[Lympho-venous shunts and thromboids in urinary obstruction]. / Lymphovenöse Shunts und Thromboide bei Harnstauungsniere.

This case of urinary obstruction with short anamnesis illuminates the early tissue reaction to urine extravasation, especially the Tamm-Horsfall protein. The latter becomes organized in the manner of a foreign body substance and drains via ectatic renal lymph vessels and reopened lymphovenous shunts into the intrarenal venous system. Polypoid formations (thromboids) with or without vessel obliteration appear to result in a clinical course of severe renal impairment.

[Acute generalized cat scratch disease in myelodysplastic syndrome]. / Akute generalisierte Katzenkratzkrankheit bei myelodysplastischem Syndrom.

In patients with normal immunity, cat scratch disease typically develop a papule at the portal of entry and no other cutaneous features. A 73 year old male patient with a myelodysplastic syndrome developed generalized petechial, papular and, vasculitic skin lesions in association with cat scratch disease. After the diagnosis was established by identifying the causative organism in a lymph node biopsy, the patient was treated with erythromycin for three weeks resulting in progressive clearance of the skin lesions. Apart from the soluble IL-2 receptor, no other serologic inflammatory parameters were elevated. IgG antibodies against Bartonella henselae and Bartonella quintana increased only slightly during acute exacerbation of the disease, but significantly increased some months later. The diagnosis was established by the positive staining of the lymph node biopsy using the Warthin-Starry stain.

Effects of specific inhibition of cyclo-oxygenase-1 and cyclo-oxygenase-2 in the rat stomach with normal mucosa and after acid challenge.

1. Effects of the cyclo-oxygenase (COX)-1 inhibitor SC-560 and the COX-2 inhibitors rofecoxib and DFU were investigated in the normal stomach and after acid challenge. 2. In healthy rats, neither SC-560 nor rofecoxib (20 mg kg(-1) each) given alone damaged the mucosa. Co-treatment with SC-560 and rofecoxib, however, induced severe lesions comparable to indomethacin (20 mg kg(-1)) whereas co-administration of SC-560 and DFU (20 mg kg(-1) each) had no comparable ulcerogenic effect 5 h after dosing. 3. SC-560 (20 mg kg(-1)) inhibited gastric 6-keto-prostaglandin (PG) F(1alpha) by 86+/-5% and platelet thromboxane (TX) B(2) formation by 89+/-4% comparable to indomethacin (20 mg kg(-1)). Rofecoxib (20 mg kg(-1)) did not inhibit gastric and platelet eicosanoids. 4. Intragastric HCl elevated mucosal mRNA levels of COX-2 but not COX-1. Dexamethasone (2 mg kg(-1)) prevented the up-regulation of COX-2. 5. After acid challenge, SC-560 (5 and 20 mg kg(-1)) induced dose-dependent injury. Rofecoxib (20 mg kg(-1)), DFU (5 mg kg(-1)) and dexamethasone (2 mg kg(-1)) given alone were not ulcerogenic but aggravated SC-560-induced damage. DFU augmented SC-560 damage 1 but not 5 h after administration whereas rofecoxib increased injury after both treatment periods suggesting different time courses. 6. Gastric injurious effects of rofecoxib and DFU correlated with inhibition of inflammatory PGE(2). 7. The findings show that in the normal stomach lesions only develop when both COX-1 and COX-2 are inhibited. In contrast, during acid challenge inhibition of COX-1 renders the mucosa more vulnerable suggesting an important role of COX-1 in mucosal defence in the presence of a potentially noxious agent. In this function COX-1 is supported by COX-2. In the face of pending injury, however, COX-2 cannot maintain mucosal integrity when the activity of COX-1 is suppressed.

Selective cyclo-oxygenase-2 inhibitors aggravate ischaemia-reperfusion injury in the rat stomach.

