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)

Prostaglandin E2 (PGE2) has been used to maintain patency of the ductus arteriosus in four neonates with cyanotic congenital heart disease due to obstructive right heart malformations. PGE2 was infused prior to surgery, and in three patients, during surgery until a satisfactory aorto-pulmonary shunt was established. PGE2 produced consistently an immediate and persistent rise in arterial oxygen saturation, which could be ascribed to dilation of the ductus arteriosus. No major side effects occurred, except for pyrexia in two infants. All patients recovered well from surgery. We propose this treatment as preparation for surgery in any infant with congenital heart defects and ductus-dependent pulmonary blood flow. The same treatment may be useful preoperatively in patients with aortic interruption who also depend on continued patency of the ductus for blood supply to the lower half of the body.
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PMID:E-type prostaglandins: a new emergency therapy for certain cyanotic congenital heart malformations. 5 43

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

A small-for-gestational-age infant with cyanosis due to double outlet right ventricle with severe pulmonary stenosis and patent ductus arteriosus was treated with oral prostaglandin E1 derivative (OP-1206). The constricting ductus arteriosus dilated and the ductus-dependent pulmonary blood flow increased. The recommended dosage was 1.5-2.0 micrograms/kg/day which was lower than that of intravenous PGE1 or of oral PGE2. The administration interval was 6 hours, which was longer than that of oral PGE2. The patient was treated as an out-patient because continuous intravenous infusion was not necessary. Treatment was continued for 2 months without complication, at which time a Blalock-Taussig shunt operation was performed. Orally administered PGE1 derivative (OP-1206) was found to be equally effective to intravenous infusion of PGE1 for both short and long-term management of cyanotic heart disease in which the pulmonary blood flow is mostly dependent on the patency of the ductus arteriosus. Oral PGE1 derivative (OP-1206) may be a possible substitute for intravenous PGE1 infusion therapy.
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PMID:Oral prostaglandin E1 derivative (OP-1206) in an infant with double outlet right ventricle and pulmonary stenosis. Effect on ductus-dependent pulmonary circulation. 177 35

Dietary fish oil containing the n-3 polyunsaturated fatty acids eicosapentaenoic acid (EPA, 20:5) and docosahexaenoic acid (DHA, 22:6) is being consumed by many individuals in an effort to reduce thrombosis and heart disease. However, little is known about how these fatty acids can affect cerebrovascular function. The purpose of the present study was to begin to examine the effects of these fatty acids on cerebral arteriolar diameter and to compare their effects with that of arachidonic acid (AA). Pial arteriolar diameter responses to the topically applied fatty acids [0.2-200 micrograms/ml cerebrospinal fluid (CSF)] were measured in rabbits using in vivo microscopy and the acute cranial window technique. Prostaglandin E2 (PGE2) formed by the brain in response to AA, EPA, and DHA was measured in CSF using radioimmunoassay. EPA induced a dose-dependent dilation response of which the maximum was 29%, whereas the maximal dilation produced by AA was 100%. The arteriolar effect of EPA was reduced by indomethacin or superoxide dismutase plus catalase, indicating vasoactivity due to oxygen radicals formed by cyclooxygenase metabolism of EPA. DHA itself had no effect on diameter or adenosine-induced dilation but reduced dilation by AA when coapplied with AA. AA induced a 65-fold maximal increase in PGE2, whereas EPA and DHA had comparatively little effect. These results imply that substitution of n-3 fatty acids for AA in brain phospholipids may result in less cyclooxygenase-dependent cerebrovascular reactivity. This alteration in reactivity may produce important effects with respect to the brain's blood flow response to a number of physiological and pathological challenges.
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PMID:Effect of fish oil n-3 fatty acids on cerebral microcirculation. 214 67

Patients with diabetes mellitus have an increased susceptibility to heart disease. The exact mechanism for this phenomenon is unclear. Abnormalities in prostaglandin (PG) production have been suggested as a possible cause. In this connection, we examined the PG synthetic capacity of cardiac microsomes from spontaneously diabetic rats. Cardiac microsomes from diabetic and control rats produced varying amounts of 6-keto-PGF1 alpha (stable degradation product of PGI2), PGE2, PGD2, PGF2 alpha, and TXB2 (stable breakdown product of TXA2). In both instances the production of 6-keto-PGF1 alpha predominated, however, microsomes from diabetic rats showed markedly greater conversion of arachidonic acid to all the PG products, especially 6-keto-PGF1 alpha. When PGF2 alpha metabolism was detected between diabetic and control heart preparations. These results show an enhanced cyclooxygenase activity in diabetic rat hearts without any change in prostaglandin dehydrogenase activity. Such a change may promote some of the cardiac alterations seen in diabetic mellitus.
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PMID:Altered myocardial prostaglandin synthesis in spontaneously diabetic rats. 251 48

