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Query: UMLS:C0018801 (
heart failure
)
72,216
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Cardiac involvement is common in
acromegaly
. Evidence for cardiac hypertrophy, dilation and diastolic filling abnormalities has been widely reported in literature. Generally, ventricular hypertrophy is revealed by echocardiography but early data referred increased cardiac size by standard X-ray. Besides, echocardiography investigates cardiac function and value disease. There are new technologic advances in ultrasonic imaging. Pulsed Tissue Doppler is a new non-invasive ultrasound tool which extends Doppler applications beyond the analysis of intra-cardiac flow velocities until the quantitative assessment of the regional myocardial left ventricular wall motion, measuring directly velocities and time intervals of myocardium. The radionuclide techniques permit to study better the cardiac performance. In fact, diastolic as well as systolic function can be assessed at rest and at peak exercise by equilibrium radionuclide angiography. This method has a main advantage of providing direct evaluation of ventricular function, being operator independent. Coronary artery disease has been poorly studied mainly because of the necessity to perform invasive procedures. Only a few cases have been reported with
heart failure
study by coronarography and having alterations of perfusion which ameliorated after somatostatin analog treatment. More recently, a few data have been presented using perfusional scintigraphy in
acromegaly
, even if coronary artery disease does not seem very frequent in
acromegaly
. Doppler analysis of carotid arteries can be also performed to investigate atherosclerosis: however, patients with active
acromegaly
have endothelial dysfunction more than clear-cut atherosclerotic plaques. In conclusion, careful assessments of cardiac function, morphology and activity need in patients with
acromegaly
.
...
PMID:Cardiovascular complications in acromegaly: methods of assessment. 1250 75
Experimental and clinical studies have recently demonstrated that the growth hormone-insulin-like growth factor-I (GH-IGF-I) system is involved in the regulation of cardiac structure and function. Patients with
acromegaly
have an increased propensity of developing cardiovascular complications, such as ventricular hypertrophy with interstitial fibrosis. Conversely, patients with GH deficiency can exhibit ventricular dysfunction, increased vascular thickness, and an increased number of atheromatous plaques. In both groups of patients these abnormalities may be partially reverted by normalizing GH-IGF-I levels. In experimental or human chronic
heart failure
(CHF), GH administration increases ventricular mass and cardiac performance and reduces pulmonary vascular resistance. The mechanism by which this occurs is still unclear, but seems to involve calcium channels and non-endothelium-mediated vasodilatation. Randomized trials studying CHF patients contradict these results, highlighting that, in patients with
heart failure
, the response to GH therapy appears to be variable, and is probably influenced either by acquired GH resistance or by baseline levels of hormones. Due to the small number of patients examined to date, larger, randomized, controlled studies are needed.
...
PMID:Does growth hormone play a role in chronic heart failure? 1263 81
Growth hormone (GH) acting through locally produced insulin--like growth factors stimulates myocardial hypertrophy and increases myocyte contractility. Many people with growth hormone deficiency (GHD) present a lower left ventricular mass, reduced ejection fraction and lower exercise tolerance. Recombinant human growth hormone (rhGH) administration gives a chance to correct these disturbances. On the other hand excessive levels of GH (for example in
acromegaly
) may induce
heart failure
too. Initially, cardiac hypertrophy is an adaptive response, but with time, in untreated cases, it leads to congestive heart failure. Mentioned information inclined many authors to undertake researches on rhGH application in severe
heart failure
in patient with idiopathic dilated cardiomyopathy and coronary disease. RhGH improved treatment let these patients reach heart transplantation.
...