1. Effects of indomethacin, the selective cyclo-oxygenase (COX)-2 inhibitors NS-398 and DFU, and dexamethasone on gastric damage induced by 30 min ischaemia followed by 60 min reperfusion (I-R) were investigated in rats. Modulation of gastric levels of COX-1 and COX-2 mRNA by I-R was evaluated using Northern blot and reverse transcription-polymerase chain reaction. 2. I-R-induced gastric damage was dose-dependently aggravated by administration of indomethacin (1 - 10 mg kg(-1)), NS-398 (0.4 - 4 mg kg(-1)) or DFU (0.02 - 2 mg kg(-1)) as assessed macroscopically and histologically. 3. Likewise, administration of dexamethasone (1 mg kg(-1)) significantly increased I-R damage. 4. Low doses of 16, 16-dimethyl-prostaglandin(PG)E(2), that did not protect against ethanol-induced mucosal damage, reversed the effects of the selective COX-2 inhibitors, indomethacin and dexamethasone. 5. I-R had no effect on gastric COX-1 mRNA levels but increased COX-2 mRNA levels in a time-dependent manner. Dexamethasone inhibited the I-R-induced expression of COX-2 mRNA. 6. I-R was not associated with a measurable increase in gastric mucosal formation of 6-keto-PGF(1alpha) and PGE(2). PG formation was substantially inhibited by indomethacin (10 mg kg(-1)) but was not significantly reduced by NS-398 (4 mg kg(-1)), DFU (2 mg kg(-1)) or dexamethasone (1 mg kg(-1)). 7. The findings indicate that selective COX-2 inhibitors and dexamethasone markedly enhance gastric damage induced by I-R. Thus, whereas COX-2 has no essential role in the maintenance of gastric mucosal integrity under basal conditions, COX-2 is rapidly induced in a pro-ulcerogenic setting and contributes to mucosal defence by minimizing injury. This suggests that in certain situations selective COX-2 inhibitors may have gastrotoxic effects.

Peptidergic and cholinergic neurons and mediators in peptone-induced gastroprotection: role of cyclooxygenase-2.

This study investigates the neural pathways, mediators, and cyclooxygenase isoenzymes involved in the gastroprotection conferred by peptone in rats. Intragastric perfusion with 8% peptone protected against gross and histological damage induced by subsequent perfusion with 50% ethanol. The gastroprotective effect of peptone was near maximally inhibited by gastrin immunoneutralization, inactivation of capsaicin-sensitive afferent neurons, calcitonin gene-related peptide (CGRP) immunoneutralization, blockade of gastrin receptors, CGRP, bombesin/gastrin-releasing peptide (GRP), or somatostatin receptors, and by the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester and was partially (46%) counteracted by atropine. Indomethacin and the selective cyclooxygenase-2 inhibitors NS-398 and L-745,337 dose dependently (50% inhibitory dose, 4.2, 0.8, and 1.5 mg/kg, respectively) attenuated the peptone-induced protection. Dexamethasone was ineffective. These results indicate that protective effects of peptone involve endogenous gastrin and possibly somatostatin and are mediated by capsaicin-sensitive afferent, cholinergic, and bombesin/GRP neurons. CGRP, NO, and prostaglandins participate as essential mediators. The study provides evidence that prostaglandins derived from a constitutive cyclooxygenase-2 contribute to mucosal defense in the presence of ulcerogens and thus participate in homeostatic functions of the stomach.

Selective cyclo-oxygenase-2 inhibitors and their influence on the protective effect of a mild irritant in the rat stomach.

