Publications by authors named "Katrin Fricke"

7 Publications

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Utility of Fetal Cardiovascular Magnetic Resonance for Prenatal Diagnosis of Complex Congenital Heart Defects.

JAMA Netw Open 2021 Mar 1;4(3):e213538. Epub 2021 Mar 1.

Clinical Physiology, Department of Clinical Sciences Lund, Lund University, Skåne University Hospital, Lund, Sweden.

Importance: Prenatal diagnosis of complex congenital heart defects reduces mortality and morbidity in affected infants. However, fetal echocardiography can be limited by poor acoustic windows, and there is a need for improved diagnostic methods.

Objective: To assess the clinical utility of fetal cardiovascular magnetic resonance imaging in cases in which fetal echocardiography could not visualize all relevant anatomy.

Design, Setting, And Participants: This cohort study was conducted between January 20, 2017, and June 29, 2020, at Skåne University Hospital (Lund, Sweden), a tertiary center for pediatric cardiology and thoracic surgery. Participants were fetuses referred for fetal cardiovascular magnetic resonance examination by a pediatric cardiologist after an inconclusive echocardiograph.

Exposures: Fetal cardiovascular magnetic resonance examination requested by the patient's pediatric cardiologist.

Main Outcomes And Measures: Any change in patient management because of diagnostic information gained from fetal cardiovascular magnetic resonance imaging.

Results: A total of 31 fetuses underwent cardiovascular magnetic resonance examination at a median gestational age of 36 weeks (range, 31-39 weeks). Overall, fetal cardiovascular magnetic resonance imaging had clinical utility, affecting patient management and/or parental counseling in 26 cases (84%). For aortic arch anatomy including signs of coarctation (20 fetuses), fetal cardiovascular magnetic resonance imaging added diagnostic information in 16 cases (80%). For assessment of univentricular vs biventricular outcome in borderline left ventricle, unbalanced atrioventricular septal defect, and pulmonary atresia with intact ventricular septum (15 fetuses), fetal cardiovascular magnetic resonance imaging visualized intracardiac anatomy and ventricular function, allowing assessment of outcome in 13 cases (87%). In 4 fetuses with hypoplastic left heart syndrome, fetal cardiovascular magnetic resonance imaging helped delivery planning in 3 cases (75%). Finally, fetal cardiovascular magnetic resonance imaging provided valuable information for parental counseling in 21 cases (68%).

Conclusions And Relevance: In this cohort study, fetal cardiovascular magnetic resonance imaging added clinically useful information to what was available from echocardiography. These findings suggest that fetal CMR has the potential to affect clinical decision-making in challenging cases of congenital heart defects with inconclusive data from echocardiography. Fetal cardiovascular magnetic resonance imaging showed an association with clinical decision-making, including mode of delivery and early postnatal care, as well as with parental counseling.
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http://dx.doi.org/10.1001/jamanetworkopen.2021.3538DOI Listing
March 2021

Fetal Echocardiographic Dimension Indices: Important Predictors of Postnatal Coarctation.

Pediatr Cardiol 2021 Mar 23;42(3):517-525. Epub 2020 Dec 23.

Lund University, Skane University Hospital, Department of Clinical Sciences Lund, Pediatric Cardiology, Lund, Sweden.

The aim of the study is to identify reliable quantitative fetal echocardiographic predictors for postnatal development of coarctation (CoA). In this retrospective study, we included 65 fetuses with a prenatally suspected, isolated CoA, born 2010-2018. Dimensions of the cardiac structures, aortic, and ductal arches expressed as ratios and Z-scores were analyzed in relation to outcome. Fetuses that developed CoA postnatally (34%) exhibited significantly smaller Z-scores of left cardiac structures from the mitral valve to the aortic isthmus. The most sensitive and specific predictors were a carotid-subclavian artery index (CSAI) of < 0.78 (92.3% sensitivity, 96.8% specificity) or a product of isthmus-to-duct ratio in the three-vessel trachea view (3VT) and the mitral-to-tricuspid valve ratio (I/DxMV/TV) of < 0.37 (100% sensitivity, 94.6% specificity). When comparing different Z-score datasets, we observed large and highly significant differences. Postnatal CoA can be predicted with high accuracy during fetal life using CSAI or I/DxMV/TV. The latter may be particularly useful if adequate sagittal aortic arch images cannot be obtained. As significant and clinically unacceptable differences in Z-scores were observed for the same measurements, this calls for a large multi-center collaboration to generate reliable fetal echocardiographic Z-scores.
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http://dx.doi.org/10.1007/s00246-020-02509-6DOI Listing
March 2021

