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)

During the winter of 1986-1987, 64 children with respiratory syncytial virus (RSV) infection were admitted to our hospital. The diagnosis was made by direct immunofluorescent antibody technique. Twenty-three children (36%) needed intensive care treatment. Nearly 11 (52%) had a preexisting disease state, identified as a risk factor i.e., prematurity (n = 8), bronchopulmonary dysplasia (n = 2), congenital heart disease (n = 1). Twelve patients (50%) were intubated and ventilated. Conditions for intubation and ventilation were repetitive apnea with or without bradycardia (n = 4), clinical deterioration (n = 3) or hypercarbia (n = 5). Seventy-five percent of the patients who needed intensive care management were under three months of age compared to 34% of the children who were admitted to the clinical ward. The mean age for ventilated patients was 7.9 weeks. The mean duration of ventilation was 5.5 days. Volume controlled ventilation was initially applied to all patients. Pulmonary complications (atelectasis, pneumonia, pneumothorax or adult respiratory distress syndrome) were present in 15 (65%) IC patients. Nine (39%) of them also had symptoms of inappropriate antidiuretic hormone secretion (IADHS). Only two patients had symptoms of IADHS and two others had convulsions. Three children (5%) died as a result of respiratory insufficiency. Two of these infants belonged to the risk group.
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PMID:Respiratory syncytial virus infections in children admitted to the intensive care unit. 281 76

Secondary hypertrophic cardiomyopathy (HCM) was diagnosed in 55 newborns and infants without heart disease. The 17 newborn infants of diabetic mothers, 23 infants given ACTH treatment for infantile spasms, 9 ventilated premature infants or babies with bronchopulmonary dysplasia and 6 infants with different underlying diseases comprising this group underwent 2-dimensional echocardiography. In almost all cases echocardiographic evidence of HCM resolved after removal of the exogenous or endogenous causative factor. Myocardial effects of several substances are known and their pathophysiological mechanisms are discussed. Since HCM may precede systemic disease or may often be the first pointer to a triggering agent, further diagnostic procedures are always indicated. Hence, the diagnosis of primary HCM should be made by exclusion.
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PMID:[Secondary myocardial hypertrophy in newborn infants and infants without congenital heart defect]. 285 96

Previously unreported lung disease found at autopsy in 2 young infants with Down's syndrome and congenital heart disease (complete atrioventricular canal malformation with left-to-right shunt) is described. The perinatal and neonatal period was unremarkable, and there was no history of mechanical ventilation or administration of high concentration of oxygen for extended periods. In 1 of the cases respiratory symptoms and hyperinflation with focal cystic changes in the lung fields on chest X-ray were noted at 5-7 months of age. Pathologically there was cystic dilatation of alveoli with focal cuboidal metaplasia of alveolar epithelium and mild to moderate focal alveolar septal fibrosis. Wilson-Mikity syndrome, congenital pulmonary lymphagiectasia, bronchopulmonary dysplasia, and idiopathic interstitial fibrosis of lungs were ruled out on clinical and/or pathologic grounds. Factors such as compression of bronchi by enlarged pulmonary arteries or cardiac chambers, peribronchiolar accumulation of fluid, pulmonary hypoplasia occurring in Down's syndrome, and episodes of pulmonary arterial hypoperfusion associated with severe congenital heart disease may be related to the pathogenesis of the lesion.
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PMID:Cystic lung disease in Down's syndrome: a report of two cases. 294 28

RSV is now understood to be the most significant viral respiratory pathogen of infants and is capable of causing both bronchiolitis and pneumonia. It is a particular risk to hospitalized infants as the virus is easily spread through close contact. The most vulnerable infants are those who suffer with either congenital heart disease or bronchopulmonary dysplasia who easily fall prey to pulmonary complications of infection. Strict environmental control and the use of protective clothing and eyewear should be implemented to decrease the nosocomial spread of RSV. Available diagnostic studies include viral isolation, fluorescent antibody stains, and enzyme immunoassays. Treatment of the disease is usually supportive but hospitalized patients frequently benefit from aerosolized ribavirin therapy. Hopefully, current vaccine trials will be successful and this pathogen will not only be treatable but will also be preventable.
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PMID:Respiratory syncytial virus. 306 24

Bronchiolitis is one of the most serious pulmonary infections commonly caused by respiratory syncytial virus (RSV). RSV disease occurs in yearly epidemics and is most severe in children 1 year of age or younger. Approximately 1 in 50 to 1 in 100 infants are hospitalized after their first infection, and mortality fluctuates between 0.5 and 5.0 per cent. Patients with underlying conditions such as congenital heart disease and bronchopulmonary dysplasia are at higher risk for morbidity and mortality. Methods for rapid diagnosis of RSV infection and the advent of specific therapy with aerosolized ribavirin have revolutionized the management of hospitalized patients with moderate to severe disease. A 3- to 5-day course of ribavirin plus supportive measures should be used in infants who prove to be infected by RSV and who are deteriorating on traditional supportive therapy, and/or who have underlying cardiac and/or pulmonary or immune defects.
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PMID:Ribavirin aerosol treatment of serious respiratory syncytial virus infection in infants. 333 96

