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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two children with congenital fibroelastosis and recurrent episodes of heart failure had overt proteinuria and hematuria; one also had a reversible nephrotic syndrome. Urinary manifestations persisted during periods of cardiac compensation. Renal biopsies revealed mesangial hyperplasia by light microscopy, identical ultrastructural lesions in the glomerular basement membrane, and deposits of fibrin in one of the biopsy specimens studied by immunofluorscence. These changes detected by electron microscopy may result in an increase in glomerular permeability independent of the renal hemodynamic disturbances associated with cardiac insufficiency. The progression of the lesions appears to be slow, although urinary manifestations may simulate an intercurrent glomerulonephritis. Pulmonary hypertension and renal venous stasis with glomerular intravascular coagulation were discussed as possible pathogenic mechanisms.
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PMID:Glomerular lesions in congenital endocardial fibroelastosis: clinical manifestations and ultrastructural studies in two patients. 58 Aug 81

This is a study of 23 cases with pulmonary plethora and cardiac failure. A "banding" of pulmonary artery was performed, to diminish the pulmonary bloodflow in order to avoid the development of pulmonary hypertensive changes and to improve the heart failure. The mean age of the cases operated upon was 16,9 months. The complications post-banding were: stenosis of the pulmonary outflow tract and necrosis or calcification of the pulmonary artery wall. There was a direct relationship between these complications and the time of persistence of the "banding". The pulmonary artery pressure, distal to the "banding", was reduced as much as 2/3 of the previous pressure in all patients below 6 months and in 63,64% of those patients above 1 year old. A patent ductus arteriosus, complicating the ventricular septal defectis closed prior to perform the "banding" in order to see its role in the pulmonary hyperkinetic hypertension. This is carried out only if pulmonary hypertension remains unaffected.
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PMID:[Pulmonary arterial bnading hemodinamic and clinical evaluation in 23 cases (author's transl)]. 60 37

Thirty-two patients with double outlet right ventricle (DORV) were studied between 1960 and 1976. Associated congenital defects frequently compounded the difficulty of clinical diagnosis. Cardiac catheterisation was performed in 27 patients, and the ventriculograms were studied with particular regard to the relative positions of the great vessels to each other and to the ventricular septal defect. These relationships determine which corrective operation is possible. Correction has been performed in 12 patients with a perioperative mortality of 25%. Although mitral-aortic discontinuity was demonstrated in all cases, consideration of the anatomical spectrum included in the term DORV suggests that discontinuity is not an essential feature. In common with other clinical data and in contrast with necropsy studies, none of our patients was found to show the normal relationship of the great vessels to each other, in which the aorta lies posterior and to the right of the pulmonary artery. The reason for this difference between the clinical and necropsy findings is not apparent. A similar disparity was shown with regard to pulmonary stenosis, which was demonstrated at catheterisation in 68% of the 27 patients (mean gradient 68 +/- 3 mmHg), in contrast with incidences of 18% and 25% in recent necropsy series. Patients in the necropsy studies were frequently neonates or infants, in whom death may have been the result of intractable cardiac failure secondary to excessive pulmonary blood flow. In older patients without pulmonary stenosis and with pulmonary hypertension, frequent observation is imperative so that surgical treatment can be instituted before the development of irreversible pulmonary vascular disease.
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PMID:Double outlet right ventricle: clinical and anatomical spectrum. 68 64

It has been our policy at Harefield Hospital since 1971 to perform primary repair of large ventricular septal defects in the first year of life if there is severe intractable cardiac failure or persistent pulmonary hypertension in infants approaching the first year of age. Twenty-six infants underwent repair; their ages were between one and twelve months. One child died early. The remaining 25 have been followed up for between 6 and 78 months (mean 30.3 months). There have been no late deaths and all children are asymptomatic. Late, postoperative cardiac catheterization was performed in 17 patients. This showed that in all the patients the pulmonary artery pressure was normal and there were no residual shunts. It is concluded that primary repair of large ventricular septal defects in the first year of life gives good results and appears to prevent pulmonary hypertension.
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PMID:[Primary repair of large ventricular septal defects in the first year of life (author's transl)]. 70 Feb 95

The frequency with which cattle develop right-heart failure during the winter at high altitude suggested that cold might contribute to hypoxic pulmonary hypertension. Indeed in a preliminary study conducted out-of-doors during early Spring, two calves with known hyperreactive pulmonary vessels showed elevated pulmonary arterial pressures attributed to their prior exposure to nighttime cold (-5 degrees C). In a second study five hyperreactive calves had increases in mean pulmonary arterial pressure from 29 to 45 Torr (+ 55%) during 48 h of exposure to cold (0 to -5 degrees C) in a climatic chamber. Three calves with less reactive lung vessels increased their pressures from 25 to 36 Torr (+ 44%). In a more complete study, six calves selected as potential hyperresponders showed increases in pulmonary arterial pressure (+ 60%), blood flow (+ 18%), and vascular resistance (+ 38%) during 48 h of cold exposure. Arterial PO2 decreased (-10 Torr) and PCO2 rose (+6 Torr) suggesting hypoventilation. Oxygen breathing returned pulmonary pressures and resistance to near control values, suggesting that cold had induced a hypoxic pulmonary vasoconstriction and an increased blood flow. Thus, a cold produced pulmonary hypertension in cattle at the modest altitude of 1,524 m and the pressor responses were greater in calves with more reactive lung vessels.
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PMID:Cold-induced pulmonary hypertension in cattle. 70 Nov 35

