Impact of fetal diagnosis of congenital heart disease on parents / 소아과

PURPOSE: This study was performed to assess how a fetal diagnosis of congenital heart disease affects parents, as regards pregnancy management and care of infants after birth. METHODS: Database search to find out abnormal fetal echocardiography performed at Seoul National University Children's Hospital from July 1988 to June 2003 revealed 370 examinations. After excluding both arrhythmias without structural cardiac disease and multiple pregnancies, 299 pregnancies remained and this data formed the basis of this analysis. We retrospectively reviewed the medical records with special attention to pregnancy outcomes and also tried to find out factors influencing parental decisions on whether to continue or terminate pregnancy. RESULTS: In this study, the mean gestation age at diagnosis was 28+/-6.0 weeks. The mean age of mothers was 30+/-3.9 years old. Younger gestational ages at diagnosis(P=0.000), more severe grades of fetal heart disease(P=0.002) and younger mothers(P=0.014) correlated with terminations of pregnanies. But the grades of fetal status, the grades of associated anomaly, whether in-vitro-fertilization was carried out or not and numbers of previous children were not significant. CONCLUSION: This study found that the earlier gestational ages at diagnosis, younger maternal age and higher grades of fetal heart disease tended to lead parent to select abortions. Fetal echocardiographies were performed too late. Moreover Koreans have a biased view that malformation is a something incurable and a tragedy not only to oneself, but also to a family. So parents select terminations of pregnancy, even in curable cases. This is very unethical.

Echocardiographic Assessment of Left Ventricular Diastolic Function in Transitional Circulation Period

BACKGROUND AND OBJECTIVES: During the transitional period from fetal to neonatal life, there are dramatic changes in the newborn circulation. Among these changes, the left ventricular diastolic function can be easily assessed by Doppler measurement of the mitral inflow. However, there are many physiologic and hemodynamic factors responsible for the mitral inflow. This study was designed to evaluate several parameters that represent the left ventricular function during the transitional circulation period. SUBJECTS AND METHODS: Eighteen normal full-term infants were studied by serial two-dimensional, Doppler and color flow echocardiography within 24 hours before and after birth, between 2 days and 6 days after birth and between 7 days and 30 days after birth). RESULTS: One day after birth, the mitral valve (MV) E velocity and E/A increased (37.9+/-7.5 vs. 60.3+/-9.0 and 0.8+/-0.1 vs. 1.1+/-0.1, p<0.01, respectively), but the MV A velocity, the velocity of propagation (Vp), the LV isovolumic relaxation time (IVRT), the corrected IVRT and the tissue Doppler ventricular septum e' and s' did not change. Although Vp/E and a' decreased (1.2+/-0.3 vs. 0.7+/-0.2 and 8.2+/-1.8 vs. 6.5+/-1.7, p<0.05, respectively), the E/e' and the systolic and diastolic pulmonary venous flow velocities increased after birth (6.3+/-1.9 vs. 11.6+/-2.9, and 26.1+/-6.7 vs. 64.5+/-9.6, and 20.9+/-4.1 vs. 63.5+/-17.2, p<0.05, respectively). CONCLUSION: Increased preload plays a key role for the increased MV E/A ratio after birth. Other unknown factors (and possibly including pericardial restriction) may be also responsible for left ventricular diastolic function.

A False Diagnosis of Hypoplastic Left Heart Syndrome in a Fetus

Typical hypoplastic left heart syndrome(HLHS) is a distinct pathologic entity with aortic atresia, mitral atresia, very hypoplastic or absent left ventricle and thread like ascending aorta. Occasionally, the lesser degree of hypoplasia is found and is called hypoplastic left heart complex(HLHC) by some authors. This HLHC is often associated with critical aortic stenosis. Fetal echocardiography has enabled us to observe human fetal heart in-utero and to diagnose congenital heart disease prenatally over the last 20 years. The diagnosis of HLHS in fetal echocardiography is based on 2-dimensional echocardio -graphic evidence of a diminutive ascending aorta, aortic atresia, mitral atresia or severe stenosis and a hypoplastic left ventricle. Abnormal flow direction through atrial septum or through isthmus greatly aids the diagnosis. This report shows a fetal case who showed hypoplastic left side chambers and retrograde isthmic flow and was diagnosed with hypoplastic left heart syndrome. After birth, although the baby had tachy-dyspnea for the first 3 weeks, she finally recovered without any intervention and showed catch up growth of left side chambers. This case illustrates the extreme difficulty of assessing left ventricle in a fetus.

