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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fourteen infants with congenital heart disease were investigated for failure to thrive. Assessment of intestinal function revealed minor absorptive abnormalities (mild steatorrhea in three patients, bile salt loss in four patients), delayed gastric emptying, and abnormal triglyceride loading tests. Low caloric intake (88.3 +/- 19.3 kcal/kg/day) seemed the main reason for failure to gain weight. Weight accession and cardiorespiratory rates were monitored daily during voluntary intake, a high-caloric diet by mouth, and nasogastric tube feeding. Providing 169 +/- 29 kcal/kg/day by tube resulted in weight gain with mild and transient elevation of respiratory rate at the end of the meal and increased heart rate 90 min after the meal. This regimen is a metabolically inexpensive and efficient method of supporting weight gain in children with congenital heart disease.
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PMID:Assessment of intestinal and cardiorespiratory function in children with congenital heart disease on high-caloric formulas. 404 36

Metabolisable energy intake, determined by bomb calorimetry of food, vomit, stool and urine, and resting metabolism, assessed by respiratory gas exchange, were studied in 21 infants with congenital heart disease and nine control infants. Weight for age, growth rates, and daily metabolisable energy intake per kg tended to be lower in infants with heart disease than in control infants. Resting oxygen consumption was high in those infants with pulmonary hypertension and persistent cardiac failure. Energy intake, as a percentage of that recommended for age, correlated with weight gain, and resting oxygen consumption correlated inversely with both percentage body mass index and relative fatness. Failure to thrive in infants with congenital heart disease may be due to a combination of low energy intakes and, in some cases, high energy requirements allowing insufficient energy for normal growth. Increasing the energy intakes of infants with congenital heart disease may be a way of improving their growth.
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PMID:Why does congenital heart disease cause failure to thrive? 409 78

Of nine patients under five months of age with cardiovascular manifestations of the rubella syndrome, six had patent ductus arteriosus. Three of these six also had pulmonary artery stenosis. One infant had bilateral isolated pulmonary artery stenosis. The significant clinical findings leading to the diagnosis of pulmonary artery stenosis were axillary murmurs in the presence of right ventricular hypertrophy. Demonstration of a gradient across the stenosis at the time of catheterization, together with cineangiography, established the diagnosis. In two cases ventricular septal defect was the only cardiac anomaly.Six babies under five months of age had interruption of a patent ductus arteriosus because of uncontrollable congestive heart failure or failure to thrive. Although growth failure was not necessarily due to heart disease, all were developing satisfactorily following operation.Diagnosis and therapy of the cardiac complications of the rubella syndrome is possible in the first few months of life. Early recognition of cardiac defects in the young infant with the rubella syndrome permits aggressive medical management and in selected instances surgical therapy.
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PMID:Rubella syndrome. Cardiovascular manifestation and surgical therapy in infants. 595 30

Four infants with congenital heart disease showed in their first months of life poor weight gain in spite of the absence of cardiac failure; a diagnosis of intolerance to cow's milk proteins was made on the basis of laboratory findings and subsequently confirmed by the success of the avoidance diet and the positivity of the challenge tests; all four children had previously received nasogastric feeding, and this may represent a favouring factor for sensitization. Intolerance to cow's milk proteins should be considered as a possible cofactor for failure to thrive in infants with congenital heart disease.
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PMID:Congenital heart disease and cow's milk intolerance. 654 11

We describe a 3-month-old female with a de novo interstitial deletion of the long arm of chromosome 1 (1q23-25). Clinical features are failure to thrive, psychomotor retardation, cleft lip and palate, short metacarpals, metatarsals and fingers and a severe congenital heart disease. The four previously reported patients with the same deletion share with ours the distinctive pattern of anomalies of the face and limbs; therefore, it seems now possible to delineate a proximal 1 q deletion syndrome.
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PMID:Interstitial deletion of chromosome 1 (q23-q25). Report of a case. 658 54

We report chromosome rearrangements and/or duplication of chromosomes 11 and/or 22. This investigation was prompted by propositi with multiple congenital anomalies and an apparently identical chromosome abnormality - ie, 47, +der(22)t(11;22)(q23;q11.2)mat in two unrelated families. The propositi had failure to thrive, development delay, cleft palate, congenital heart disease, meningomyelocele, and hydrocephaly. The breakage points identified on chromosomes 11 and 22 are site-specific and occur in a nonrandom fashion. Band 11q23 corresponds to the gap produced in some individuals by special treatment of the chromosome preparation with mercaptoethanol and may provide a method to identify individuals at risk for chromosome breakage and rearrangements during gametogenesis.
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PMID:Duplication of distal 11q and 22p occurrence in two unrelated families. 723 4