Ischemic myocardial and papillary muscle dysfunction has considerable implication in newborn infants and children with normal or malformed hearts. Papillary muscle dysfunction in adults primarily involves coronary artery occlusion and ischemic necrosis in the left ventricle and papillary muscles. Infants and children rarely develop coronary artery occlusion. Their myocardial dysfunction and injury occurs with nearly equal frequency in both ventricles as a result of underperfusion from a wide range of causes, including severe birth asphyxia, congenital heart disease, and complications of premature delivery. A history of cardiogenic shock, acute congestive heart failure with cyanosis and atrioventricular murmur, or persistent fetal circulation in a newborn without congenital heart disease should alert the pathologist to the possibility of ischemic myocardial necrosis (IMN). Older infants with ventricular hypertrophy, persistent pulmonary hypertension (PPHN), bronchopulmonary dysplasia (BPD), and those with malformed hearts involving severe ventricular hypertension due to outflow obstruction or pulmonary hypertension may have IMN, fibrosis, or dystrophic calcification alone or in combination. Animal models of adult ischemic cardiac injury may not be suitable for study of the newborn.
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PMID:Ischemic myocardial necrosis and papillary muscle dysfunction in infants and children. 333 39

Technical aspects and indications for the use of digital subtraction angiography of thorax in 109 children are discussed, and the interest of this exploratory method emphasized in chronic respiratory disease in children. Results obtained are compared with other investigations for screening of bronchopulmonary dysplasia. Although generally reliable for exploration of thoracic aorta anomalies (coarctation and abnormal vascular arch) it is considered to be incompletely effective for investigation of congenital heart disease.
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PMID:[Digitalized angiography of the thorax in children]. 351 7

Although the pulmonary circulation in infants with advanced bronchopulmonary dysplasia (BPD) is characterized by abnormal structure and vasoreactivity, metabolic lung functions have not been studied in these infants. To test the hypothesis that patients with severe BPD may have abnormal metabolic lung function, we assessed the pulmonary vascular extraction of circulating norepinephrine in six children with BPD during cardiac catheterization. Plasma norepinephrine levels were measured from simultaneously drawn mixed venous (main pulmonary artery) and left atrium or femoral artery samples. In comparison with four infants with mild heart disease without pulmonary hypertension, we found that infants with BPD extract proportionately less norepinephrine than non-BPD infants [-7 +/- 50% (BPD) versus +27 +/- 6% (non-BPD); P less than 0.001, t test]. Three infants with BPD had higher arterial than mixed venous concentrations of plasma norepinephrine, suggesting net production across the lung. Plasma catecholamine levels and percent extraction correlated poorly with cardiac index and systemic and pulmonary vascular resistance indices. However, this study group was characterized by a high incidence of pulmonary (6/6) and systemic (4/6) hypertension, left ventricular hypertrophy (4/6), and subsequent death (3/6). We conclude that infants with severe BPD and pulmonary hypertension have decreased pulmonary vascular clearance or net production of circulating norepinephrine, but links between altered pulmonary catecholamine metabolism and pulmonary hypertension, or other cardiovascular abnormalities associated with BPD, remain speculative.
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PMID:Pulmonary vascular extraction of circulating norepinephrine in infants with bronchopulmonary dysplasia. 369 7

A randomized trial was conducted of dexamethasone therapy in infants with bronchopulmonary dysplasia who were dependent on respirators and were not progressing clinically despite conventional treatment. Babies were admitted to the study if they had a roentgenogram and clinical diagnosis of bronchopulmonary dysplasia, were 2 to 6 weeks in age, weighed less than 1,500 g, had made no progress in weaning for the preceding five days, and were free of sepsis, patent ductus arteriosus, and congenital heart disease, and had had no intravenous fat for at least 24 hours. After parental consent was obtained, infants were randomly assigned to control or treatment groups. The study hypothesis was that with steroid treatment, babies could be weaned from the respirator within 72 hours and would show a significant improvement in lung compliance within that time. Sequential analysis exceeded criterion (P less than .05) when seven consecutive untied pairs showed weaning with dexamethasone and failure to wean in control infants. Pulmonary compliance improved by 64% in the treated group and 5% in the control group (P less than .01). No significant intergroup differences were noted in mortality, length of hospital stay, sepsis, hypertension, hyperglycemia, or electrolyte abnormalities. Study design permits the conclusion that dexamethasone can produce substantial short-term improvement in lung function, often permitting rapid weaning from the respirator, but long-term efficacy and safety must be demonstrated by further investigations.
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PMID:Controlled trial of dexamethasone in respirator-dependent infants with bronchopulmonary dysplasia. 388 Aug 79

This article has reviewed current thought on the pathophysiology, medical management, and nursing implications of PDA in the premature newborn. The ductus arteriosus is a normal vascular channel that provides a route for blood flow to the descending aorta in the fetus; and it is an abnormal channel in the newborn that allows additional pulmonary blood flow to be shunted from the higher pressured aorta. Left heart volume overload and additional insults in connection with concurrent RDS and BPD were discussed. Current management for closure advocates indomethacin administration, and ligation, should indomethacin fail or be contraindicated. Continued patency with prostaglandin administration is the objective in cyanotic neonates with congenital heart disease and diminished pulmonary blood flow and in acyanotic neonates with aortic arch abnormalities that lead to decreased descending aortic flow. Nursing responsibilities encompass the well-being of the newborn as well as the family. The neonate must be assessed frequently for signs of cardiopulmonary deterioration. The neonate's responses to drug administration must be monitored for their effect on the ductus and the minimization of side effects. Care of the parents regarding support and information was discussed.
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PMID:Patent ductus arteriosus in the premature neonate. 388 36


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