Prenatal features of ductus arteriosus constriction and restrictive foramen ovale in d-transposition of the great arteries.
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BACKGROUND: Although most neonates with d-transposition of the great arteries (TGA) have an uncomplicated preoperative course, some with a restrictive foramen ovale (FO), ductus arteriosus (DA) constriction, or pulmonary hypertension may be severely hypoxemic and even die shortly after birth. Our goal was to determine whether prenatal echocardiography can identify these high-risk fetuses with TGA. METHODS AND RESULTS: We reviewed the prenatal and postnatal echocardiograms and outcomes of 16 fetuses with TGA/intact ventricular septum or small ventricular septal defect. Of the 16 fetuses, 6 prenatally had an abnormal FO (fixed position, flat, and/or redundant septum primum). Five of the 6 had restrictive FO at birth. Five fetuses had DA narrowing at the pulmonary artery end in utero, and 6 had a small DA (diameter z score of <-2.0). Of 4 fetuses with the most diminutive DA, 2 also had an abnormal appearance of the FO, and both died immediately after birth. One other fetus had persistent pulmonary hypertension. Eight fetuses had abnormal Doppler flow pattern in the DA (continuous high-velocity flow, n=1; retrograde diastolic flow, n=7). CONCLUSIONS: Abnormal features of the FO, DA, or both are present in fetuses with TGA at high risk for postnatal hypoxemia. These features may result from the abnormal intrauterine hemodynamics in TGA. A combination of restrictive FO and DA constriction in TGA may be associated with early neonatal death. (+info)
Inducible NO synthase inhibition attenuates shear stress-induced pulmonary vasodilation in the ovine fetus.
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Recent studies have suggested that type II (inducible) nitric oxide (NO) synthase (NOS II) is present in the fetal lung, but its physiological roles are uncertain. Whether NOS II activity contributes to the NO-mediated fall in pulmonary vascular resistance (PVR) during shear stress-induced pulmonary vasodilation is unknown. We studied the hemodynamic effects of two selective NOS II antagonists [aminoguanidine (AG) and S-ethylisothiourea (EIT)], a nonselective NOS antagonist [nitro-L-arginine (L-NNA)], and a nonselective vasoconstrictor (U-46619) on PVR during partial compression of the ductus arteriosus (DA) in 20 chronically prepared fetal lambs (mean age 132 +/- 2 days, term 147 days). At surgery, catheters were placed in the left pulmonary artery (LPA) for selective drug infusion, an ultrasonic flow transducer was placed on the LPA to measure blood flow, and an inflatable vascular occluder was placed loosely around the DA for compression. On alternate days, a brief intrapulmonary infusion of normal saline (control), AG, EIT, L-NNA, or U-46619 was infused in random order into the LPA. The DA was compressed to increase mean pulmonary arterial pressure (MPAP) 12-15 mmHg above baseline values and held constant for 30 min. In control studies, DA compression reduced PVR by 42% from baseline values (P < 0.01). L-NNA treatment completely blocked the fall in PVR during DA compression. AG and EIT attenuated the decrease in PVR by 30 and 19%, respectively (P < 0.05). Nonspecific elevation in PVR by U-46619 did not affect the fall in PVR during DA compression. Immunostaining for NOS II identified this isoform in airway epithelium and vascular smooth muscle in the late-gestation ovine fetal lung. We conclude that selective NOS II antagonists attenuate but do not block shear stress-induced vasodilation in the fetal lung. We speculate that stimulation of NOS II activity, perhaps from smooth muscle cells, contributes in part to the NO-mediated fall in PVR during shear stress-induced pulmonary vasodilation. (+info)
Cyclooxygenase-2 plays a significant role in regulating the tone of the fetal lamb ductus arteriosus.