The preliminary results of our experience with the "inverted" subxiphoid approach for 2D echocardiographic visualisation of patent ductus arteriosus (PDA) in premature neonates and infants are reported. Eight premature ventilated neonates weighting 870 to 1,200 g with an isolated PDA were examined by this technique using a mechanical sector scanner and a 7.5 MHz transducer; three views were obtained (left ventricular outflow tract or "long axis"; an oblique view through the two atria and aortic arch; short axis view of the ventricles). A PDA was directly visualised in 6 of the 8 patients. It was possible to measure its diameter and observe its tortuous or rectilinear trajectory; the outcome of Indomethacin therapy or surgical ligature could also be evaluated. In the 2 patients in whom the PDA was not visualised, there were no clinical symptoms or echocardiographic signs of shunt: these PDA were therefore probably extremely small. In the neonate and infant, it is relatively easy to demonstrate a PDA by this approach. The PDA can also be followed up in "ductus dependent" congenital heart disease during treatment with Prostaglandin E. In conclusion, the subxiphoid approach represents an interesting alternative for the visualisation of PDA, especially in premature neonates in whom the suprasternal and parasternal views are often difficult to obtain.
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PMID:[Value of the subxiphoid approach in 2-dimensional echocardiography for the diagnosis of ductus arteriosus in premature infants and infants]. 309 73

Maintaining patency of the ductus arteriosus pending surgical intervention can be critical to the survival of the neonate with ductal dependent congenital heart disease. Spontaneously delayed ductal closure has been observed clinically and experimentally in newborns with critical pulmonic stenosis. Infants with ductal dependent congenital heart lesions were therefore studied to ascertain whether there was an endogenous increase in dilator prostaglandins prolonging ductal patency. Six neonates with cyanotic lesions (group 1) and six with left ventricular obstructive lesions (group 2) were studied. Circulating PGE2 was not increased in either group. The levels of plasma 6 keto PGF1 alpha, a stable hydrolysis product of prostacyclin, were found to be elevated, but only in the cyanotic group (3143 +/- 1844 vs 404 +/- 250 pg/ml; p less than 0.05; normal less than 500 pg/ml). As expected, PaO2's were also different (36 +/- 15 vs 72 +/- 34 mmHg; p less than 0.05). It is speculated, therefore, that increased synthesis and/or release of prostacyclin, possibly mediated by the hypoxia of the cyanotic ductal dependent lesion, contributes to persistent patency of the ductus arteriosus.
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PMID:Endogenous dilator prostaglandins in congenital heart disease. 332 70

Prostaglandin E2 was administered to 22 newborns with ductus-dependent cyanotic congenital heart disease. Twelve patients had pulmonary atresia and ten simple dextrotransposition of the great arteries. Patients were classified into two groups: group 1 (n = 11) received prostaglandin E2 by the intravenous route (dose: 0.01-0.05 microgram/kg per min); group 2 (n = 11) received prostaglandin E2 by the oral route (dose: 35-65 micrograms/kg per 1-4 h). Treatment lasted for 1-90 days. All infants except one of group 2 showed a significant (greater than 10 Torr) increase in PaO2 following PGE2 administration. The mean increase in PaO2 was higher (P less than 0.01) in group 1 (21.8 +/- 1.7, Torr) than in group 2 (15.8 +/- 1.5, Torr). PaO2 fell significantly (P less than 0.01) in five patients of group 1 who continued treatment orally with satisfactory (greater than 30 Torr) levels in four of them. Severe side effects were observed only in group 1. The data show that similarly to prostaglandin E1 infusions, prostaglandin E2, given i.v. or orally, is useful in the management of infants with ductus-dependent cyanotic congenital heart disease. Oral prostaglandin E2, administration is less effective than i.v. infusions, but can be used for long-term, therapy being more convenient and causing minimal morbidity.
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PMID:Prostaglandin E2 administration in infants with ductus-dependent cyanotic congenital heart disease. 347 49

Prostaglandin E2 was given orally to 59 infants with ductus dependent congenital heart disease, and intravenous infusions were substituted for varying periods in 27 of them. An additional three neonates received intravenous treatment alone. Mean oral maintenance dose was 27 micrograms/kg per hour and the mean intravenous dose was 0.005 micrograms/kg per minute. Mean duration of treatment was 49 days (range 16 hours to 272 days). Oral treatment was almost always effective and was especially suitable for long term use. Low dose intravenous treatment was readily substituted when indicated. Complications were usually 'minor'. Growth of the infants and of their pulmonary arteries facilitated later surgical management.
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PMID:Evaluation of oral and low dose intravenous prostaglandin E2 in management of ductus dependent congenital heart disease. 386 36

We present two patients with subcutaneous fat necroses (SCFN) in whom endocrinologic studies revealed an association with elevated prostaglandin E (PGE) levels. A boy born after prolonged labor complicated by meconium aspiration developed erythematous, indurated plaques over the back, arms, buttocks, and cheeks at 4 days of age. A biopsy specimen of involved skin showed panniculitis with foci of necrotic adipocytes containing radially arranged, needle-shaped clefts and a granulomatous infiltrate in the septae. Laboratory studies revealed hypercalcemia of 13.6 mg/dl (normal 8.8-10.1 mg/dl), elevated 1.25-1.25(OH)2D3, and increased urinary excretion of PGE2. The child was hospitalized and treated with systemic steroids and diuretics, with resolution of SCFN and hypercalcemia. The second patient was a girl born with cyanotic heart disease. A diagnosis of Ebstein anomaly was made, and intravenous PGE1 was started to keep patent the ductus arteriosus. Four days later erythematous, indurated plaques were noted on the knee, back, and anterior chest. A skin biopsy specimen revealed SCFN. There was no associated laboratory abnormality. On discontinuing PGE1, no new lesions formed and the existing panniculitis resolved. These two cases demonstrate the association between SCFN and elevated PGE levels (endogenous in patient 1, exogenous in patient 2). No previous reports of SCFN after the administration of PGE1 have appeared in the literature.
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PMID:Subcutaneous fat necrosis, hypercalcemia, and prostaglandin E. 779 19


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