Growth in children with congenital heart disease (CHD) is often compromised. For several decades, investigators have tried to identify the factors affecting growth in children with CHD. Cardiac malformations are undoubtedly responsible for malnutrition, which may range from mild undernutrition to severe failure to thrive (FTT). Malnutrition may then significantly undermine the outcome of corrective surgical operations and postoperative recovery. Mechanisms linking CHD to malnutrition may be related either to decreased energy intake and/or to increased energy requirements. Decreased energy intake can involve deficiencies of specific nutrients, or insufficient total caloric intake. Increased respiratory rate accompanying congestive heart failure may be responsible for increased energy requirements. Different types of cardiac malformations and consequent interventions may have different effects on growth and require diverse strategies. Most treatment strategies aim to facilitate "catch-up" growth, providing extra calories and protein that exceed the Recommended Dietary Allowance for age. However, there is no generally accepted set of guidelines that define appropriate caloric intake for catch-up growth. We attempt to identify the most important causes of malnutrition and highlight the most effective nutrition strategies for children with CHD.
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PMID:Children with congenital heart disease: a nutrition challenge. 781 52

Intestinal absorption and its relationship to increased total body water was studied in seven infants with congenital heart disease receiving regular diuretics due to congestive heart failure. All infants and six age-matched healthy controls were studied for a 3-d period during which time all food intake was recorded, stools were collected, and total body water content (TBW) and extracellular water were measured. All the anthropometric measurements were lower in the infants with congenital heart disease compared with healthy controls. Energy and fat excretion in the stools were significantly increased in the group of patients, but when expressed as a percentage of daily caloric intake or as a percentage of the specific intake (e.g. fat excretion/fat intake x 100), no statistical differences were found. TBW as a percentage of body weight was increased in our patients compared with our controls (84.95 +/- 5.82% versus 68.65 +/- 4.60%; p = 0.01) and so was extracellular water as a percentage of predicted (200.0 +/- 18.6% versus 100.9 +/- 7.2%; p = 0.001). A positive correlation was found between energy and fat excretion as a percentage of the intake and TBW as a percentage of predicted; energy and fat malabsorption did not exceed 8% in the patients with the highest body water content (120% of predicted). It is concluded that malabsorption is not a significant factor in failure to thrive of patients with congenital heart disease who are receiving regular diuretics. Based on the significant negative correlation between excess body water and fat and calorie absorption, however, it is suggested to monitor TBW in patients who fail to gain weight.
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PMID:Malabsorption in infants with congenital heart disease under diuretic treatment. 781 30

One hundred and seventy nine children reporting to the paediatric cardiac clinic were studied consecutively over a 2 year period (1991-1993) using medical history, physical examination, chest x-ray, electrocardiography, echocardiography and complete haemogram. 100 (56%) of them had congenital heart disease, 70(39%) had rheumatic heart disease, four had cardiomyopathy and in five children no abnormality was detected. 58 of patients with congenital heart disease were females and 42 were males. Their age ranged between two weeks and 15 years and four months. Symptoms started in infancy in 89% of 94 symptomatic patients. The commonest symptoms were breathlessness, failure to thrive, repeated chest infections and cynosis. The other six patients were detected incidentally. Almost all types of defects were represented, the commonest being ventricular septal defect (VSD), Fallot's tetralogy, pulmonary stenosis, patent ductus arteriosus, atrioventricular septal defect and secondum atrial septal defect. Five patients with VSD were preterms. 91% of patients with VSD were symptomatic. VSD was small in one-third of patients. six patients with VSD aged 5-11 years had evidence of pulmonary hypertension, one of whom had Eisenmenger with cynosis and one found inoperable because of pulmonary vascular disease. Twenty patients had extracardiac malformations in 65% of whom more than one system was involved. 53% patients were anaemic. 47% of patients were underweight and 33% were marasmic while only 14% of controls were underweight and none of them was marasmic.
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PMID:Pattern of congenital heart disease in Sudanese children. 787 91

Growth failure is a well recognised consequence of severe congenital heart disease. Total daily energy expenditure (TDEE) was investigated in eight infants with severe congenital heart disease to determine whether an increase in this parameter is an important factor in their failure to thrive, and to estimate the energy intake that would be required to allow normal growth. The infants were studied over a seven day period before surgery using the doubly labelled water method. Growth failure was evident; their mean age standardised body mass index was 80% of the expected value. Mean TDEE was 425 kJ/kg, significantly greater than in healthy infants (mean TDEE/kg SD score = +1.4; 95% confidence interval +0.27 to +2.57). In contrast, their energy intake was only 82% of the estimated average requirements. It was estimated that in early infancy a gross energy intake of 600 kJ/kg/day is required for normal growth in patients with congenital heart disease. This is unlikely to be achieved by energy supplements alone and early recourse to nasogastric feeding should be considered.
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PMID:Energy expenditure in congenital heart disease. 811 8


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