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Katherine Bianco, MD

  • Director, Maternal Congenital Heart Program
  • Clinical Associate Professor
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Locations and Hours

Obstetrics Clinic

770 Welch Rd Ste 201
MC 5880
Palo Alto, CA 94304
Phone: (650) 498-4069
Fax: (650) 725-2062
Map, Directions & Parking

Obstetrics and Gynecology

300 Pasteur Dr Rm HH333
MC 5317
Stanford, CA  94305
Phone: (650) 497-8928
Fax: (650) 498-6583
Map, Directions & Parking

Specialties

Obstetrics & Gynecology

Work and Education

Professional Education

Central University of Venezuela, Caracas, Venezuela, 6/13/1997

Internship

Yale School Of Medicine Office of Student Affairs, New Haven, CT, 6/30/2004

Residency

Yale School Of Medicine Office of Student Affairs, New Haven, CT, 6/30/2004

Fellowship

University of California San Francisco, San Francisco, CA, 8/31/2008

Board Certifications

Clinical Genetics, American Board of Medical Genetics and Genomics

Maternal & Fetal Medicine, American Board of Obstetrics and Gynecology

Obstetrics & Gynecology, American Board of Obstetrics and Gynecology

Services

Obstetrics

All Publications

Chronic antepartum maternal hyperoxygenation in a case of severe fetal Ebstein's anomaly with circular shunt physiology. Annals of pediatric cardiology Arunamata, A., Axelrod, D. M., Bianco, K., Balasubramanian, S., Quirin, A., Tacy, T. A. ; 10 (3): 28487

Abstract

Perinatal mortality remains high among fetuses diagnosed with Ebstein's anomaly of the tricuspid valve. The subgroup of patients with pulmonary valve regurgitation is at particularly high risk. In the setting of pulmonary valve regurgitation, early constriction of the ductus arteriosus may be a novel perinatal management strategy to reduce systemic steal resulting from circular shunt physiology. We report the use of chronic antepartum maternal oxygen therapy for constriction of the fetal ductus arteriosus and modulation of fetal pulmonary vascular resistance in a late presentation of Ebstein's anomaly with severe tricuspid valve regurgitation, reversal of flow in the ductus arteriosus, and continuous pulmonary valve regurgitation.

View details for PubMedID 28928616

Postpartum Depression Among Women with Cardiac Disease: Considerations During the Delivery Admission Panelli, D., Sherwin, E. B., Lee, C. J., Suharwardy, S., Miller, H. E., Tolani, A. T., Girsen, A. I., Leonard, S. A., Warshawsky, S., Judy, A., Khandel-Wal, A., Bianco, Y. K. SPRINGER HEIDELBERG. 2020: 246A

View details for Web of Science ID 000525432601113

Perinatal Outcomes in Women With Cardiac Arrhythmia. Lee, J., Sie, L., Sherwin, E. B., Girsen, A. I., Tolani, A. T., Miller, H. E., Panelli, D. M., Do, S. C., Khandelwal, A., Bianco, K. SPRINGER HEIDELBERG. 2020: 161A

View details for Web of Science ID 000525432600268

Cellular Aging in Pregnancy: Telomere Dynamics Across Gestation. Panelli, D. M., Leonard, S. A., Wong, R. J., Girsen, A. I., Baskovic, M., Stevenson, D. K., Bianco, K. SPRINGER HEIDELBERG. 2020: 127A128A

View details for Web of Science ID 000525432600181

Changes in pregnancy-related serum biomarkers early in gestation are associated with later development of preeclampsia. PloS one Hao, S., You, J., Chen, L., Zhao, H., Huang, Y., Zheng, L., Tian, L., Maric, I., Liu, X., Li, T., Bianco, Y. K., Winn, V. D., Aghaeepour, N., Gaudilliere, B., Angst, M. S., Zhou, X., Li, Y. M., Mo, L., Wong, R. J., Shaw, G. M., Stevenson, D. K., Cohen, H. J., Mcelhinney, D. B., Sylvester, K. G., Ling, X. B. 2020; 15 (3): e0230000