1. The effects of the non-selective cyclo-oxygenase (COX) inhibitor indomethacin and the selective COX-2 inhibitors, N-[2-(cyclohexyloxy)-4-nitrophenyl] methanesulphonamide (NS-398), 5-methanesulphonamido-6-(2,4-difluorothio-phenyl)-1-indan one (L-745,337) and 5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulphonyl) phenyl-2(5H)-furanone (DFU), on the protection induced by the mild irritant 20% ethanol were investigated in the rat stomach. 2. Instillation of 20% ethanol (1 ml, p.o.) effectively protected against gastric mucosal injury induced by subsequent instillation of 70% or 96% ethanol (1 ml, p.o.). 3. Oral administration of indomethacin (1.25-20 mg kg[-1]) dose-dependently counteracted the protective effect of 20% ethanol (ID50: 3.5 mg kg[-1]). 4. Likewise, NS-398 (0.1-1 mg kg[-1]), L-745,337 (0.2-2 mg kg[-1]) and DFU (0.02-0.2 mg kg[-1]) inhibited the protective effect of 20% ethanol in a dose-dependent manner with ID50 values of 0.3 mg kg(-1), 0.4 mg kg(-1) and 0.06 mg kg(-1), respectively. 5. Inhibition of mild irritant-induced protection was also found when NS-398 (1 mg kg[-1]) was administered s.c. or when 96% ethanol was used to damage the mucosa. 6. Pretreatment with 16,16-dimethyl-prostaglandin (PG)E2 at 4 ng kg(-1), a dose that did not protect against ethanol (70%)-induced mucosal damage when given alone, completely reversed the effect of the selective COX-2 inhibitors on the mild irritant-induced protection. 7. Pretreatment with dexamethasone (3 mg kg(-1), 24 and 2 h before instillation of 20% ethanol) did not affect the protective activity of the mild irritant, indicating that enzyme induction is not involved. 8. Indomethacin (20 mg kg(-1), p.o.) did not prevent the protection conferred by sodium salicylate (100 mg kg[-1]), dimercaprol (30 microg kg[-1]), iodoacetamide (50 mg kg[-1]) and lithium (20 mg kg[-1]). Likewise, the protective effect of these agents was not counteracted by NS-398 (1 mg kg(-1), p.o.). 9. Whereas indomethacin (20 mg kg(-1), p.o.) near-maximally inhibited gastric mucosal formation of PGE2, 6-keto-PGF1alpha and thromboxane (TX) B2 as well as platelet TXB2 release, the selective COX-2 inhibitors were ineffective. 10. The findings show that selective COX-2 inhibitors, although lacking in ulcerogenic activity, prevent the protection conferred by a mild irritant. Prostaglandis generated by a constitutive COX-2 could thus contribute to physiological functions involved in gastric homeostasis, although at present a non-COX-2-related mechanism underlying the effect of the selective COX-2 inhibitors tested on mild irritant-induced protection cannot be completely excluded.

Diagnostic and perinatal management of fetal extrasystole.

Fifty fetuses referred to the Polish Mother's Memorial Hospital for fetal echocardiography between January 1, 1991 and June 1, 1995 were evaluated. The mean fetal gestational age at the time of diagnosis of arrhythmia was 34.1 weeks, and the mean gestational age at the time of delivery was 38.7 weeks. Checkup echocardiographic examinations were performed every 10-14 days, for a mean 2.4 studies per fetus. In most cases (48/50, 96%), premature atrial contractions were present during the first echocardiography examination. The fetal heart study was normal in 30 cases; in 7 (14%) there was tricuspid valve regurgitation, in 7 (14%) an atrial septal aneurysm, in 4 congenital heart defects, in 1 myocardial hypertrophy, and in 1 disproportion in the four-chamber view. Of the 50 fetuses, 43 underwent regular echocardiographic monitoring alone; in 7 cases, based on the presence of additional echocardiographic findings, pharmacotherapy was applied (digoxin, verapamil, or both). Three neonates died after delivery owing to malformations in two cases (one critical aortic stenosis, one spina bifida plus hygroma colli) and due to myocarditis in one case. In six of seven newborns treated in utero, myocarditis was diagnosed after birth (including the one with neonatal demise). Most of the newborns were in good condition after birth, their mean Apgar score being 8.6 and the mean birth weight 3259 g. We concluded that most extrasystoles represent an isolated anomaly, not affecting the fetal condition. Their presence should not influence the obstetric care and may require only echocardiographic monitoring. In most of our cases the premature contractions subsided after birth, although sometimes they preceded fetal supraventricular tachycardia or appeared after congenital myocarditis.

