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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitric oxide (NO) induces vasodilatatory, antiaggregatory, and antiproliferative effects in vitro. To delineate potential beneficial effects of NO in preventing vascular disease in vivo, we generated transgenic mice overexpressing human erythropoietin. These animals induce polyglobulia known to be associated with a high incidence of vascular disease. Despite hematocrit levels of 80%, adult transgenic mice did not develop hypertension or thromboembolism. Endothelial NO synthase levels, NO-mediated endothelium-dependent relaxation and circulating and vascular tissue NO levels were markedly increased. Administration of the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) led to vasoconstriction of peripheral resistance vessels, hypertension, and death of transgenic mice, whereas wild-type siblings developed hypertension but did not show increased mortality. L-NAME-treated polyglobulic mice revealed acute left ventricular dilatation and vascular engorgement associated with pulmonary congestion and hemorrhage. In conclusion, we here unequivocally demonstrate that endothelial NO maintains normotension, prevents cardiovascular dysfunction, and critically determines survival in vivo under conditions of increased hematocrit.
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PMID:Nitric oxide prevents cardiovascular disease and determines survival in polyglobulic mice overexpressing erythropoietin. 1102 59

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

The aim of the study was to examine the relationship between white matter changes on magnetic resonance imaging (MRI), brain atrophy and ventricular dilation in late-life dementias. T(1)-weighted, T(2)-weighted, and proton density MRI scans were acquired in subjects with Alzheimer's disease (AD, N=25) and dementia with Lewy bodies (DLB, N=27). Total brain and ventricular volumes were measured and white matter lesions rated using a semi-quantitative scale. Periventricular hyperintensities (PVH) were found to independently correlate with advancing age and increasing ventricular dilatation in all subjects. In contrast, deep white matter hyperintensities (DWMH) did not correlate with measures of brain atrophy, ventricular dilatation or age, but were associated with a history of hypertension. These findings support the hypothesis that PVH and DWMH are pathologically diverse and that white matter change in AD and DLB may be determined by similar processes. In particular, PVH appear to be linked to atrophic processes involving ventricular enlargement and DWMH to ischaemic risk factors.
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PMID:MRI volumetric correlates of white matter lesions in dementia with Lewy bodies and Alzheimer's disease. 1104 73

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

The persistence of right ventricular dilatation and paradoxical interventricular septal motion are two echocardiographic abnormalities rarely reported after surgical closure of atrial septal defects. The aim of this study was to identify the predictive factors of these abnormalities in the long-term and to study their functional consequences. One hundred and two patients aged 18 +/- 14 years (range 1-62 years) underwent closure of atrial septal defects. Thirty-five patients were under 10 years of age, 33 were 10 to 20 years of age and 34 were over 20. Fifty-six patients were female. The rhythm was sinus in the great majority of cases (97%). Three patients, all over 40 years of age, were in atrial fibrillation. Before surgery, right ventricular dilatation was observed in 95 patients (91.2%), paradoxical septal wall motion in 93 patients (91.2%), the ratio of pulmonary/systemic output was 2.7 +/- 0.6 (range 1.7 to 7.4) and over 2 in 90% of patients: pulmonary systolic pressure was 32.3 +/- 12 mmHg and over 40 mmHg in 18 patients (17.6%). Ninety-four patients were followed up regularly with a mean follow-up time of 5.5 +/- 3.6 years (1-14 years). The right ventricle remained dilated in 37 patients (39.4%) after surgery: the right ventricular dimension decreased from 36 +/- 1 to 27.8 +/- 6.2 mm (p = 0.001). The ratio of end diastolic right ventricular/left ventricular dimension also decreased from 1.07 +/- 0.31 to 0.56 +/- 0.12 (p = 0.0001). Multivariate analysis identified two predictive factors of persistent right ventricular dilatation: age > 40 years (p = 0.009) and a pulmonary/systemic flow ratio > 3 (p = 0.03). Interventricular septal wall motion remained paradoxical in 21 patients (22%). Multivariate analysis identified two predictive factors of persistent paradoxical septal motion: age > 40 years (p = 0.02) and systolic pulmonary pressures > 40 mmHg (p = 0.03). These abnormalities remained asymptomatic in all but two patients with persistent long-term hypertension and a residual atrial septal defect. The persistence of right ventricular dilatation and paradoxical septal motion was quite common, with older age at surgery, systolic pulmonary artery pressure > 40 mmHg and a ratio of pulmonary/systemic blood flow > 3, being predisposing factors. These abnormalities were clinically asymptomatic when isolated.
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PMID:[Right ventricular dilatation and intraventricular septal motion after surgical closure of atrial septal defect]. 1133 55

We report a 18 years old woman that was admitted with a history of four days of cardiac failure with acute pulmonary edema, high blood pressure, left ventricular dilatation and moderate to severe systolic dysfunction. Twenty four hours after admission she had a miscarriage, expelling a mole. The diagnosis of hyperthyroidism caused by a mole and early pre eclampsia was confirmed and the patient was managed with diuretics and dopamine. Symptoms abated, thyroid function tests, cardiac function and size returned to normal values and the patient was discharged asymptomatic, ten days after admission.
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PMID:[Gestational hyperthyroidism: a case associated to molar pregnancy]. 1137 99