Abstract

Placental protein expression plays a crucial role during pregnancy. We hypothesized that: (1) circulating levels of pregnancy-associated, placenta-related proteins throughout gestation reflect the temporal progression of the uncomplicated, full-term pregnancy, and can effectively estimate gestational ages (GAs); and (2) preeclampsia (PE) is associated with disruptions in these protein levels early in gestation; and can identify impending PE. We also compared gestational profiles of proteins in the human and mouse, using pregnant heme oxygenase-1 (HO-1) heterozygote (Het) mice, a mouse model reflecting PE-like symptoms.Serum levels of placenta-related proteins-leptin (LEP), chorionic somatomammotropin hormone like 1 (CSHL1), elabela (ELA), activin A, soluble fms-like tyrosine kinase 1 (sFlt-1), and placental growth factor (PlGF)-were quantified by ELISA in blood serially collected throughout human pregnancies (20 normal subjects with 66 samples, and 20 subjects who developed PE with 61 samples). Multivariate analysis was performed to estimate the GA in normal pregnancy. Mean-squared errors of GA estimations were used to identify impending PE. The human protein profiles were then compared with those in the pregnant HO-1 Het mice.An elastic net-based gestational dating model was developed (R2 = 0.76) and validated (R2 = 0.61) using serum levels of the 6 proteins measured at various GAs from women with normal uncomplicated pregnancies. In women who developed PE, the model was not (R2 = -0.17) associated with GA. Deviations from the model estimations were observed in women who developed PE (P = 0.01). The model developed with 5 proteins (ELA excluded) performed similarly from sera from normal human (R2 = 0.68) and WT mouse (R2 = 0.85) pregnancies. Disruptions of this model were observed in both human PE-associated (R2 = 0.27) and mouse HO-1 Het (R2 = 0.30) pregnancies. LEP outperformed sFlt-1 and PlGF in differentiating impending PE at early human and late mouse GAs.Serum placenta-related protein profiles are temporally regulated throughout normal pregnancies and significantly disrupted in women who develop PE. LEP changes earlier than the well-established biomarkers (sFlt-1 and PlGF). There may be evidence of a causative action of HO-1 deficiency in LEP upregulation in a PE-like murine model.

View details for DOI 10.1371/journal.pone.0230000

View details for PubMedID 32126118

Trisomy 21 is Associated with Caspase-2 Upregulation in Cytotrophoblasts at the Maternal-Fetal Interface REPRODUCTIVE SCIENCES Leon-Martinez, D., Robinson, J. F., Zdravkovic, T., Genbacev, O., Gormley, M., Mcmaster, M., Fisher, S. J., Bianco, K. 2020; 27 (1): 100109

Abstract

Impaired placentation is implicated in poor perinatal outcomes associated with Trisomy 21. Earlier studies revealed abnormal cytotrophoblast differentiation along the invasive pathway as a contributing mechanism. To further elucidate the causes, we evaluated Caspase-2 expression at the protein level (immunolocalization and immunoblot) in samples from Trisomy 21 (n = 9) and euploid (n = 4) age-matched placentas. Apoptosis was investigated via the TUNEL assay. An immunolocalization approach was used to characterize Caspase-3, Fas (CD95), and Fas ligand in the same samples. Caspase-2 was significantly overexpressed in Trisomy 21 placentas, with the highest expression in villous cores and invasive cytotrophoblasts. Immunolocalization showed that Caspase-3 had a similar expression pattern as Caspase-2. Using the TUNEL approach, we observed high variability in the number of apoptotic cells in biopsies from different regions of the same placenta and among different placentas. However, Trisomy 21 placentas had more apoptotic cells, specifically in cell columns and basal plates. Furthermore, Caspase-2 co-immunolocalized with Fas (CD95) and FasL in TUNEL-positive extravillous cytotrophoblasts, but not in villous cores. These results help explain the higher levels of apoptosis among placental cells of Trisomy 21 pregnancies in molecular terms. Specifically, the co-expression of Caspase-2 and Caspase-3 with other regulators of the apoptotic process in TUNEL-positive cells suggests these molecules may cooperate in launching the observed apoptosis. Among trophoblasts, only the invasive subpopulation showed this pattern, which could help explain the higher rates of adverse outcomes in these pregnancies. In future experiments, this relationship will be further examined at a functional level in cultured human trophoblasts.