Reversal of diastolic flow in the middle cerebral artery of the fetus during the second half of pregnancy.

This study obtained data on 22 fetuses in whom reversal of diastolic flow in the middle cerebral artery (MCA) was seen. In 59% of cases there was normal heart function and in 28% there was isolated tricuspid valve regurgitation. The majority (73%) of cases presented with normal fetal anatomy and most (82%) had a normal amniotic fluid index and normal fetal growth. In all cases, Doppler results of the umbilical artery and vein were normal. Of the women, 65% were on no medication and 73% did not smoke during pregnancy. The reversal of diastolic flow in the MCA was seen temporarily in the majority of cases (for 2-30 min); however, in one case with rhesus factor disease and a rim of ascites, it was observed for a longer period (about 2 h) and on the following day, intrauterine demise was recorded. In most of the cases without structural malformations, the neonatal outcome was normal. We conclude that reversed diastolic flow in the MCA is a rare and usually transient event. In one of our cases prolonged reversed flow preceded intrauterine demise. Therefore, this may be an ominous sign and careful fetal surveillance should be undertaken when this observation is made. There are a few possible pathomechanisms of reversed diastolic flow in the MCA. In the majority of cases the cause of the observed phenomenon remains unknown, but an increased pressure in the right ventricle and possible tricuspid regurgitation should be considered.

Fetal functional pulmonary atresia with ascites resolving spontaneously before birth. A case report.

In this case we report functional pulmonary atresia in a fetus with significant tricuspid valve regurgitation and severe ascites, with spontaneous improvement without prenatal intervention and a subsequent follow-up at 8 weeks after birth.

Parvovirus particles in a fetal-heart with myocarditis: ultrastructural and immunohistochemical study.

We report on the occurrence of parvovirus particles and VP1 (84 kDa) and VP2 (58 kDa) viral antigens in the heart of a case of fatal myocarditis in a fetus of a 26 year old women. Numerous cells containing intranuclear inclusions were identified within the blood vessels of the heart in a close apposition to muscle fibers. These cells were characterized by plentiful mitochondria and were consistent with erythroblasts. Typically, inclusions consisted of electrondense marginated chromatin and granular and amorphous "cores". At higher magnification, parvovirus particles, approximately 23 nm in diameter, were visualized either as relatively small clusters or forming large paracrystalline arrays. Virus buds were never observed. In addition, unusual membrane proliferation was seen. These findings support a notion that parvovirus may invade the fetal heart.

Tachykinin-induced increase in gastric mucosal resistance: role of primary afferent neurons, CGRP, and NO.

The tachykinins [Ala5,beta-Ala8]neurokinin A-(4-10) {[Ala5,beta-Ala8]NKA-(4-10)} and NKA-(4-10) dose dependently protected against ethanol-induced gastric mucosal damage in rats (half-maximal inhibitory dose, 46 and 48 nmol/kg, respectively). These effects were abolished by primary afferent nerve denervation, calcitonin gene-related peptide (CGRP) immunoneutralization, the CGRP receptor antagonist human (h) hCGRP-(8-37), and inhibition of nitric oxide (NO) biosynthesis by NG-nitro-L-arginine methyl ester. Tachykinin-induced protection occurred despite marked depression of gastric mucosal blood flow and was not associated with increased acid secretion. NK2-receptor blockade antagonized the protective effects of [Ala5,beta-Ala8]NKA-(4-10) and NKA-(4-10), whereas NK1-receptor blockade was ineffective. Blockade of NK2 but not NK1 receptors prevented by 65% the protection evoked by topical capsaicin without affecting capsaicin-induced hyperemia. We conclude that the increase in gastric mucosal resistance evoked by tachykinins is NK2 receptor-mediated and involves primary afferent neurons, CGRP, and NO. Gastric mucosal hyperemia and increased acid secretion do not participate in the effect. Tachykinins activating NK2 receptors contribute to the increase in gastric mucosal resistance but not the increment in mucosal blood flow after primary afferent nerve stimulation by capsaicin.

