH (or IGF-I) induces mRNA expression for specific contractile proteins and myocyte hypertrophy. Furthermore, GH increases the force of contraction and determines myosin phenoconversion toward the low ATPase activity V3 isoform. These data provide plausible explanations for the cardiac abnormalities observed in clinical settings of excessive or defective GH production. In acromegaly, the functional consequences of GH excess initially prevail (hyperkinetic syndrome), followed by alterations of cardiac function when myocardial hypertrophy develops. This involves both ventricles and is purposeless because it occurs without increased wall stress. Hypertrophy also entails proliferation of the myocardial fibrous tissue that leads to interstitial remodeling. The functional consequence is an impaired ventricular relaxation that causes a diastolic dysfunction, followed by impairment of systolic function. In untreated disease, cardiac performance slowly but inexorably deteriorates and heart failure eventually develops. Several lines of evidence support the specificity of heart disease in acromegaly. Particularly demonstrative are the recent studies in which GH production was suppressed by octreotide, with a consequent significant regression of hypertrophy and improvement of cardiac dysfunction. It is not yet established whether full recovery of normal cardiac morphology and function is possible after correction of GH excess. The point is not a minor one since the possibility to revert, albeit partially, myocardial fibrosis is of great relevance to the control of cardiac hypertrophy in general. GHD leads to a reduced mass of both ventricles and to impaired cardiac performance with low heart rate (hypokinetic syndrome). These alterations are particularly evident during physical exercise and might provide an important contribution to the reduced exercise capacity of GHD patients, in addition to the reduced muscle mass and strength. The data also support a role of GH in the maintenance of a normal cardiac structure and performance. The hypokinetic syndrome is well documented in young patients in whom GHD began very early in their childhood. In contrast, the data in adult-onset GHD are less consistent. This suggests that the consequences of GHD are more relevant if the disorder starts during early heart development. As observed with other abnormalities associated with GHD, cardiac dysfunction is also susceptible to marked improvement by hrGH. This observation lends further support to the proposal to treat these patients with replacement therapy.
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PMID:Growth hormone and the heart. 784 68


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