View details for DOI 10.1007/s43032-019-00002-x

View details for Web of Science ID 000525433300011

View details for PubMedID 32046398

Contraception uptake among women with cardiovascular disease: The impact of a multidisciplinary team care approach Miller, H. E., Sie, L., Lee, C. J., Panelli, D. M., Sherwin, E. B., Noon, B., Girsen, A., Bianco, K. MOSBY-ELSEVIER. 2020: S707S708

View details for DOI 10.1016/j.ajog.2019.11.1161

View details for Web of Science ID 000504997301467

Impact of gender, rank and research productivity on salary in obstetrics and gynecology Miller, H. E., Seckel, E., Sanchez, D., White, C., Mueller, C., Bianco, K. MOSBY-ELSEVIER. 2020: S356

View details for DOI 10.1016/j.ajog.2019.11.569

View details for Web of Science ID 000504997300552

Maternal Outcomes in Planned and Unplanned Pregnancies in Women with Cardiac Disease. Do, S. C., Tolani, A. T., Sie, L., Girsen, A. I., Lee, C. J., Sherwin, E., Panelli, D. M., El-Sayed, Y. Y., Khandelwal, A., Blumenfeld, Y. J., Bianco, K. SAGE PUBLICATIONS INC. 2019: 323A

View details for Web of Science ID 000459610400771

A Multidisciplinary Approach to Care of Pregnant Patients with History of Open Heart Surgery. Do, S. C., Lee, C. J., Sie, L., Tolani, A. T., Sherwin, E., Girsen, A. I., El-Sayed, Y. Y., Khandelwal, A., Bianco, K., Blumenfeld, Y. J. SAGE PUBLICATIONS INC. 2019: 323A324A

View details for Web of Science ID 000459610400772

Care of the pregnant cardiac patient e the importance of a multidisciplinary approach Tolani, A. T., Do, S. C., Blumenfeld, Y. J., Sie, L., Girsen, A. I., Lee, C. J., Sherwin, E. B., Tsur, A., El-Sayed, Y. Y., Khandelwal, A., Bianco, K. MOSBY-ELSEVIER. 2019: S536

View details for DOI 10.1016/j.ajog.2018.11.842

View details for Web of Science ID 000454249402297

Outcomes of women with primary and secondary pulmonary hypertension during pregnancy Blumenfeld, Y. J., Girsen, A. I., Druzin, M. L., Lyell, D. J., Bianco, K. Y., Herrero, T., Bentley, J., Seckel, E., Zamanian, R. T., El-Sayed, Y. Y. MOSBY-ELSEVIER. 2019: S405

View details for DOI 10.1016/j.ajog.2018.11.633

View details for Web of Science ID 000454249402093

Donor-derived circulating cell-free DNA (ccfDNA) reference materials for concordance studies Konigshofer, Y., Butler, M. G., Dickens, J., Bianco, K., Sylvester, K. G., Anekella, B., Garlick, R. K. AMER ASSOC CANCER RESEARCH. 2018

View details for DOI 10.1158/1538-7445.AM2018-5569

View details for Web of Science ID 000468819504548

Hospital variations in the use of forceps assisted delivery - results from a state-wide analysis Bentley, J., Lee, H., Lyell, D., El-Sayed, Y., Ness, A., Bianco, K., Spiegel, A., Blumenfeld, Y. MOSBY-ELSEVIER. 2018: S344

View details for Web of Science ID 000423616600074

Maternal morbidity after forceps vs vacuum assisted delivery - Outcomes from a large state-wide cohort Bentley, J., Lyell, D., El-Sayed, Y., Ness, A., Foeller, M., Bianco, K., Spiegel, A., Martin, B., Do, S., Blumenfeld, Y. MOSBY-ELSEVIER. 2018: S345

View details for Web of Science ID 000423616600075

Gene expression network analysis in aneuploid human trophoblast progenitor cells (TBPC) reveals modular structures Leon-Martinez, D., Ling, X., Hao, S., Sylvester, K., Bianco, K. MOSBY-ELSEVIER. 2018: S163S164

View details for Web of Science ID 000422946900255

Fetal intolerance to labor in pregnancies complicated by marginal and eccentric cord insertion Young-Lin, N., Lutz, A., Leon-Martinez, D., Ye, C., Torosis, M., Jazayeri, Y., Pugh, B., Bianco, K. MOSBY-ELSEVIER. 2018: S285