[Analysis of the questionnaire for prenatal ultrasonography in women delivering at the Polish Mother's Memorial Hospital in the year 1995]. / Analiza ankiet dotyczacych prenatalnych badan USG U kobiet rodzacych w CZMP w 1995 roku.

After delivery at the Polish Mother's Memorial Hospital, Lódz Poland (PMMH), 1658 women were asked to fulfill the questionnaire regarding US studies during their pregnancy. At least one US study had 94% (1559) of pregnant women, 6% (99) had none. Three-US studies (the optimal number recommended by the authors) had 26%, 2-US studies had 33%, 1-US studies had 22%. Our data confirm that the series of 3-US studies during the low risk pregnancy, as it is recommended in most European countries needs further promotion and implementation in Poland. In our center, in the majority of cases, 4 or more US studies were performed in high risk pregnancies.

[Evaluation of the diagnostic usefulness for ultrasonographic and echocardiographic lethal markers in fetal pulmonary hypoplasia. Analysis of 11 cases]. / Ocena przydatnosci diagnostycznej ultrasonograficznych i echokardiograficznych cech letalnej postaci hipoplazji pluc plodu. Analiza 11 przypadków.

Results of ultrasonographic and echocardiographic studies of 11 fetuses were analysed retrospectively in relation to their pulmonary hypoplasia. Congenital malformations, quality of hydramnios and echocardiographical measurements of fetal chest were estimated. The best symptoms of pulmonary hypoplasia were: oligo/ahydramnios, absence of fetal breathing movements and malformations in fetal chest cavity (diaphragmatic hernia, cardiomegaly, hydrothorax). Systemic malformations were present in each case. The measurements such as CC, CA, HA, (CA-HA) x 100/CA were not accurate enough and we did not find any statistical differences between the control and the studied group. Finding several factors predisposing to lung hypoplasia means that its lethal form may be present in fetus.

[Prenatal echocardiography of aortic stenosis]. / Stenoza aortalna wykrywana prenatalnym badaniem echokardiograficznym.

UNLABELLED: Between 1991-1995 five cases of fetal critical aortic stenosis were diagnosed by fetal echocardiography at the Polish Mother's Memorial hospital. The main cause for referral for fetal ECHO was fetal ascites detected during routine obstetrical ultrasound scan in four cases and positive family history in one case. Pregnant women had fetal echocardiography monitoring as in-patients. During the first examination, the mean aortic valve size was 3.9 mm, mean shortening fraction of LV was 15.8%, mean heart/chest area ratio was 0.51. In one case pharmacological treatment with digoxin (due to fetal congestive heart failure) and steroids (to stimulate fetal lung maturity) was introduced. Amniocentesis due to severe polyhydramnios and fetal ascites drainage were also performed in this case. The were 2 fetal demises at 26 and 28 weeks of pregnancy, 3 cesarean section due to fetal distress during the first period of labour. The pH of umbilical blood was > 7.2. The newborns died between days 2-4 of life. CONCLUSIONS: Aortic valve stenosis can be diagnosed prenatally. This type of fetal heart defect has a poor prognosis.

Fetal echocardiography guidelines to predict survival of fetuses with ascites.

