Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

RGS family members are GTPase-activating proteins (GAPs) for heterotrimeric G proteins. There is evidence that altered RGS gene expression may contribute to the pathogenesis of cardiac hypertrophy and failure. We investigated the ability of RGS4 to modulate cardiac physiology using a transgenic mouse model. Overexpression of RGS4 in postnatal ventricular tissue did not affect cardiac morphology or basal cardiac function, but markedly compromised the ability of the heart to adapt to transverse aortic constriction (TAC). In contrast to wild-type mice, the transgenic animals developed significantly reduced ventricular hypertrophy in response to pressure overload and also did not exhibit induction of the cardiac "fetal" gene program. TAC of the transgenic mice caused a rapid decompensation in most animals characterized by left ventricular dilatation, depressed systolic function, and increased postoperative mortality when compared with nontransgenic littermates. These results implicate RGS proteins as a crucial component of the signaling pathway involved in both the cardiac response to acute ventricular pressure overload and the cardiac hypertrophic program.
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PMID:RGS4 causes increased mortality and reduced cardiac hypertrophy in response to pressure overload. 1048 71

Hypertension is an important risk factor for cardiovascular morbidity and mortality. Hypertension is associated with the development of congestive heart failure by way of left ventricular hypertrophy, with left ventricular dilatation and through myocardial ischemia and left ventricular damage. Reports on the natural history of untreated hypertension indicate that at least 50% of affected subjects develop congestive heart failure. Hypertension is an important precursor of heart failure, and still the most common risk factor for congestive heart failure in the population. In clinical trials, particularly in elderly patients, a reduction in the incidence of congestive heart failure has been observed. Despite increments in the use of antihypertensive drugs, mortality from congestive heart failure among the elderly is increasing. Moreover, several patients with hypertension are unaware, untreated and uncontrolled for the most important risk factor for congestive heart failure. For the primary prevention of heart failure, improvements in blood pressure control are of vast importance.
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PMID:Hypertension: an important precursor of heart failure. 1080 84

Cardiomyopathy is a common, heterogeneous and important cause of cardiac morbidity and mortality in uraemic patients. The risks of ischaemic heart disease, cardiac failure, and death increase progressively from lowest risk in patients with concentric left-ventricular hypertrophy, to medium risk in patients with left-ventricular dilatation but intact systolic function, to highest risk in patients with systolic dysfunction. Anaemia and hypertension are the reversible risk factors most consistently linked with the development of cardiomyopathy in these patients. Longitudinal data show that anaemia predisposes individuals to initial left ventricular dilatation, with compensatory hypertrophy, which may progress to systolic dysfunction. This process typically begins at glomerular filtration rates between 25 and 50 ml/min, and haemoglobin concentrations that are even slightly below normal are associated with progressive cardiac enlargement. Several observational studies have suggested that the correction of anaemia may reduce mortality and hospitalization rates in dialysis patients. The available evidence supports maintaining haemoglobin concentrations to greater than 11 g/dl. Whether a haemoglobin threshold exists above which no further benefit is seen remains controversial, partially because recent randomized controlled trials have intervened relatively late in the anaemia cardiomyopathy cardiac failure death continuum. One large randomized controlled trial showed no benefit from normalizing the haemoglobin concentration in haemodialysis patients with well-established cardiac disease; however, these patients had been exposed to anaemia for long periods of time and were at the extreme end of the cardiorenal disease spectrum. Other researchers have demonstrated a protective effect of normalizing the haemoglobin concentration in patients with asymptomatic, and hence presumably early, cardiomyopathy. The psychological benefits and improvements in exercise tolerance and quality of life resulting from normalization of the haemoglobin concentration are becoming clearer. However, conclusive evidence of the cardiovascular benefits of earlier, more aggressive treatment of renal anaemia as well as of the exact target haemoglobin concentration at which risk begins to develop is still lacking. The results of ongoing trials should help to clarify both of these issues within the next 5 years.
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PMID:Effects of anaemia on cardiovascular status. 1103 53