View details for Web of Science ID 000422946900475

Neonatal outcomes after operative vaginal delivery - are forceps or vacuum safer? Bentley, J. P., Lee, H., Lyell, D., El-Sayed, Y., Ness, A., Bianco, K., Yeaton-Massey, A., Blumenfeld, Y. MOSBY-ELSEVIER. 2018: S343S344

View details for Web of Science ID 000423616600073

Placental transcriptomes in the common aneuploidies reveal critical regions on the trisomic chromosomes and genome-wide effects PRENATAL DIAGNOSIS Bianco, K., Gormley, M., Farrell, J., Zhou, Y., Oliverio, O., Tilden, H., McMaster, M., Fisher, S. J. 2016; 36 (9): 812-822

Abstract

Chromosomal aberrations are frequently associated with birth defects and pregnancy losses. Trisomy 13, Trisomy 18 and Trisomy 21 are the most common, clinically relevant fetal aneusomies. This study used a transcriptomics approach to identify the molecular signatures at the maternal-fetal interface in each aneuploidy.We profiled placental gene expression (13-22weeks) in T13 (n=4), T18 (n=4) and T21 (n=8), and in euploid pregnancies (n=4).We found differentially expressed transcripts (2-fold) in T21 (n=160), T18 (n=80) and T13 (n=125). The majority were upregulated and most of the misexpressed genes were not located on the relevant trisomic chromosome, suggesting genome-wide dysregulation. A smaller number of the differentially expressed transcripts were encoded on the trisomic chromosome, suggesting gene dosage. In T21, <10% of the genes were transcribed from the Down syndrome critical region (21q21-22), which contributes to the clinical phenotype. In T13, 15% of the upregulated genes were on the affected chromosome (13q11-14), and in T18, the percentage increased to 24% (18q11-22 region).The trisomic placental (and possibly fetal) phenotypes are driven by the combined effects of genome-wide phenomena and increased gene dosage from the trisomic chromosome. 2016 John Wiley & Sons, Ltd.

View details for DOI 10.1002/pd.4862

View details for Web of Science ID 000384096800002

View details for PubMedID 27328057

View details for PubMedCentralID PMC5104283

Human trophoblast progenitor cell (TBPC) lines derived from aneuploid placentas: studying fundamental aspects of trophoblast biology Bianco, K., Leon-Martinez, D., Farrell, J., Gormley, M., McMaster, M., Fisher, S. J. MOSBY-ELSEVIER. 2016: S331

View details for DOI 10.1016/j.ajog.2015.10.666

View details for Web of Science ID 000367092800614

Integrative analysis of 111 reference human epigenomes. Nature Kundaje, A., Meuleman, W., Ernst, J., Bilenky, M., Yen, A., Heravi-Moussavi, A., Kheradpour, P., Zhang, Z., Wang, J., Ziller, M. J., Amin, V., Whitaker, J. W., Schultz, M. D., Ward, L. D., Sarkar, A., Quon, G., Sandstrom, R. S., Eaton, M. L., Wu, Y., Pfenning, A. R., Wang, X., Claussnitzer, M., Liu, Y., Coarfa, C., Harris, R. A., Shoresh, N., Epstein, C. B., Gjoneska, E., Leung, D., Xie, W., Hawkins, R. D., Lister, R., Hong, C., Gascard, P., Mungall, A. J., Moore, R., Chuah, E., Tam, A., Canfield, T. K., Hansen, R. S., Kaul, R., Sabo, P. J., Bansal, M. S., Carles, A., Dixon, J. R., Farh, K., Feizi, S., Karlic, R., Kim, A., Kulkarni, A., Li, D., Lowdon, R., Elliott, G., Mercer, T. R., Neph, S. J., Onuchic, V., Polak, P., Rajagopal, N., Ray, P., Sallari, R. C., Siebenthall, K. T., Sinnott-Armstrong, N. A., Stevens, M., Thurman, R. E., Wu, J., Zhang, B., Zhou, X., Beaudet, A. E., Boyer, L. A., De Jager, P. L., Farnham, P. J., Fisher, S. J., Haussler, D., Jones, S. J., Li, W., Marra, M. A., McManus, M. T., Sunyaev, S., Thomson, J. A., Tlsty, T. D., Tsai, L., Wang, W., Waterland, R. A., Zhang, M. Q., Chadwick, L. H., Bernstein, B. E., Costello, J. F., Ecker, J. R., Hirst, M., Meissner, A., Milosavljevic, A., Ren, B., Stamatoyannopoulos, J. A., Wang, T., Kellis, M. 2015; 518 (7539): 317-330