In a retrospective analysis of the standard protocols for fetal echocardiographic examination, 27 fetuses (mean gestational age 29 +/- 5.4 weeks) with ascites were evaluated. Fetal cardiomegaly (increased heart area/chest area ratio), the presence or absence of atrioventricular valve regurgitation, inferior vena cava and ductus venosus Doppler flow velocity and umbilical vein pulsation were evaluated quantitatively in a group of survivors and non-survivors. A statistically significant difference between the two groups was found for the presence of atrioventricular valve regurgitation (p = 0.003), and for cardiomegaly (p = 0.009). There was no statistical difference for the presence of abnormal venous flow and umbilical pulsation (p > 0.05). Abnormal venous Doppler flow velocities in the inferior vena cava and ductus venosus were observed more frequently than umbilical vein pulsation. The mean heart area/chest area ratios in the group of survivors and in the group of non-survivors were 0.34 +/- 0.09 and 0.48 +/- 0.08, respectively (p < 0.001). The mean gestational ages at the time of diagnosis of ascites in the groups of survivors and non-survivors were 33 +/- 3.3 weeks and 28 +/- 5.1 weeks, respectively (p < 0.05); the mean gestational ages at the time of delivery were 35.6 +/- 2.3 weeks and 33.3 +/- 4.9 weeks, respectively (p = 0.33). In terms of different echocardiographic features as well as the gestational age of the unborn patient with ascites, there is apparently no single indicator of a poor prognosis. Our results suggest that the prognosis is usually poor in a fetus with ascites, when cardiomegaly is detected, as well as the presence of tricuspid and mitral valve regurgitation. This is regardless of the type of venous flow and regardless of the etiology of the ascites.

Functional ablation of sensory neurons impairs healing of acute gastric mucosal damage in rats.

Healing of ethanol-injured gastric mucosa was studied in rats treated with a neurotoxic dose of capsaicin to induce functional ablation of sensory nerves. Capsaicin treatment delayed the healing of mucosal damage in the glandular region and promoted the development of deep ulcerations predominantly in the antrum. These lesions occupied 86% of the antral surface and were associated with marked invasion of inflammatory cells and 18-fold elevation of gastric myeloperoxidase activity compared with vehicle-pretreated rats. Inhibition of cyclooxygenase, 5-lipoxygenase, or nitric oxide synthase did not affect the development of antral lesions after ethanol challenge in capsaicin-pretreated rats. In vehicle-pretreated rats, inhibition of nitric oxide synthase did not mimic the effect of functional ablation of sensory neurons. The findings suggest that in the gastric mucosa sensory neurons contribute to repair processes and limit the inflammatory response to injury. These effects do not involve arachidonic acid metabolites or nitric oxide.

Protection by gastrin in the rat stomach involves afferent neurons, calcitonin gene-related peptide, and nitric oxide.

BACKGROUND & AIMS: Certain gut peptides exert gastroprotective effects. However, the underlying mechanism is not fully understood. This study examines the contribution of afferent neurons, calcitonin gene-related peptide, and nitric oxide to the protection conferred by gastrin 17 in the rat stomach. METHODS: Gastroprotection by gastrin 17 against ethanol-induced gross and histological damage was studied after capsaicin-induced defunctionalization of afferent neurons, pretreatment with the calcitonin gene-related peptide receptor antagonist human calcitonin gene-related peptide8-37, anti-calcitonin gene-related peptide antibodies, and the NO synthase inhibitor NG-nitro-L-arginine. RESULTS: Gastrin 17 (1-25 pmol/kg) dose-dependently prevented mucosal damage caused by ethanol. Protection was inhibited by functional ablation of afferent neurons or pretreatment with human calcitonin gene-related peptide8-37 (50% inhibitory dose, 86 pmol.kg-1.min-1), anticalcitonin gene-related peptide antibodies, or NG-nitro-L-arginine (50% inhibitory dose, 1 mg/kg). L-Arginine but not D-arginine reversed the effect of NG-nitro-L-arginine. Effects on gross damage were paralleled by histology. Protective doses of gastrin 17 increased gastric mucosal blood flow and, in addition, elevated plasma gastrin concentrations to the same extent as intragastric peptone perfusion. CONCLUSIONS: Gastrin 17 has potent gastroprotective activity that involves afferent neurons, calcitonin gene-related peptide, and NO.