PMID:[Clinical and metabolic effects of recombinant human growth hormone in cardiac insufficiency]. 1459 78
Short-term GH or IGF-I excess provides a model of physiological cardiac growth associated with functional advantage. The physiological nature of cardiac growth is accounted for by the following: (i) the increment in cardiomyocyte size occurs prevalently at expense of the short axis. This is the basis for the concentric pattern of left ventricular (LV) hypertrophy, with consequent fall in LV wall stress and functional improvement; (ii) cardiomyocyte growth is associated with improved contractility and relaxation, and a favourable energetic setting; (iii) the capillary density of the myocardial tissue is not affected; (iv) there is a balanced growth of cardiomyocytes and nonmyocyte elements, which accounts for the lack of interstitial fibrosis; (v) myocardial energetics and mechanics are not perturbed; and (vi) the growth response is not associated with the gene re-programming that characterizes pathologic cardiac hypertrophy and
heart failure
. Overall, the mechanisms activated by GH or IGF-I appear to be entirely different from those of chronic
heart failure
. Not to be neglected is also the fact that GH, through its nitric oxide (NO)-releasing action, contributes to the maintenance of normal vascular reactivity and peripheral vascular resistance. This particular kind of interaction of GH with the cardiovascular system accounts for: (i) the lack of cardiac impairment in short-term
acromegaly
; (ii) the beneficial effects of GH and IGF-I in various models of
heart failure
; (iii) the protective effect of GH and IGF-I against post-infarction ventricular remodelling; (iv) the reversal of endothelial dysfunction in patients with
heart failure
treated with GH; and (v) the cardiac abnormalities associated with GH deficiency and their correction after GH therapy. If it is clear that GH and IGF-I exert favourable effects on the heart in the short term, it is equally undeniable that GH excess with time causes pathologic cardiac hypertrophy and, if it is not corrected, eventually leads to
cardiac failure
. Why then, at one point in time in the natural history of
acromegaly
, does physiological cardiac growth become maladaptive and translate into heart failure? Before this transition takes places, the acromegalic heart shares very few features with other models of chronic
heart failure
. None of the mechanisms involved in the progression of
heart failure
is clearly operative in
acromegaly
, save for the presence of insulin-resistance and mild alterations of lipoproteins and clot factors. Is this enough to account for the development of heart failure? Probably not. On the other hand, it must be stressed that GH and IGF-I activate several mechanisms that play a protective role against the development of
heart failure
. These include ventricular unloading, deactivation of neurohormonal components, antiapoptotic effect and enhanced vascular reactivity. Ultimately, all data available concur to hypothesize that acromegalic cardiomyopathy represents a progressive model of cardiac hypertrophy in which the cardiotoxic and pro-remodelling effect is intrinsic to the excessive and unrestrained myocardial growth.
...
PMID:Growth hormone, acromegaly, and heart failure: an intricate triangulation. 1497 6
Cardiovascular morbidity and mortality are increased in
acromegaly
. In fact, GH and IGF-I excess induces a specific cardiomyopathy. The early stage of
acromegaly
is characterized by the hyperkinetic syndrome (high heart rate and increased systolic output). Frequently, concentric biventricular hypertrophy and diastolic dysfunction occur in
acromegaly
, leading to an impaired systolic function ending in
heart failure
if the disease is untreated or unsuccessfully untreated. Besides, abnormalities of cardiac rhythm and of valves have been also described in
acromegaly
. The coexistence of other complications, such as arterial hypertension and diabetes, aggravates the acromegalic cardiomyopathy. The suppression of GH/IGF-I following an efficacious therapy could decrease left ventricular mass and improve cardiac function. In conclusion, a careful evaluation of cardiac function, morphology and activity seems to be mandatory in
acromegaly
.
...
PMID:Cardiovascular complications in acromegaly. 1528 42
Cardiovascular disease is claimed to be one of the most severe complications of
acromegaly
, contributing significantly to mortality in this disease. In fact, an excess of growth hormone (GH) and insulin-like growth factor 1 (IGF-I) causes a specific derangement of cardiomyocytes, leading to abnormalities in cardiac muscle structure and function, inducing a specific cardiomyopathy. In the early phase of
acromegaly
the excess of GH and IGF-I induces a hyperkinetic syndrome, characterized by increased heart rate and increased systolic output. Concentric hypertrophy is the most common feature of cardiac involvement in
acromegaly
, found in more than two thirds of patients at diagnosis. This abnormality is commonly associated with diastolic dysfunction and eventually with impaired systolic function ending in
heart failure
, if the GH/IGF-I excess is left untreated. In addition, abnormalities of cardiac rhythm and of heart valves have also been described in
acromegaly
. The coexistence of other complications, such as arterial hypertension and diabetes mellitus, aggravates acromegalic cardiomyopathy. Successful control of
acromegaly
induces a decrease in left ventricular mass and an improvement in diastolic function, while the effects of GH/IGF-I suppression on systolic function are more variable. However, since cardiovascular alterations in young patients with short disease duration are milder than in those with longer disease duration, it is likely to be easier to reverse and/or arrest acromegalic cardiomyopathy in young patients with early-onset disease. In conclusion, careful assessments of cardiac function, morphology, and activity are required in patients with
acromegaly
. An early diagnosis and prompt effective treatment are important in order to reverse acromegalic cardiomyopathy.
...