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Nonselective cyclooxygenase (COX) inhibitors are potent tocolytic agents but have adverse effects on the fetal ductus arteriosus. We hypothesized that COX-2 inhibitors may not affect the ductus if the predominant COX isoform is COX-1. To examine this hypothesis, we used ductus arteriosus obtained from late-gestation fetal lambs. In contrast to our hypothesis, fetal lamb ductus arteriosus expressed both COX-1- and COX-2-immunoreactive protein (by Western analysis). Although COX-1 was found in both endothelial and smooth muscle cells, COX-2 was found only in the endothelial cells lining the ductus lumen (by immunohistochemistry). The relative contribution of COX-1 and COX-2 to PGE2 synthesis was consistent with the immunohistochemical results: in the intact ductus, PGE2 formation was catalyzed by both COX-1 and COX-2 in equivalent proportions; in the endothelium-denuded ductus, COX-2 no longer played a significant role in PGE2 synthesis. NS-398, a selective inhibitor of COX-2, was 66% as effective as the selective COX-1 inhibitor valeryl salicylate and the nonselective COX inhibitor indomethacin in causing contraction of the ductus in vitro. At this time, caution should be used when recommending COX-2 inhibitors for use in pregnant women. (+info)
The effects of maternal indomethacin therapy on human fetal branch pulmonary arterial vascular impedance.
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OBJECTIVE: To examine whether maternal indomethacin therapy affects human fetal pulmonary arterial vascular impedance without constriction of the ductus arteriosus and to determine the changes in the pulmonary arterial vascular impedance in the presence of ductal constriction. STUDY DESIGN: In this cross-sectional study, 52 normal fetuses without maternal medication (control group), 33 fetuses without ductal constriction (Study group I) and 11 fetuses with ductal constriction (Study group II) during maternal indomethacin therapy between 24 and 34 weeks of gestation were examined by Doppler echo-cardiography. Blood velocity waveforms across the proximal right or left pulmonary artery were obtained and the pulsatility index (PI) of the proximal pulmonary arteries was calculated. RESULTS: In the control group, the proximal pulmonary artery PI was higher (p < 0.0001) at 24-25 weeks (n = 7) (3.73 +/- 0.33; mean +/- SD) than at 33-34 week of gestation (n = 11) (2.98 +/- 0.27). The PI was constantly greater (p < 0.005) in Study group I than in the control group. However, in this group the mean average weekly decrease in the PI of the proximal pulmonary arteries was similar to that in the control group. After 26 weeks of gestation, the PI values in Study group II were significantly higher than in the control group (27 weeks: 4.12 vs. 3.34 (p < 0.005); 30 weeks: 4.48 vs. 3.14 (p < 0.0001); 34 weeks: 4.96 vs. 3.00 (p < 0.0001), respectively). CONCLUSIONS: Human fetal pulmonary arterial vascular impedance is increased by maternal indomethacin therapy even without ductal constriction. In the presence of ductal constriction, the magnitude of the increase in the vascular impedance is related to the gestational age. (+info)
Biventricular repair approach in ducto-dependent neonates with hypoplastic but morphologically normal left ventricle.
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OBJECTIVES: Increased afterload and multilevel LV obstruction is constant. We assumed that restoration of normal loading conditions by relief of LV obstructions promotes its growth, provided that part of the cardiac output was preoperatively supported by the LV, whatever the echocardiographic indexes. BACKGROUND: Whether to perform uni- or biventricular repair in ducto dependent neonates with hypoplastic but morphologically normal LV (hypoplastic left heart syndrome classes II & III) remains unanswered. Echocardiographic criteria have been proposed for surgical decision. METHODS: Twenty ducto dependent neonates presented with this anomaly. All had aortic coarctation associated to multilevel LV obstruction. Preoperative echocardiographic assessment showed: mean EDLW of 12.4 +/- 3.03 ml/m2 and mean Rhodes score of -1.73 +/-0.8. Surgery consisted in relief of LV outflow tract obstruction by coarctation repair in all associated to aortic commissurotomy in one and ASD closure in 2. RESULTS: There were 3 early and 2 late deaths. Failure of biventricular repair and LV growth was obvious in patients with severe anatomic mitral stenosis. The other demonstrated growth of the left heart. At hospital discharge the EDLVV was 19.4+/-3.12 ml/m2 (p = 0.0001) and the Rhodes score was -0.38+/-1.01 (p = 0.0003). Actuarial survival and freedom from reoperation rates at 5 years were 72.5% and 46%, respectively. CONCLUSIONS: Biventricular repair can be proposed to ducto dependent neonates with hypoplastic but morphologically normal LV provided that all anatomical causes of LV obstruction can be relieved. Secondary growth of the left heart then occurs; however, the reoperation rate is high. (+info)
Coanda effect on ductal flow in the pulmonary artery.