Fetal echocardiography during indomethacin treatment.

Fetal echocardiograms were evaluated in 315 studies performed in 107 fetuses exposed to indomethacin. In the majority of cases, the results of the fetal echocardiography study were within normal limits (74%). The most common abnormal phenomena were tricuspid valve regurgitation (10%), ductal constriction (6%), tricuspid valve regurgitation and ductal constriction (5%), an increased ductal velocity (2%), and other (3%). The difference between the prevalence of ductal constriction in the whole series of studies (11%) compared to the prevalence of ductal constriction per fetus (25%) (p < 0.001) suggests that this phenomenon was only temporary and disappeared when medication was discontinued. The mean gestational age for detection of tricuspid valve regurgitation was 27.7 +/- 2.8 weeks and for ductal constriction, 30.9 +/- 2.1 weeks (t-test, p < 0.01). Trivial tricuspid valve regurgitation was detected at a mean of 26.7 +/- 2.2 weeks and significant tricuspid valve regurgitation at 29.6 +/- 2.3 weeks (t-test, p < 0.01). We conclude that indomethacin treatment is relatively safe for the fetal heart. The most common side-effects are tricuspid valve regurgitation and ductal constriction. Tricuspid valve regurgitation may be detected before ductal constriction, but by itself it is not a contraindication for the continued use of indomethacin.

[Clinical follow up in a case of fetal arrhythmia--review of the literature]. / Postepowanie kliniczne w przypadku arytmii u plodu--przeglad pismiennictwa.

Fetal heart arrhythmias are divided into 3 categories: 1. extrasystoles 2. tachycardia and 3. bradycardia. In each of these fetal echocardiography follow-up is necessary during the pregnancy. Extrasystoles are usually evaluated every 2 weeks, are mostly benign and no pharmacological treatment is necessary. Vaginal delivery is recommended. Tachycardia should be monitored every week for any evidence of incoming fetal heart failure. In such circumstances pregnant women should be in hospitalized and pharmacological treatment is strongly recommended, usually with digoxin or digoxin and verapamil. Furthermore, other drugs were reported. In a case of bradycardia fetal echocardiography should be performed every week. Fetal heart failure usually leads to cesarean sections, similar like in cases of tachycardia.

The prevalence and clinical significance of fetal tricuspid valve regurgitation with normal heart anatomy.

OBJECTIVE: Our purpose was to assess the prevalence, cause, and clinical significance of fetal tricuspid valve regurgitation in structurally normal hearts during indicated fetal echocardiographic examination. STUDY DESIGN: The prevalence of fetal tricuspid regurgitation was retrospectively evaluated in a group of 733 singleton fetuses referred for routine fetal echocardiography. RESULTS: The prevalence of this abnormality was 6.8%. Tricuspid valve regurgitation was most frequent in the group referred for fetal echocardiography to evaluate indomethacin exposure, followed by maternal diabetes. Factors associated with tricuspid valve regurgitation included ductal constriction, abnormal heart rhythm, atrial septal aneurysm, congestive heart failure, pericardial effusion, myocardial hypertrophy, and extracardiac malformations. Fetal tricuspid valve regurgitation was trivial in 80% (nonholosystolic, maximum velocity < 2 m/sec) and was significant in 20% (holosystolic, maximum velocity > 2 m/sec). Neonatal follow-up of tricuspid valve regurgitation was unremarkable. CONCLUSIONS: Fetal tricuspid valve regurgitation with normal heart anatomy was a frequent finding during indicated fetal echocardiographic examination and may indicate abnormal physiologic characteristics (increased preload or afterload, myocardial impairment, or arrhythmia). In the majority of cases (92%) the possible cause may be established. In other cases (8%) there may be "idiopathic" tricuspid valve regurgitation.