Summary The case is described of a 12-year-old girl presenting with raised intracranial pressure without ventricular dilatation and a type 1 Chiari malformation. This was taken to be a coincidental association of pseudotumour cerebri and the Chiari malformation. Treatment of the pseudotumour with Diamox gave rapid and sustained relief of the intracranial hypertension without change in the Chiari malformation. In addition, a series of 156 cases of pseudotumour cerebri was reviewed for evidence of the Chiari malf ormation. An overall incidence of 1.3%, rising to 2.7% in patients with MR scanning [excluding the case described] was found.
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PMID:Pseudotumour cerebri occurring in association with the Chiari malformation. 1174 33

Left ventricular remodeling is the process by which ventricular size, shape, and function are regulated by mechanical, neurohormonal, and genetic factors. Remodeling may be physiological and adaptive during normal growth or pathological due to myocardial infarction, cardiomyopathy, hypertension, or valvular heart disease. Postinfarction remodeling has been divided into an early phase within 72 hours and a late phase beyond 72 hours. The early phase involves expansion of the infarct zone, which may result in early ventricular rupture or aneurysm formation. Late remodeling involves the left ventricle globally and is associated with time-dependent dilatation, the distortion of ventricular shape, and mural hypertrophy. Hypertrophy and collagen degradation are adaptive responses during postinfarction remodeling. Myocardial repair is triggered by cytokines released from injured myocytes. Ventricular remodeling is influenced most by infarct artery patency. Once infarct evolution has occurred, pharmacological intervention, like ACE inhibition and beta-adrenoreceptor blocking agents, may minimize infarct expansion and ventricular dilatation and improve the long-term prognosis.
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PMID:[Pathophysiology and therapeutic aspects of left ventricular "remodeling" in the post-infarct phase]. 1177 72

OBJECTIVE - To describe clinical observations of marked improvement in ventricular dysfunction in a medical office environment under circumstances differing from those in study protocols and multicenter studies performed in hospital or with outpatient cohorts. METHODS - Eleven cardiac failure patients with marked ventricular dysfunction receiving treatment at a doctors office between 1994 and 1999 were studied. Their ages ranged from 20 and 66 years (mean 39.42+/-14.05 years); 7 patients were men, 4 were women. Cardiopathic etiologies were arterial hypertension in 5 patients, peripartum cardiomyopathy in 2, nondefined myocarditis in 2, and alcoholic cardiomyopathy in 4. Initial echocardiograms revealed left ventricular dilatation (average diastolic diameter, 69.45+/-8.15mm), reduced left ventricular ejection fraction (0.38+/-0.08) and left atrial dilatation (43.36+/-5.16mm). The therapeutic approach followed consisted of patient orientation, elimination of etiological or causal factors of cardiac failure, and prescription of digitalis, diuretics, and angiotensinconverting enzyme inhibitors. RESULTS - Following treatment, left ventricular ejection fraction changed to 0.63+/-0.09; left ventricular diameters changed to 57.18+/-8.13mm, and left atrium diameters changed to 37.27+/-8.05mm. Maximum improvement was noted after 16.9+/-8.63 (6 to 36) months. CONCLUSION - Patients with serious cardiac failure and ventricular dysfunction caused by hypertension, alcoholism, or myocarditis can experience marked improvement in ventricular dysfunction after undergoing appropriate therapy within the venue of the doctor's office.
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PMID:Reversibility of ventricular dysfunction. Clinical experience in a medical office. 1179 29

Congestive heart failure is a leading cause of mortality in developed countries. Myocardial hypertrophy resulting from hypertension often precedes heart failure. Understanding the signaling underlying cardiac hypertrophy and failure is of major interest. Here, we identified Fas receptor activation, a classical death signal causing apoptosis via activation of the caspase cascade in many cell types, as a novel pathway mediating cardiomyocyte hypertrophy in vitro and in vivo. Fas activation by Fas ligand induced a hypertrophic response in cultured cardiomyocytes, which was dependent on the inactivation of glycogen synthase kinase 3 beta (GSK3 beta) by phosphorylation. In vivo, lpr (lymphoproliferative disease) mice lacking a functional Fas receptor demonstrated rapid-onset left ventricular dilatation and failure, absence of compensatory hypertrophy, and significantly increased mortality in response to pressure overload induction that was accompanied by a failure to inhibit GSK3 beta activity. In contrast, Fas ligand was dispensable for the development of pressure overload hypertrophy in vivo. In vitro, neonatal cardiomyocytes from lpr mice showed a completely abrogated or significantly blunted hypertrophic response after stimulation with Fas ligand or angiotensin II, respectively. These findings indicate that Fas receptor signaling inhibits GSK3 beta activity in cardiomyocytes and is required for compensation of pressure overload in vivo.
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PMID:Fas receptor signaling inhibits glycogen synthase kinase 3 beta and induces cardiac hypertrophy following pressure overload. 1182 97


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