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 15,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-seven patients with acromegaly had echocardiograms performed to delineate the ventricular septum, left ventricular posterior wall and mitral valve. Left ventricular function was assessed by calculating the systolic internal dimensional shortening of the left ventricle. Six patients met the criteria for asymmetric septal hypertrophy and eight had concentric left ventricular hypertrophy. The remaining 13 patients were categorized as "normal," although six had septal measurements greater than 11 mm. The group with asymmetric septal hypertrophy had significantly greater percentage of internal dimensional shortening during systole than either the normal group (p less than 0.05) or the group with left ventricular hypertrophy (p less than 0.01). Initial mean growth hormone levels were considerably higher in the group with left ventricular hypertrophy than in the normal group (93 versus 34 ng/ml). Thus, echocardiographic abnormalities are common in acromegaly, and patients with asymmetric septal hypertrophy and acromegaly appear to have significantly increased ventricular ejection. Many of the patients with left ventricular hypertrophy have no evidence of clinical cardiovascular disease, and their left ventricular hypertrophy may be related to higher initial growth hormone levels.
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PMID:Acromegaly and the heart. An echocardiographic study. 15 93

Cardiac enlargement and dysfunction are common in patients with acromegaly. Whether these changes are a direct consequence of growth hormone excess is obscured by the high frequency of hypertension, diabetes mellitus, or atherosclerosis in acromegalic patients. In this study, the effects of chronic elevations of growth hormone (GH) upon the heart were studied in rats with GH-producing tumours implanted subcutaneously for 4 weeks. Geometric measurements and histology were employed to detect the presence of cardiac changes. Increased mass was observed in the tumour-bearing animals. When compared with controls, in tumour-bearing rats there were significantly greater (P less than 0.05) right (0.17 +/- 0.03 v. 0.13 +/- 0.01 g) and left (0.62 +/- 0.05 v. 0.50 +/- 0.04 g) ventricular weights, external cardiac dimensions, and myocardial fibre diameters (9.4 +/- 0.6 v. 8.3 +/- 0.4 micron). However, these increases were linearly-related to increased body mass in the tumour-bearing group so that the ratios of ventricular weights to body weight were similar in both groups. Furthermore, no pathologic changes such as myocardial fibrosis or asymmetric septal hypertrophy were present in the tumour-bearing rats. Thus, under the conditions of this study, growth hormone excess induced cardiac growth, which appeared to represent a manifestation of generalized body growth rather than a distinct pathologic process.
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PMID:Cardiac morphology in rats with growth hormone-producing tumours. 293 34

M-mode echocardiography was used to study cardiac involvement in 78 patients with acromegaly. Proportionate concentric or eccentric left ventricular hypertrophy (LVH) was a common finding. Calculated left ventricular mass (LVM) was increased significantly in a hormonally active disease group compared to an inactive disease group or a control group (153 +/- 7 vs. 96 +/- 8 and 89 +/- 3 g/m2 resp.; p less than 0.001 for both). The increase of LVM in hormonally active disease is due to predominantly LV dilatation, whereas associated hypertension, if present, aggravates the LVH exclusively due to thickening of the LV wall. Hypocorticalism, if present, does not influence the degree of LVH. Asymmetric septal hypertrophy was not found to be specific for acromegaly and was seen in only 7.7% of patients. There was no correlation between LVM and both the plasma levels of growth hormone and duration of disease. On the basis of a retrospective analysis of LVM in successfully treated patients the authors conclude that specific heart muscle disease in acromegaly, manifesting itself as LVH, is slowly reversible after cessation of the growth hormone hyperproduction.
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PMID:The nature of cardiac hypertrophy in acromegaly: an echocardiographic study. 316 77

We used echocardiography to study anatomic and functional changes of the heart in 25 patients with acromegaly. Asymmetric septal hypertrophy was found in 10 patients, in the range of 12 to 30 mm, with an average of 16 mm. The degree of septum-thickness was severe in 1 case, marked in 5 cases and mild in 4 cases. Concentric left ventricular hypertrophy was present in 1 patient. In 8 patients the left ventricle was normal and left ventricular dilatation of more than 60 mm was present in 6 cases. Except in one patient, the ejection fraction was decreased in the dilated group, indicating diminished myocardial contractility. The growth hormone level was higher in patients with left ventricular hypertrophy as compared to those patients with normal or dilated left ventricles. In acromegaly primary myocardial hypertrophy may be related to the growth hormone level.
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PMID:The heart in acromegaly: an echocardiographic study. 622 Sep 83

Clinical examinations including echocardiography were performed for 14 acromegalic patients (five men and nine women, whose mean age was 48.6 years). Three of these had hypertension (HT) above 160/95 mmHg, three had diabetes mellitus (DM). Their cardiac sizes and functions were correlated with the durations of disease and plasma growth hormone (GH) levels. The incidences of HT and DM were also evaluated. Three of 14 patients (22%) had increased cardiothoracic ratios (greater than 55%). Electrocardiographic abnormalities were noted in three patients including two with left ventricular hypertrophy (LVH) and one with interventricular conduction defects with abnormal Q waves. By echocardiography (Table 2), nine patients (64%) were judged to be normal. The remaining five patients (36%) had abnormal echocardiograms. These included LVH (sums of the interventricular and posterior wall thicknesses greater than or equal to 25 mm) in two (25 mm in Case 10, 30 mm in Case 11), increased left ventricular end-diastolic dimension (EDD greater than or equal to 55 mm) in one (72 mm in Case 14) and both abnormalities in two patients (Cases 12 and 13). Two patients (Case 13 and 14), whose %FS were 17% and 22%, respectively, had definite evidence of congestive heart failure. Two patients (Case 11 and 13) met the diagnostic criteria for asymmetric septal hypertrophy. One patient with echocardiographic LVH and another who had increased EDD with LVH had histories of HT (Case 11 and 12). Plasma GH levels in patients with LVH were greater than 100 ng/ml (Cases 10 and 11). The left ventricular hypertrophy and/or increased EDD observed in these patients seemed related to the duration of acromegaly but not to the presence of DM. Myocardial biopsy of the right ventricle in two patients with congestive heart failure disclosed myocardial hypertrophy, myocardial fiber disarray, interstitial fibrosis and large nuclei.
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PMID:[The heart in acromegaly: an echocardiographic study]. 624 54

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

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.
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PMID:Doppler echocardiographic patterns in patients with acromegaly. 865 20