Abstract

The reference human genome sequence set the stage for studies of genetic variation and its association with human disease, but epigenomic studies lack a similar reference. To address this need, the NIH Roadmap Epigenomics Consortium generated the largest collection so far of human epigenomes for primary cells and tissues. Here we describe the integrative analysis of 111 reference human epigenomes generated as part of the programme, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression. We establish global maps of regulatory elements, define regulatory modules of coordinated activity, and their likely activators and repressors. We show that disease- and trait-associated genetic variants are enriched in tissue-specific epigenomic marks, revealing biologically relevant cell types for diverse human traits, and providing a resource for interpreting the molecular basis of human disease. Our results demonstrate the central role of epigenomic information for understanding gene regulation, cellular differentiation and human disease.

View details for DOI 10.1038/nature14248

View details for PubMedID 25693563

View details for PubMedCentralID PMC4530010

Pregnancy complications are increased among women with cardiomyopathy compared to those with other cardiac diseases Bianco, K., Harris, I., Henry, D., Killion, M., Bosco, V., Thiet, M., Gonzalez, J. MOSBY-ELSEVIER. 2015: S68S69

View details for DOI 10.1016/j.ajog.2014.10.148

View details for Web of Science ID 000361140900104

Congenital Heart Disease and Perinatal Outcomes. Henry, D., Clay, J., Gonzalez, J. M., Harris, I. S., Tilden, H., Bianco, K. SAGE PUBLICATIONS INC. 2014: 148A

View details for Web of Science ID 000333813001212

Reversal of gene dysregulation in cultured cytotrophoblasts reveals possible causes of preeclampsia JOURNAL OF CLINICAL INVESTIGATION Zhou, Y., Gormley, M. J., Hunkapiller, N. M., Kapidzic, M., Stolyarov, Y., Feng, V., Nishida, M., Drake, P. M., Bianco, K., Wang, F., McMaster, M. T., Fisher, S. J. 2013; 123 (7): 286272

Abstract

During human pregnancy, a subset of placental cytotrophoblasts (CTBs) differentiates into cells that aggressively invade the uterus and its vasculature, anchoring the progeny and rerouting maternal blood to the placenta. In preeclampsia (PE), CTB invasion is limited, reducing placental perfusion and/or creating intermittent flow. This syndrome, affecting 4%-8% of pregnancies, entails maternal vascular alterations (e.g., high blood pressure, proteinuria, and edema) and, in some patients, fetal growth restriction. The only cure is removal of the faulty placenta, i.e., delivery. Previously, we showed that defective CTB differentiation contributes to the placental component of PE, but the causes were unknown. Here, we cultured CTBs isolated from PE and control placentas for 48 hours, enabling differentiation and invasion. In various severe forms of PE, transcriptomics revealed common aberrations in CTB gene expression immediately after isolation, including upregulation of SEMA3B, which resolved in culture. The addition of SEMA3B to normal CTBs inhibited invasion and recreated aspects of the PE phenotype. Additionally, SEMA3B downregulated VEGF signaling through the PI3K/AKT and GSK3 pathways, effects that were observed in PE CTBs. We propose that, in severe PE, the in vivo environment dysregulates CTB gene expression; the autocrine actions of the upregulated molecules (including SEMA3B) impair CTB differentiation, invasion and signaling; and patient-specific factors determine the signs.

