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)

15 infants with cyanotic congenital heart disease (pulmonary atresia, Ebstein-Syndrom) were treated with Prostaglandin E1. During treatment there was a significant rise of PO2 and SO2 in the arterial, capillary and central venous blood. There was a minor rise of pH and HCO3; the arterial pCO2 fell slightly. We used PGE1-therapy as pretreatment before the heart operation, so that the critical babies go to the operation well oxygenated and in a better state. The side effects we observed (tachypnoe, tachycardia, hyperpyrexia, augmented urine output, erythemas, apnoic spells) seemed less important than the great advantage of a better oxygenation of these hypoxic babies.
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PMID:[Prostaglandin E1: effect on blood gases in infants with cyanotic congenital heart disease (author's transl)]. 2 23

Prostaglandin-E (PGE) infusions have been used in an attempt to increase ductal patency in 11 infants aged one to 99 days with cyanotic heart disease. PGE1 was used in nine infants and PGE2 in two. Five patients had pulmonary atresia, four extreme pulmonary stenosis, one Ebstein's anomaly and one simple transposition of the great arteries. All but the oldest infant showed a satisfactory increase in oxygen saturation (average 36%) attributed to dilatation of the ductus. The failure in one infant may have been due largely to hypoplasia of the left pulmonary artery. The only important side effect was apnea in one infant receiving PGE2. The efficacy of this form of treatment is confirmed in infants dependent on ductal patency for survival. PGE is an important asset in saving the lives of neonates requiring an aorticopulmonary shunt operation. The recommended starting dose is 0.1 mug/kg/min of PGE1 given by constant infusion.
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PMID:Palliation of cyanotic congenital heart disease in infancy with E-type prostaglandins. 6 17

Prostaglandin E1 (PGE1) has been used for successful palliation in nine infants with congenital heart disease. Seven patients had pulmonary atresia with ductal-dependent pulmonary blood flow. In this group, systemic O2 saturation increased from a mean value of 45% to 79% after infusion of PGE1, and surgical palliation was successfully done with the infants in stable condition, without hypoxemia or acidemia. An additional patient with coarctation of the aorta had marked ductal dilatation after PGE1 infusion as indicated by umbilical artery pulse pressure. The coarctation was repaired, with the infant in stable condition. The final patient had neonatal tricuspid insufficiency with right to left atrial shunting. Systemic O2 saturation was improved after PGE1 infusion, though the ductus was closed. The improved oxygenation was believed to be due to a reduction in pulmonary vascular resistance by PGE1. Prostaglandin E1 provides a powerful new tool for palliation of critical congenital heart disease in infants whose ductal constriction can markedly influence their clinical status.
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PMID:Pharmacologic dilatation of the ductus arteriosus with prostaglandin E1 in infants with congenital heart disease. 8 28

Six unselected neonates with cyanotic congenital heart disease and life-threatening degrees of arterial oxygen desaturation have been managed by a protocol that includes administration of prostaglandin E1 (PGE1) and early Blalock-Taussig shunting. In 5 patients (seven paired observations) partial pressure of arterial oxygen (PaO2) rose from 19 mm Hg to a mean of 32.9 mm Hg within 20 minutes of initiation of PGE1 (0.1 to 0.2 microgram/kg/hr), infused intravenously or through an aortic catheter placed at ductal level or with both methods. The nonresponsive patient was older than the patients showing a positive response (1 month versus 24 to 96 hours). Following catheterization, immediate palliative operation including a Blalock-Taussig shunt was carried out. Although all had a satisfactory PaO2 (mean, 49 mm Hg) postoperatively, the PGE1-nonresponsive patient experienced serious intraoperative bradycardia, hypotension, and acidosis in contrast to the PGE1-responsive group. In this study, the use of PGE1 was not associated with any apparent serious side effects.
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PMID:The use of prostaglandin E1 and Blalock-Taussig shunts in neonates with cyanotic congenital heart disease. 45 28

The patient with complex congenital heart disease, severe pulmonary outflow obstruction, and visceral heterotaxia, may have 'silent' obstruction of the pulmonary venous return. Severe reduction of pulmonary blood flow secondary to pulmonary stenosis or atresia in such patients may prevent the usual radiographic appearance of pulmonary oedema. If such obstructed anomalous pulmonary venous connections are not diagnosed before operation, construction of a systemic to pulmonary artery anastomosis will unmask the obstruction, usually resulting in pulmonary oedema and death. We have recently 'challenged' a neonate with dextrocardia, vesceral heterotaxia, presumed asplenia, and complex congenital heart disease including pulmonary atresia, with an infusion of prostaglandin E1 to increase pulmonary blood flow via his ductus arteriosus. This resulted in severe pulmonary oedema which partially resolved after the infusion was discontinued. This was interpreted as consistent with obstructed total anomalous pulmonary venous return. This was confirmed at necropsy. Thus, the infusion of prostaglandin E1 before operation in the patient with asplenia or similar cardiac disease may be of aid in unmasking 'silent' obstructions of the pulmonary veins, and is of obvious value in the preoperative assessment of such patients.
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PMID:The prostaglandin challenge. Test to unmask obstructed total anomalous pulmonary venous connections in asplenia syndrome. 62 71

