Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aerosolized ribavirin was evaluated in the treatment of respiratory syncytial virus lower respiratory tract disease in 53 infants, 36 of whom had underlying diseases. Of the total infants, 26 were studied in a double-blind, placebo-controlled manner; 14 received ribavirin and 12 received placebo, a water aerosol, for an average of five days. When the infants with bronchopulmonary dysplasia and congenital heart disease treated with ribavirin were compared with those receiving placebo, the treated infants showed a significantly faster rate of improvement in their illness severity score. The degree of improvement in the total group of infants receiving ribavirin compared with those receiving placebo was similarly greater, and at the end of therapy significantly greater improvement was also demonstrated in their arterial blood gas values and in the amount of virus shed from their nasal washes. No toxic or adverse effects of the aerosol therapy were observed in any of the 53 infants studied, and resistance to ribavirin did not develop in any of the respiratory syncytial virus strains isolated, despite prolonged treatment in some of the more ill infants.
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PMID:Ribavirin treatment of respiratory syncytial viral infection in infants with underlying cardiopulmonary disease. 390 39

Bronchopulmonary dysplasia is a serious chronic lung disease of infancy but despite numerous problems such as poor growth, recurrent lower respiratory tract infections, and cor pulmonale, steady improvement and recovery may generally be expected. We report four infants with bronchopulmonary dysplasia in whom the cardiopulmonary course did not show the usual steady improvement. Each infant was found to have an unsuspected cardiopulmonary lesion in addition to lung disease: two had congenital heart disease and two upper airway obstruction. Three improved after surgical intervention but one patient died immediately after this. Persistent right ventricular hypertrophy in patients with bronchopulmonary dysplasia maintained on supplemental oxygen, and a particularly slow rate of recovery from the need for supplemental oxygen are markers that should lead to evaluation for coexisting cardiopulmonary abnormalities.
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PMID:Unsuspected cardiopulmonary abnormalities complicating bronchopulmonary dysplasia. 623 74

Pulmonary edema is an important feature of many newborn lung diseases, including respiratory distress from severe perinatal asphyxia, heart failure, hyaline membrane disease, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often results from increased filtration pressure in the microcirculation of the lungs. This occurs during sustained hypoxia, in left ventricular failure associated with congenital heart disease or myocardial dysfunction, following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution, and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema) or fibrosis (long-standing lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the lungs and its relationship to neonatal respiratory distress. 657 79

Pulmonary edema is an important cause of respiratory distress in newborn infants. It occurs with severe perinatal asphyxia, heart failure, hyaline membrane disease, persistent patency of the ductus arteriosus, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often develops from increased pressure in the microcirculation of the lungs. This may occur in conjunction with sustained hypoxia; left ventricular failure associated with congenital heart disease or myocardial dysfunction; following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema of fibrosis (chronic lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen-breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. Epithelial protein leaks may develop when the transpulmonary pressure needed to inflate the lungs increases because of high surface tension at the air-liquid interface. Fibrin clots from in some of the air spaces, which in combination with atelectasis and edema constitute the pathologic features of hyaline membrane disease. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen fluid filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the newborn lung. 676 Oct 39

Three newborn infants are described with a distinctive pulmonary arterial lipid lesion, characterized by a wide foamy layer of intima partially occluding the lumen of small muscular pulmonary arteries. Lipid stains indicated lipid infiltration of the walls of these arteries, involving not only the intimal layer, but media and adventitia as well. All three infants had received intravenous lipid infusions. All three infants also had histologic evidence of pulmonary hypertension, one on the basis of chronic lung disease (BPD) and two on the basis of congenital heart disease. A retrospective autopsy study of long-term neonatal ICU dwellers receiving such infusions revealed two additional patients with lipid deposits in pulmonary arterial walls. It is speculated that the pulmonary arterial lipid deposits were derived from the lipid infusions and were dependent on antecedent or concurrent vascular damage from pulmonary hypertension.
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PMID:Pulmonary arterial lipid deposit in newborn infants receiving intravenous lipid infusion. 743 Nov 76

Respiratory syncytial virus (RSV) is the only viral respiratory pathogen that produces an annual epidemic of respiratory illness. Infants with cardiac disease or infants born prematurely with or without bronchopulmonary dysplasia are at increased risk of severe RSV disease. A recently developed RSV immunoglobulin (RSVIG) was studied to determine safety and efficacy in prevention of severe RSV disease in such children who are high risk for severe RSV illness. Results from this prospective, blinded trial involving 249 children (102 with broncho-pulmonary dysplasia, 87 with congenital heart disease and 60 who were born prematurely) indicate that high dose RSVIG reduced the incidence and severity of RSV lower respiratory tract infection. It is a safe and effective means of RSV prophylaxis in selected high risk children.
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PMID:Role of antibody and the use of respiratory syncytial virus immunoglobulin in the prevention of respiratory syncytial virus disease in preterm infants with and without bronchopulmonary dysplasia. 807 36