View details for DOI 10.1172/JCI66966

View details for Web of Science ID 000321316700016

View details for PubMedID 23934129

View details for PubMedCentralID PMC3999620

Decidua-Placental Interface Show Abnormal Epigenetic Profiles in Common Aneuploidies Houshdaran, S., Tilden, H., Bianco, K. SAGE PUBLICATIONS INC. 2013: 254A

View details for Web of Science ID 000329543100649

Genomic profiles in common aneuploidies: a combination of dose effects and whole genome misregulation Bianco, K., Gormley, M., Tilden, H., McMaster, M., Fisher, S. MOSBY-ELSEVIER. 2013: S30

View details for DOI 10.1016/j.ajog.2012.10.224

View details for Web of Science ID 000313393500053

Human Placenta Undergoes Global DNA Methylation Modification during Normal Gestation Houshdaran, S., Goldfien, G. A., Bianco, K. SAGE PUBLICATIONS INC. 2012: 383A384A

View details for Web of Science ID 000329543603283

Genomic imprinting in offspring conceived with assisted reproductive technology 31st Annual Scientific Meeting of the Society-of-Maternal-Fetal-Medicine (SMFM) Norton, M., Haston, K., Reijo-Pera, R., Chueh, J., Blumenfeld, Y., Bianco, K., Zlatnik, M. MOSBY-ELSEVIER. 2011: S284S285

View details for Web of Science ID 000285927500719

Stem Cells in Hepatic Regeneration After Injury ADVANCES IN WOUND CARE, VOL 1 Kuscuoglu, U., Bianco, K., Sylvester, K. G., Sen, C. K. 2010; 1: 52631

View details for DOI 10.1089/awc.2009.0101

View details for Web of Science ID 000277780600085

Effect of estradiol on oocyte development INTERNATIONAL JOURNAL OF GYNECOLOGY & OBSTETRICS Bianco, K., Mahutte, N. G., Arici, A., Sakkas, D., Taylor, H. S. 2009; 104 (3): 23032

Abstract

To determine whether elevated serum estradiol (E(2)) concentrations in oocyte donors affect assisted reproduction outcome.In a retrospective cohort study of 58 consecutive oocyte donation cycles, donors were stratified into 2 groups according to E(2) concentration, group 1 (n=32; E(2)2000 pg/mL [range, 2062-6957 pg/mL]). Data were analyzed using the t test and chi(2) test.Donors in group 1 produced significantly less oocytes than donors in group 2 (19.3+/-1.7 vs 12.0+/-1.4; P<0.001), and recipients of oocytes from group 1 had significantly fewer numbers of embryos available for transfer (10.4+/-1.1 vs 6.4+/-0.8; P=0.003). However, the mean number (3.3) of embryos transferred and the pregnancy rate were the same in both groups.Elevated estradiol concentration in oocyte donors did not affect pregnancy outcome, suggesting that estradiol levels in donors do not affect oocyte development.

View details for DOI 10.1016/j.ijgo.2008.10.015

View details for Web of Science ID 000264255600015

View details for PubMedID 19056082

View details for PubMedCentralID PMC3107851

Operative vaginal delivery: Now or later? Cheng, Y. W., Bianco, K., Shaffer, B. L., Lyell, D., Caughey, A. B. MOSBY-ELSEVIER. 2007: S97

View details for DOI 10.1016/j.ajog.2007.10.328

View details for Web of Science ID 000251708500313

Fetal cerebellar hemorrhage in parvovirus-associated non-immune hydrops fetalis JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE Glenn, O. A., Bianco, K., Barkovich, A., Callen, P. W., Parer, J. T. 2007; 20 (10): 76972

Abstract

We report two cases of fetal cerebellar hemorrhage in the setting of parvovirus-associated hydrops fetalis and fetal blood transfusion. In both cases, the cerebellar hemorrhage was diagnosed by fetal magnetic resonance imaging after intrauterine blood transfusion. To our knowledge, this is the first report of fetal cerebellar hemorrhage in the setting of parvovirus-associated hydrops fetalis, and may be the result of cerebrovascular changes both during and after the transfusion.

View details for DOI 10.1080/14767050701580960

View details for Web of Science ID 000250402500011

View details for PubMedID 17763280

Second-trimester ductus venosus measurement and adverse perinatal outcome in fetuses with congenital heart disease JOURNAL OF ULTRASOUND IN MEDICINE Bianco, K., Small, M., Julien, S., Kershaw, T., Michon, M., Copel, J. 2006; 25 (8): 97982