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The Coanda effect (the tendency of a jet stream to adhere to a boundary wall), and the relevant anatomy, may explain the location of ductal jets within the main pulmonary artery. With the usual insertion of the duct close to the left pulmonary artery, during right ventricular ejection, the ductal jet adheres to the left wall of the main pulmonary artery. When right ventricular ejection is absent in pulmonary atresia, the ductal jet streams down the right wall of the pulmonary artery to the pulmonary valve, reverses, and maintains a parallel column back toward the bifurcation. If the reversed flow is mistaken for ejection from the right ventricle, the diagnosis of pulmonary atresia may be missed. (+info)
Fate of the stented arterial duct.
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BACKGROUND: The technical aspects of ductal stenting have been reported, but little is known of the fate of the duct after stent implantation. METHODS AND RESULTS: Nineteen patients underwent stent implantation to maintain ductal patency. Eight had hypoplastic left heart (HLH) syndrome, 10 had pulmonary atresia, and 1 had tricuspid atresia. Median survival with HLH was 57 (12 to 907) days. Stent implantation was successful in all cases of HLH, but there were no long-term survivors. Two well-palliated infants died at transplantation. Median survival with duct-dependent pulmonary flow was 183 (0 to 1687) days, with 3 patients well at latest follow-up (56, 55, and 9 months, respectively). There were 2 operative deaths due to ductal spasm and 4 late deaths, 1 due to duct thrombosis, 1 due to chronic lung disease, and 2 of unknown cause. Stent implantation failed in 4 of the 11 cases. Assessment of endothelialization was possible in 13 cases; the stent was partially covered in 3 and fully endothelialized in all 10 cases assessed >8 weeks after implantation. In patients stented for inadequate pulmonary flow, ductal intimal hyperplasia occurred by 9 months in all 3 survivors but responded to repeated dilation. CONCLUSIONS: Ductal stenting cannot be recommended. In patients with HLH, it provides only short-term palliation even when combined with pulmonary artery banding. With duct-dependent pulmonary blood flow, the procedure carries high risk, and duration of palliation is poor. In patients with bilateral ducts and absent central pulmonary arteries, good palliation may be achieved, but repeated angioplasty is necessary to counteract intimal hyperplasia. (+info)
Ductus venosus blood velocity in persistent pulmonary hypertension of the newborn.
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AIMS: To investigate the ductus venosus flow velocity (DVFV) in infants with persistent pulmonary hypertension of the newborn (PPHN); to evaluate the DVFV pattern as a possible diagnostic supplement in neonates with PPHN and other conditions with increased right atrial pressure. METHODS: DVFV was studied in 16 neonates with PPHN on days 1-4 of postnatal life using Doppler echocardiography. DVFV was compared with that in mechanically ventilated neonates with increased intrathoracic pressure, but without signs of PPHN (n=11); with neonates with congenital heart defects resulting in right atrial pressure (n=6); and with preterm neonates without PPHN (n=46); and healthy term neonates (n=50). RESULTS: Infants with PPHN and congenital heart defects with increased right atrial pressure were regularly associated with an increased pulsatile pattern and a reversed flow velocity in ductus venosus during atrial contraction. A few short instances of reversed velocity were also noted in normal neonates before the circulation had settled during the first day after birth. CONCLUSIONS: A reversed velocity in the ductus venosus during atrial contraction at this time signifies that central venous pressure exceeds portal pressure. This negative velocity deflection is easily recognised during Doppler examination and can be recommended for diagnosing increased right atrial pressure and PPHN. (+info)