From July 1990 to April 1993, 36 lung transplantations in 33 patients were performed in our pediatric transplant program (0.25 to 23 years, mean age 10.3 years). Eight children had been continuously supported with a ventilator for 3 days to 4.5 years before transplantation and three were supported by extracorporeal membrane oxygenation. Indications for lung transplantation in this pediatric population included the following: cystic fibrosis (n = 13), pulmonary hypertension, and associated congenital heart disease (n = 10), pulmonary atresia, ventricular septal defect and nonconfluent pulmonary arteries (n = 3), pulmonary fibrosis (n = 6), and acute respiratory distress syndrome (n = 1). Three children underwent retransplantation for acute graft failure (n = 2) or chronic rejection (n = 1). Pulmonary fibrosis was related to complications of treatment of acute of myelogenous leukemia with bone marrow transplantation in two children and to bronchiolitis obliterans, bronchopulmonary dysplasia, interstitial pneumonitis, and Langerhans cell histiocytosis in four others. Thirteen children underwent lung transplantation and concomitant cardiac repair. Bilateral lung transplantation, ventricular septal defect closure and pulmonary homograft reconstruction of the right ventricular outflow tract to the transplanted lungs was performed in three children by means of a new technique that avoids the need for combined heart-lung transplantation. Two patients had ventricular septal defect closure and single lung transplant for Eisenmenger's syndrome, two had ligation of a patent ductus arteriosus and transplantation, three additional children underwent atrial septal defect closure and lung transplantation, and two underwent lung transplantation for congenital pulmonary vein stenosis. Eight early deaths and three late deaths occurred (actuarial 1-year survival 62%). Lung transplantation in children has been associated with acceptable early results, although modification of the adult implantation technique has been necessary. Lung transplantation and repair of complex congenital heart defects is possible; heart-lung transplantation may only be required for patients with severe left heart dysfunction and associated pulmonary vascular disease. Bronchiolitis obliterans remains a major concern for long-term graft function in pediatric lung transplant recipients.
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PMID:Pediatric lung transplantation. Indications, techniques, and early results. 815 51

The single most important respiratory pathogen in infancy and early childhood is respiratory syncytial virus (RSV). Approximately 40% of primary RSV infections in children result in lower respiratory tract disease. Approximately 1% of RSV-infected children require hospitalization. Especially in high-risk children, primary RSV infection results in significant morbidity and, sometimes, death. This high-risk group includes children with bronchopulmonary dysplasia, children with congenital heart disease, premature infants less than 6 months of age, and children with immunodeficiency diseases. It has been estimated that, in the United States, 14,000 infants with chronic lung disease and 16,400 infants with heart disease will be identified by 12 months of age. More than 91,000 children are hospitalized annually with lower respiratory tract disease caused by RSV, and 4500 deaths occur. In 1985 a report from the Institute of Medicine calculated that the annual hospitalization costs attributable to RSV infection were $300 million. Data collected at the New England Medical Center in 1991 show that the average cost of hospitalization of a child with RSV was $808 each day. Because of difficulty in developing a safe and effective RSV vaccine, attention is now focused on passive immunization using an RSV immune globulin. On the basis of a recently completed multiinstitutional trial, RSV immune globulin appears to be a safe and cost-effective option for prevention of severe RSV disease in high-risk children.
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PMID:Economic impact of viral respiratory disease in children. 816 53

Infants with cardiac disease or infants born prematurely with or without bronchopulmonary dysplasia are at increased risk of severe respiratory syncytial virus (RSV) disease. A recently developed RSV immune globulin (RSVIG) was studied in a 3-year multicenter trial to determine safety and efficacy in the prevention of severe RSV disease in children who are at high risk of severe RSV illness. Two hundred forty-nine children were studied; 102 had bronchopulmonary dysplasia, 87 had congenital heart disease, and 60 were born prematurely. RSVIG was given on a monthly basis to 81 children at a high dose of 750 mg/kg (15 ml/kg) and to 79 children at a low dose of 150 mg/kg (3 ml/kg). The 89 children in the control group did not receive RSVIG. There were 64 episodes of RSV infection: 19 in the high-dose group, 16 in the low-dose group, and 29 in the control group. High-dose recipients had significantly fewer RSV lower respiratory tract infections, hospitalizations, hospital days, intensive care unit days, and less use of ribavirin compared with control subjects. Only 19 adverse events were reported during the 580 infusions administered (3%). No death was attributed to RSV disease or RSVIG therapy. Treated children did not acquire exaggerated RSV illness in a subsequent year. Thus high-dose RSVIG reduced the incidence and severity of RSV lower respiratory tract infection. It is a safe and effective means of RSV prophylaxis in selected high-risk children.
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PMID:Role of antibody and use of respiratory syncytial virus (RSV) immune globulin to prevent severe RSV disease in high-risk children. 816 55

Bronchiolitis, a lower respiratory tract illness most often caused by respiratory syncytial virus, generally affects children under two years of age, commonly during the winter months. Necrosis of epithelial cells in the small airways leads to inflammation and airway obstruction, causing decreased oxygen saturation, with cough and wheezing. Hospital admission should be considered for children with pulse oximetry levels less than 95 percent at rest. Treatment consists of humidified oxygen, intravenous hydration and administration of nebulized albuterol. Infants with mild disease who are identified early in the course of illness should be reevaluated in 24 hours. Infants with congenital heart disease, bronchopulmonary dysplasia or a history of prematurity, who are at high risk for severe disease, should be treated with ribavirin.
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PMID:Bronchiolitis. 784 31


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