Abstract

The purpose of this study was to determine whether Doppler velocimetry of the ductus venosus (DV) predicts adverse perinatal outcome in congenital heart disease (CHD).We conducted a retrospective cohort study of all pregnant women undergoing fetal echocardiography for CHD in a single perinatal center during a 2-year period. We compared outcomes for fetuses having a diagnosis of CHD in the second trimester and abnormal DV Doppler velocimetric findings with those having CHD and normal DV Doppler findings. Karyotype, gestational age at delivery, fetal loss rate, and rate of termination were assessed. The referral value for an abnormal DV pulsatility index was above the 95th percentile for gestational age. Statistical analysis included the t test, Fisher exact test, and chi(2) test.The incidence of CHD in our population was 7%. There were 98 patients with CHD; of those, 31 had DV measurement. A total of 9 patients had an abnormal DV. Three of this group (33%) had intrauterine fetal death or perinatal death. In patients with CHD and normal DV measurements, 83% had living children versus 33% in the group with an abnormal DV (P < .05). There was no statistically significant difference in the rate of aneuploidy between the normal DV (15%) and abnormal DV (20%) groups (P = .65). The mean gestational age at delivery was similar between the normal (37.63 weeks) and abnormal (38.33 weeks) DV groups (P = .71). There was no difference in the rate of pregnancy termination.Abnormal second-trimester DV measurements are predictive of adverse perinatal outcome in patients with CHD, independent of karyotype or gestational age at delivery. This information may have a role in the counseling of parents with CHD.

View details for DOI 10.7863/jum.2006.25.8.979

View details for Web of Science ID 000239445000005

View details for PubMedID 16870891

History of miscarriage and increased incidence of fetal aneuploidy in subsequent pregnancy OBSTETRICS AND GYNECOLOGY Bianco, K., Caughey, A. B., Shaffer, B. L., Davis, R., Norton, M. E. 2006; 107 (5): 10981102

Abstract

The purpose of this study was to examine the association between history of spontaneous abortion and aneuploidy in a subsequent pregnancy.This was a retrospective cohort study of women who underwent fetal karyotype analysis with amniocentesis or chorionic villus sampling at a single prenatal diagnosis center. Information on spontaneous abortions, parity, maternal age, ethnicity, type of prenatal diagnosis, and karyotype was assessed. Univariable and multivariable analyses were conducted.A total of 46,939 women were included in our analysis. Women with no prior spontaneous abortions had a 1.39% risk for any aneuploidy. In women with one prior spontaneous abortion, this risk increased to 1.67%; for women with 2 previous spontaneous abortions, the risk increased to 1.84%; and for those women who had had 3 or more prior spontaneous abortions, the risk increased further to 2.18% (P < .007). When controlling for maternal age, parity, ethnicity, and mode of prenatal diagnosis and compared with women with no prior spontaneous abortions, women with one prior spontaneous abortion (adjusted odds ratio [AOR] 1.21, 95% confidence interval [CI] 1.01-1.47) or 3 or more prior spontaneous abortions (AOR 1.51, 95% CI 1.02-2.25) had a statistically significant increase in aneuploidy in a subsequent pregnancy. Women with 2 prior spontaneous abortions had an AOR of 1.26 for aneuploidy, but the 95% CI contained unity.An increased risk of karyotypic abnormality identified at the time of prenatal diagnosis is demonstrated in patients with an increasing number of spontaneous abortions. This study provides information regarding this risk among women presenting for prenatal diagnosis. According to our data, for a woman with an a priori risk of 1 in 300 for Down syndrome, 3 prior spontaneous abortions would increase that risk by 47% to 1 in 204. These results should be confirmed in low-risk populations.

View details for DOI 10.1097/01.AOG.0000215560.86673.22

View details for Web of Science ID 000241296500019

View details for PubMedID 16648416

Second trimester ductus venosus measurements as a predictor of adverse perinatal outcome in congenital heart disease Bianco, K., Small, M., Browne, N., Julien, S., Kershaw, T., Michon, M., Copel, J. MOSBY, INC. 2004: S173

View details for DOI 10.1016/j.ajog.2004.10.516

View details for Web of Science ID 000225925500608

Elevated estradiol levels in oocyte donation cycles do not impair ART outcomes for the recipients. Bianco, K., Mahutte, N. G., Arici, A., Duleba, A. J., Taylor, H. S., Sakkas, D. ELSEVIER SCIENCE INC. 2003: S165

View details for Web of Science ID 000185672400441