PMID:Cardiac abnormalities in acromegaly. Pathophysiology and implications for management. 1533 Jun 78
Several experimental and clinical studies have indicate that the heart is an end-organ of GH action. Patients with either childhood- or adulthood-onset GH deficiency (GHD) have abnormalities of cardiac structure and function, such as reduced cardiac mass, impaired diastolic filling and reduced left ventricular response at peak exercise. These cardiovascular abnormalities can be reversed, at least partially, after GH replacement therapy. On the other hand, the chronic overproduction of GH and IGF-I in
acromegaly
leads to the development of a specific cardiomyopathy. Concentric cardiac hypertrophy occurs in more than two-thirds of patients at diagnosis and is commonly associated with diastolic dysfunction. In later stages, impaired systolic function ending in
heart failure
can occur if GH/IGF-I excess is not controlled. Additionally, acromegalic cardiomyopathy is complicated by abnormalities of cardiac rhythm and cardiac valves. Successful control of
acromegaly
is accompanied by a decrease of the left ventricular mass and improvement of cardiac function. These beneficial effects appear earlier in young patients with short disease duration than in elderly patients. In conclusion, GH and IGF-I play a main role in the regulation of cardiac development and performance.
...
PMID:The heart: an end-organ of GH action. 1533 52
Cardiomyopathy is a major cause of death in overt
acromegaly
. Recent progress in research has increasingly revealed the molecular mechanisms concerning growth hormone and insulin-like growth factor in the development of
heart failure
. In this article, we propose mechanisms according to which
heart failure
occurs, and we aim to extrapolate this knowledge to more general processes involved in
heart failure
.
...
PMID:Acromegaly and heart failure: revisions of the growth hormone/insulin-like growth factor axis and its relation to the cardiovascular system. 1547 31
Cardiovascular complications are a major cause of morbidity and mortality in patients with
acromegaly
. Normalization of GH secretion is associated with an improvement in structural and functional cardiac abnormalities. However, the long-term cardiac effects of treatment for
acromegaly
have not been studied in patients who have already developed chronic congestive heart failure (CHF). We reviewed the charts of 330 consecutive patients with
acromegaly
treated in two French and Belgian centers since 1985. Ten patients with both
acromegaly
and CHF (eight men, two women, mean age 49.7 yr) were studied retrospectively. One of them was excluded because CHF was due to severe aortic stenosis.CHF (New York Heart Association stages III-IV and echocardiography showing dilated hypokinetic cardiomyopathy with left ventricular systolic dysfunction and a left ventricular ejection fraction less than 45%) was diagnosed before, concomitantly, or after
acromegaly
in, respectively, two, five, and two patients. Three patients were referred with terminal
heart failure
requiring transplantation.One patient had transient CHF associated with a hypertensive crisis. The other eight patients had symptomatic chronic CHF. Control of GH hypersecretion failed, totally or partially, in three patients: one had a long-term survival, and the two others died at 1 and 5 yr. Good GH control was achieved in five patients: four of these are still alive 2-16 yr after diagnosis of CHF, their clinical status is stable or improved, and their quality of life is good. Overall, the 1- and 5-yr mortality (or transplantation) rates for patients with chronic symptomatic CHF were 25% (2 of 8 patients) and 37.5% (3 of 8 patients), respectively. In conclusion, less than 3% of acromegalic patients developed CHF in this study. Although effective treatment of
acromegaly
improved short-term cardiovascular status, its impact on long-term survival is questionable.
...
PMID:Long-term outcome of patients with acromegaly and congestive heart failure. 1553 75
Clinical studies in patients with
acromegaly
have shown that growth hormone (GH) exerts both short- and long-term effects on the structure and function of the heart. Moreover, chronic growth hormone deficiency (GHD) has been associated with impaired cardiac performance, low heart rate and impaired left ventricular systolic function. Exercise capacity in patients with GHD is significantly reduced and in some severely affected individuals, dilated cardiomyopathy and
heart failure
has been reported. GHD has also been associated with a number of risk factors for cardiovascular disease. Altered lipoprotein metabolism and elevated fibrinogen and plasminogen activator inhibitor-1 activity are associated with GHD, and the risk of hypertension is increased in GH-deficient men. Subcutaneous and intra-abdominal fat mass have also been found to be abnormally high in these patients. These effects may contribute to an increased risk of death from cardiovascular disease. GH is therefore an important factor in the development and function of the cardiovascular system. In this paper, the effects of GH on the physiological mechanisms of the cardiovascular system are discussed, including the effect of GHD on cardiovascular disease risk. We will also discuss the effects of long-term GH replacement therapy in this patient population.
...
PMID:Cardiovascular disease and risk factors: the role of growth hormone. 1559 64
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