Cardiac catheterization is now a relatively safe procedure when performed by an experienced pediatric cardiology team in a medical center with full ancillary pediatric services as well as cardiac surgery available on a 24 hour basis. Advances in equipment and techniques such as improved radiological equipment, newer catheters, and angled angiocardiographic views have improved diagnostic studies such that intraoperative changes in the preoperative diagnoses fortunately are rare. The use of prostaglandin E1 in neonates with either pulmonary atresia or the coarctation syndrome to achieve ductal dilatation with resultant marked clinical improvement preoperatively is a major advance that should become a standard method of therapy over the next few years. Newer catheterization techniques include devices for enlarging atrial septal defects (balloons and blades), closing atrial septal defects, closing a patent ductus, and performing myocardial biopsies in infants. All of these latter techniques hold promise for extending the pediatric cardiologist's role in providing newer diagnostic as well as therapeutic techniques in the care of infants and children with heart disease.
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PMID:Advances in invasive cardiac diagnosis and management. 73 63

Heart-lung transplantation was, for many years, conceptualized as a possible treatment for patients with combined end-stage cardiac and pulmonary disease. As experience grew with heart transplantation, particularly in the 1970s, the difficulties of performing the orthotopic operation in patients with fixed pulmonary hypertension became apparent. This further impetus for combined heart-lung transplantation led to successful animal experiments in the late 1970s, and the first successful heart-lung transplant operation was performed in 1981. There has been significant evolution in the operative technique for the recipient operation, with emphasis on preservation of the phrenic, vagal, and recurrent laryngeal nerves and on meticulous hemostasis, with particular attention to the bronchial vessels of the posterior mediastinum. Donor procurement is of critical importance to the success of the operation, and criteria for donor selection have been well established. Lung preservation remained, for many years, a significant limitation, but current techniques involving the use of prostaglandin E1 have led to safe distant procurement with ischemic times up to 6 hours. The heart-lung transplant operation remains an effective modality for the treatment of patients with congenital heart disease, primary pulmonary hypertension, chronic obstructive pulmonary disease, and cystic fibrosis.
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PMID:Technique of combined heart-lung transplantation. 148 24

Prostaglandin E1 intravenous infusion is used in infants with ductal-dependent congenital heart disease to maintain ductal patency and prolong life until palliative or corrective surgery is feasible. Complications of prostaglandin administration include fever, diarrhoea, hypotension, apnoea, bradycardia, pseudowidening of the cranial sutures, underossification of the calvarial bones, periostitis, and skin edema [1-3]. This paper presents dramatic plain radiographic features of prostaglandin-induced bone disease, including periosteal proliferation and the unusual bone-within-bone appearance, and provides the previously unpublished CT correlation.
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PMID:Plain film and CT observations in prostaglandin-induced bone changes. 152 47

Plasma concentrations of prostaglandin (PG) E1 (12-150, median 25 pg ml-1) and 13,14-dihydro-PGE1 (3-62, median 45.5 pg ml-1) were measured by gas chromatography-mass spectrometry in eight newborns with ductus arteriosus-dependent congenital heart disease during continuous intravenous infusion of PGE1. Formation of 13,14-dihydro-PGE1 was demonstrated for the first time in neonates. Since 13,14-dihydro-PGE1 has similar biological activities as the parent compound PGE1, pharmacological effects during PGE1 infusion are most likely related to both PGE1 and the generation and action of 13,14-dihydro-PGE1.
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PMID:Formation of biologically active 13,14-dihydro-prostaglandin E1 during intravenous infusion of prostaglandin E1 in newborns with ductus arteriosus-dependent congenital heart disease. 157 56

Prostaglandin administration is the main therapy for ductal-dependent congenital heart disease prior to definitive therapy. We report a case in which tetralogy of Fallot and Noonan syndrome were diagnosed, complicated by small pulmonary arteries, which occasioned a delay in surgery. Treatment was started with prostaglandins, which were given for a total of 2 months, and a diffuse periosteal reaction occurred secondary to the administration of intravenous prostaglandin E1.
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PMID:Periosteal reaction induced by prostaglandins. 162 19


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