Congenital heart lesions are found in 0.8% of all newborns; four-fifths of them are correctable. Two thirds of all surgical procedures are done in acyanotic malformations, mainly in septal defects, patent ductus arteriosus, coarctations of the aorta and valvular stenosis. Within the last twenty years corrective repair has been established with good results in these lesions. Therapeutic problems still remain in cases of late diagnosis and in some rare and complex anomalies like malformations of the aortic arch, of the coronary arteries, in some types of aortopulmonary window and atrioventricular canal. Surgery becomes urgent in babies suffering from severe heart disease because of progressive pulmonary hypertension, inadequate growth or severe heart failure (despite intensive medical treatment). For certain lesions corrective repair (patent ductus arteriosus, coarctation) is definitely indicated, for others (ventricular septal defect, atrioventricular canal) urgent palliation or early total repair is debatable. In most patients with uncomplicated lesions treated in time during childhood a low operative mortality below 1% was observed. A higher mortality rate was found (10 to 50%) in patients with pulmonary artery disease or associated pulmonary lesions. A significantly higher mortality could also be observed in the advanced age group (4.7%) and in infants below one year of age (11,5%), underlining the important point of the age at operations. Recurrence of lesions occured in 1% of our patients after closure of ventricular septal defects, reconstructions of mitral valve disease and early corrected coarctations. Nevertheless, most of these patients can expect a normal growth, life span and ability to work.
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PMID:[Surgery of congenital acyanotic cardiac malformations (author's transl)]. 72 Oct 31

Three fatal cases of idiopathic arterial calcification in infancy are reported. The infants' ages ranged from 9 days to 3 months. Death was due to cardiac failure; in two cases caused by myocardial ischaemia, and in one by pulmonary hypertension. The histological findings are described and aetiology of the condition is discussed.
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PMID:Idiopathic arterial calcification in infancy. 73 Jan 23

Three cases of persistent pulmonary hypertension in newborn infants are reported. One patient developed this syndrome following a normal pregnancy and uneventful delivery, whilst the others had a history of fetal or perinatal distress. Cardiac catheterization showed pulmonary hypertension in two cases in the absence of cardiac or pulmonary disease or metabolic disorders; one of these babies died unexpectedly following initial improvement. The second infant died from massive cardiac failure before cardiac catheterization could be carried out. The surviving infant was reinvestigated at the age of 7 months and showed normal pulmonary pressure and no evidence of cardiac disease. Aetiology, haemodynamics and clinical picture of this syndrome are discussed in relation to the varying clinical features manifested by our patients and the course taken.
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PMID:[Persistent pulmonary hypertension in newborn infants (author's transl)]. 74 50

Leucocidin from Pseudomonas aeruginosa causes cardiovascular failure in rats and mice. The time between i.v. injection and death depends on the dose. After injection of high doses (500 mug/kg) the arterial blood pressure decreases rapidly and cardiac irregularities and AV block occur within about 5 min. In contrast to endotoxin shock no pulmonary hypertension was observed, whereas portal hypertension was seen in our experiments. Injection of lower doses (less than 200 mug/kg) caused peripheral vascular damage with lung oedema, vascular disturbances in various tissues, exudation and bleeding. Finally cardiac insufficiency predominated. Dexamethasone delayed the symptoms but did not prevent death in either rats or mice. Heparin was ineffective in this type of shock.
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PMID:Cardiovascular reactions induced by leucocidin from Pseudomonas aeruginosa. 82 38

Fibrosing alveolitis is a rare, diffuse lung disease characterized by varying combinations of two histological features: thickening of alveolar walls and the presence of large mononuclear cells in the alveolar spaces. Clinical details of 10 children with fibrosing alveolitis are reported. The main symptoms in children are tachypnoea or dyspnoea, cough, poor weight gain, and cyanosis. The condition is similar to that in adults, but it is usually a more acute illness, and if untreated, more predictably fatal. Respiratory failure, pulmonary hypertension, and cardiac failure are the major complications. Less commonly, superimposed bacterial infection and pneumothorax occur. Chest x-rays often show a sequence of changes with a ground-glass appearance and fine mottling in the early stage of the disease, progressing to a picture of mainly hilar linear markings in those children who recover. The histological features at lung biopsy or necropsy are described; these correlated poorly with the radiological features, steroid responsiveness, and clinical course. Lung function tests in 3 older children showed evidence of markedly reduced lung volumes in 2. Static lung compliance in 4 children in the acute stage of the illness was normal in 3 and diminished in one. The response to steroid therapy was analysed in cases from the literature and the 10 reported cases. No spontaneous remissions occurred, all the survivors having been treated with corticosteroids. In children fibrosing alveolitis is almost always a corticosteroid-responsive disease. An appropriate course of prednisolone would be of at least 4 week's, but preferably of 8 weeks' duration, at a minimum daily dose of 2 mg/kg. After improvement the steroid withdrawal should be cautious and protracted, comprising at least a year's continuous treatment.
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PMID:Fibrosing alveolitis in infancy and childhood. 83 51


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