Congestive heart failure is a multiple aetiology, high prevalence, poor prognosis cardiovascular disorder. Medical treatment of dilated cardiomyopathy is aimed at alleviating the symptoms of heart failure. Diuretics, ACE inhibitors and very recently, beta-blockers have been shown to have favourable effects on symptoms, exercise capacity and mortality. Growth hormone (GH) and insulin-like growth factor (IGF)-1 are involved in several physiological processes such as the control of muscle mass and function, body composition and regulation of nutrient metabolism. The roles of GH and IGF-1 as modulators of myocardial structure and function are well established. Receptors for both GH and IGF-1 are expressed by cardiac myocytes; therefore, GH may act directly on the heart or via the induction of local or systemic IGF-1, whereas IGF-1 may act by endocrine, paracrine or autocrine mechanisms. Patients with acromegaly have an increased propensity to develop ventricular hypertrophy and cardiovascular diseases and, in addition, an impaired cardiac efficiency is observed in patients with GH deficiency. Animal models of pressure and volume overload have demonstrated up-regulation of cardiac IGF-1 production and expression of GH and IGF-1 receptors, implying that the local regulation of these factors is influenced by haemodynamic changes. Moreover, experimental studies suggest that GH and IGF-1 have stimulatory effects on myocardial contractility, possibly mediated by changes in intracellular calcium handling. Heart failure is caused by ventricular dilatation with abnormal wall thickening, which leads to impaired cardiac performance; therefore, based on the evidence available for GH we would expect beneficial effects from the use of GH in these patients. Several papers highlight the positive influence of GH in the regulation of heart development and performance. In patients with GH deficiency, GH administration dramatically improves cardiac function. In small nonblind studies, both short and long term GH treatment have demonstrated beneficial effects in patients with heart failure secondary to ischaemic or idiophatic cardiomyopathy. Recently, two randomised, placebo-controlled studies, did not show significant GH-mediated improvement in cardiac performance in patients with dilated cardiomyopathy, despite significant increases in IGF-1. Acquired GH resistance, might be an important feature of severe heart failure and explain the different responses to GH therapy seen in different patients. Whether GH treatment will finally find a place, and with which modalities, in the treatment of heart failure remains to be established.
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PMID:Role of growth hormone in chronic heart failure. Therapeutic implications. 1108 97

Cardiovascular illness is an important contributor to the morbidity of kidney disease. The spectrum of cardiovascular disease (CVD) in patients with chronic renal insufficiency (CRI) includes left ventricular hypertrophy (LVH) and dilatation, ischemic heart disease, and peripheral vascular disease. Both "traditional" and "uremia-specific" factors contribute to the occurrence and progression of cardiac disease in renal patients. A growing body of recent evidence indicates that the processes contributing to CVD commence early in CRI, leading to concentric LVH, left ventricular dilatation, congestive heart failure, and ischemic heart disease. Many of the coexisting conditions that have been identified consistently as contributing to the burden of cardiovascular illness in renal populations can be modified through medical interventions. Specific therapies exist for hypertension, anemia, hyperparathyroidism, and dyslipidemia. Studies to date have demonstrated that treatment of many of these factors-such as anemia and hypertension during end-stage renal disease-appear to benefit the cardiovascular system. Earlier intervention may offer the best opportunity to reduce the burden of illness in all groups of CRI patients. Identification of patients at the onset of kidney disease and attention to the known traditional and "uremic" risk factors are emerging as promising strategies. Long-term interventional studies are needed to determine costs, benefits, and risks of such strategies.
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PMID:Cardiovascular disease in chronic renal insufficiency. 1111 55

15 years after recombinant erythropoietin (EPO) has become available for the treatment of renal anemia, the target hemoglobin concentration to be achieved is still controversial. A positive impact of partial correction of renal anemia on quality of life has been conclusively demonstrated. Several more recent studies indicate that further improvement of well-being can be achieved with normalization of hemoglobin levels. In addition, there is increasing evidence that anemia is associated with the progression of left-ventricular hypertrophy and mortality. These findings imply that correction of renal anemia has the potential to improve patient prognosis. However, in patients with advanced cardiac disease, the US normal hematocrit failed to demonstrate a prognostic benefit and instead suggested that the attempt to normalize hemoglobin may be harmful. Nevertheless, in patients with less advanced cardiac disease complete correction of renal anemia may prevent progressive ventricular dilatation. The impact of early anemia correction is currently tested in several trials in predialysis patients. Irrespective of the uncertainties about the upper target range, current US and European guidelines have defined a hemoglobin concentration of 11 g/dl as the lower target range on the basis of both symptomatic and prognostic considerations. In the majority of patients these minimum requirements are not yet achieved. Less then 10% of patients receive EPO prior to the onset of dialysis, the mean hemoglobin level at the start of dialysis is not higher than 9 g/dl and a significant proportion of patients permanently remain below 11 g/dl.
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PMID:Target hemoglobin in patients with renal failure. 1154 95