Enhancement of cyclosporine-induced oxidative damage of kidney mitochondria by iron

The present study investigated the stimulatory effects of iron (or ascorbate) on cyclosporine-induced kidney mitochondrial damage. Damaging effect of 50 muM cyclosporine plus 20 muM Fe2+ on mitochondrial lipids and proteins of rat kidney and hyaluronic acid was greater than the summation of oxidizing action of each compound alone, except sulfhydryl oxidation. Cyclosporine and 100 muM ascorbate showed an enhanced damaging effect on lipids but not on proteins. The peroxidative action of cyclosporine on lipids was enhanced with increasing concentrations of Fe2+. Ferric ion (20 muM) also interacted with cyclosporine to stimulate lipid peroxidation. Damaging action of cyclosporine on mitochondrial lipids was enhanced by ascorbate (100 muM and 1 mM). Iron chelators, DTPA and EDTA, attenuated carbonyl formation induced by cyclosporine plus ascorbate. Cyclosporine (100 muM) and 50 muM Fe2+ (or 100 muM ascorbate) synergistically stimulated degradation of 2- alpha deoxyribose. Cyclosporine (1 to 100 muM) reduced ferric ion in a dose dependent manner, which is much less than ascorbate action. Addition of Fe2+ caused a change in absorbance spectrum of cyclosporine in 230~350 nm of wavelengths. The results show that cyclosporine plus iron (or ascorbate) exerts an enhanced damaging effect on kidney mitochondria. Iron and ascorbate appear to promote the nephrotoxicity induced by cyclosporine.

Depression of Ca2+ influx in complement C5a-stimulated neutrophils by calmodulin inhibitors

Role of Ca2+/calmodulin complex in intracellular Ca2+ mobilization in neutrophils has not been clearly elucidated. In this study, effects of chlorpromazine, trifluoperazine and imipramine on the intracellular Ca2+ mobilization, including Ca2+ influx, in C5a-activated neutrophils were investigated. Complement C5a-stimulated superoxide production and myeloperoxidase release in neutrophils were inhibited by chlorpromazine, trifluoperazine and imipramine, except no effect of imipramine on myeloperoxidase release. A C5a-elicited elevation of (Ca2+)i in neutrophils was inhibited by chlorpromazine, trifluoperazine, imipramine, staurosporine, genistein, EGTA, and verapamil but not affected by pertussin toxin. The intracellular Ca2+ release in C5a-activated neutrophils was not affected by chlorpromazine and imipramine. Chlorpromazine and imipramine inhibited Mn2+ influx by C5a-activated neutrophils. Thapsigargin-evoked Ca2+ entry was inhibited by chlorpromazine, trifluoperazine, imipramine, genistein, EGTA and verapamil, while in the activation process of neutrophils. The depressive action of calmodulin inhibitors on the elevation of cytosolic Ca2+ level in C5a-activated neutrophils appears to be accomplished by inhibition of Ca2+ influx from the extracellular medium.

Comparison of regulatory action of cAMP and cGMP on the activation of neutrophil responses

The regulatory role of cyclic nucleotides in the expression of neutrophil responses has been examined. fMLP-stimulated superoxide production in neutrophils was inhibited by dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), histamine, adenosine + theophylline, cAMP elevating agents, and 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP) and sodium nitroprusside, cGMP elevating agents. Staurosporine, a protein kinase C inhibitor, genistein, a protein tyrosine kinase inhibitor and chlorpromazine, a calmodulin inhibitor, inhibited superoxide production by fMLP, but they did not further affect the action of DBcAMP on the stimulatory action of fMLP. DBcAMP, histamine, adenosine + theophylline and genistein inhibited myeloperoxidease release evoked by fMLP, whereas BrcGMP, sodium nitroprusside and staurosporine did not affect it. The elevation of (Ca2+)-i evoked by fMLP was inhibited by genistein and chlorpromazine but was not affected by staurosporine. DBcAMP exerted little effect on the initial peak in (Ca2+)-i response to fMLP but effectively inhibited the sustained rise. On the other hand, BrcGMP significantly inhibited both phases. fMLP-induced Mn-2+ influx was inhibited by either DBcAMP or BrcGMP. These results suggest that fMLP-stimulated neutrophil responses may be regulated by cAMP more than cGMP. cAMP and cGMP appear not affect stimulated responses by direct protein kinase C activation. Their regulatory action on the stimulated neutrophil responses may be not influenced by other activation processes.

Midterm Result after Transcatheter Occlusion of Patent Ductus Arteriosus with Rashkind PDA Umbrella Device

No abstract available.

Quantitative assessment of the diameters of tricuspid valve, mitral valve and great arteries in the normal human fetus

No abstract available.