Ambulatory blood pressure monitoring has been steadily growing in popularity as equipment becomes more accurate, affordable, and patient-friendly. In addition, software packages are more powerful and physician-customizable, and more physicians are accepting of ambulatory blood pressure monitoring's advantages. Summarizing the studies that deal mainly with hemodialysis patients, there are clear advantages to using more than isolated pre- and posthemodialysis blood pressure readings. If enough predialysis blood pressure readings are taken and averaged, this is a reasonable guide to end-organ damage (ie, left ventricular hypertrophy). Home and ambulatory blood pressure-derived values are complementary, and only this approach can discern any further contribution from diurnal blood pressure elevation. The cross-sectional association between blood pressure and end-organ damage is very weak in end-stage renal disease patients if the blood pressure values are "casual," but the relationship is much stronger when ambulatory blood pressure monitoring-derived measurements are used. One prospective study clearly linked the sustained loss of diurnal blood pressure fall with sleep with progressive left ventricular dilatation. Loss of circadian variation in blood pressure is associated with an increased mortality rate for dialysis patients and for diabetic patients, regardless of diabetes type. The combination of nondipping in renal impairment leads to a high mortality rate. Much more work is needed to dissect out the causes for abnormal diurnal blood pressure rhythm and attempt to modulate this parameter. Obstructive sleep apnea may be a promising target for intervention.
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PMID:Ambulatory blood pressure measurement in the renal patient. 1221 55

Patients with chronic renal failure have, as compared with age-matched controls with normal renal function, a markedly higher cardiovascular mortality. The reason is probably accelerated atherosclerosis and left ventricular hypertrophy as a result of accumulation of "classical" cardiovascular risk factors and the presence of some risk factors relatively specific for "uraemia" (e.g. anaemia, hyperhydratation, dyslipidaemia). It is assumed that the reversibility of left ventricular hypertrophy is limited in chronic renal failure due to more marked myocardial fibrosis ("uraemic cardiomyopathy"). Its regression can be achieved by treatment of hypertension with inhibitors of angiotensin converting enzyme with a positive effect on cardiovascular mortality. Regression of left ventricular hypertrophy occurs also in some patients after renal transplantation. Treatment of anaemia reduces the risk of progressive left ventricular dilatation. The cardiovascular risk increases probably already a relatively slight decline of glomerular filtration which need not lead to a significant rise of serum creatinine. The cardiovascular risk obviously increases further with progression of chronic renal insufficiency. Patients with a reduced renal function and chronic renal insufficiency have lower target blood pressure and should have also lower target values e.g. of serum cholesterol. Therapeutic procedures in these patients should not be focused only on a slower progression of chronic renal insufficiency but also on reduction of their high cardiovascular risk.
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PMID:[Cardiovascular complications in patients with chronic renal insufficiency and chronic kidney failure]. 1290 73

A forty-one-year-old male, with no risk factors for coronary artery disease (CAD) and with moderate alcohol intake, was admitted in 1992 to Portalegre Hospital with heart failure due to viral cardiomyopathy. He was re-admitted in 1998 with acute pulmonary edema and was put on mechanical ventilation for 48 hours, and transferred to Pulido Valente Hospital when stable. The physical exam was without abnormalities. ECG showed first degree AV block, left ventricular hypertrophy and 2 mm ST depression in the precordial leads. The echocardiogram revealed left ventricular dilatation and depressed systolic function. Coronary angiography showed single-vessel CAD and coronary artery anomaly. Dobutamine stress echocardiography was halted due to hypertension, making it impossible to evaluate ischemic response. Holter monitoring showed five-complex ventricular tachycardia. The patient was discharged medicated with amiodarone, with indication for cardiac scintigraphy and electrophysiological study.
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PMID:Left main coronary artery originating in the right sinus of Valsalva. 1500 65

Long-term consequences of cardiac alteration in children with chronic renal failure and after renal transplantation are largely unknown. In chronic uremia, cardiomyopathy manifests itself as systolic dysfunction, concentric left ventricular hypertrophy (LVH) or left ventricular dilatation. The correction of uremic state by renal transplantation leads to normalization of left ventricular contractility, regression of LVH and improvement of cavity volume and so dialysis patients with uremic cardiomyopathy would benefit from renal transplantation. We studied 73 patients, aged 17 yr or less, who underwent renal transplantation in our center. This cross-sectional study was performed 4.6 yr (median) after transplantation. Of the total, 48 were males and 25 were females. Transthoracic echocardiographic examination was performed for all cases. The effects of clinical, demographic, biochemical and therapeutic data on echocardiographic parameters were assessed. Multivariate analysis was used to assess the relation between the risk factors and the left ventricular muscle mass index. The most common echocardiographic abnormalities were the LVH (47.9%), left atrial enlargement (31.5%) and left ventricular dilatation and systolic dysfunction (13.7% for each). The pretransplant dialysis, arteriovenous fistula, acute rejection, cumulative steroid dose per square meter surface area, post-transplant hypertension, anemia and graft dysfunction were significant risk factors for LVH by univariate analysis. The significant factors by multivariate analysis were pretransplant dialysis, post-transplant hypertension and anemia. From this study we may conclude that LVH is a common problem among renal transplant children and adolescents. Early transplantation, control of hypertension and correction of anemia may be beneficial regarding left ventricular function and structure.
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PMID:Echocardiographic changes and risk factors for left ventricular hypertrophy in children and adolescents after renal transplantation. 1517 62


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