Detection and clinical manifestation of placental malaria in southern Ghana.

Malar J 2006 Dec 13;5:119. Epub 2006 Dec 13.

Institute of Tropical Medicine and International Health, Charité--University Medicine, Berlin, Germany.

Background: Plasmodium falciparum can be detected by microscopy, histidine-rich-protein-2 (HRP2) capture test or PCR but the respective clinical relevance of the thereby diagnosed infections in pregnant women is not well established.

Methods: In a cross-sectional, year-round study among 839 delivering women in Agogo, Ghana, P. falciparum was screened for in both, peripheral and placental blood samples, and associations with maternal anaemia, low birth weight (LBW) and preterm delivery (PD) were analysed.

Results: In peripheral blood, P. falciparum was observed in 19%, 34%, and 53% by microscopy, HRP2 test, and PCR, respectively. For placental samples, these figures were 35%, 41%, and 59%. Irrespective of diagnostic tool, P. falciparum infection increased the risk of anaemia. Positive peripheral blood results of microscopy and PCR were not associated with LBW or PD. In contrast, the HRP2 test performed well in identifying women at increased risk of poor pregnancy outcome, particularly in case of a negative peripheral blood film. Adjusting for age, parity, and antenatal visits, placental HRP2 was the only marker of infection associated with LBW (adjusted odds ratio (aOR), 1.5 (95%CI, 1.0-2.2)) and, at borderline statistical significance, PD (aOR, 1.4 (1.0-2.1)) in addition to anaemia (aOR, 2.3 (1.7-3.2)). Likewise, HRP2 in peripheral blood of seemingly aparasitaemic women was associated with PD (aOR, 1.7 (1.0-2.7)) and anaemia (aOR, 2.1 (1.4-3.2)).

Conclusion: Peripheral blood film microscopy not only underestimates placental malaria. In this highly endemic setting, it also fails to identify malaria as a cause of foetal impairment. Sub-microscopic infections detected by a HRP2 test in seemingly aparasitaemic women increase the risks of anaemia and PD. These findings indicate that the burden of malaria in pregnancy may be even larger than thought and accentuate the need for effective anti-malarial interventions in pregnancy.
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http://dx.doi.org/10.1186/1475-2875-5-119DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1716171PMC
December 2006

Effects of the renal natriuretic peptide urodilatin (ularitide) in patients with decompensated chronic heart failure: a double-blind, placebo-controlled, ascending-dose trial.

Am Heart J 2005 Dec;150(6):1239

Kerckhoff-Klinik, Bad Nauheim, Germany.

Background: Urodilatin (ularitide), a natriuretic peptide, is produced within the kidneys. The aim of this study was to define the role of 24-hour intravenous infusions of urodilatin in the treatment of decompensated chronic heart failure (DHF).

Methods: In this randomized, double-blind, ascending-dose safety study, 24 patients with DHF (cardiac index 1.91 +/- 0.34 L/min per square meter, pulmonary capillary wedge pressure 26 +/- 6 mm Hg, right atrial pressure 11 +/- 4 mm Hg) received urodilatin (7.5, 15, or 30 ng/(kg.min)) or placebo infusions over 24 hours.

Results: Compared with baseline, urodilatin decreased pulmonary capillary wedge pressure by 10 mm Hg in the 15 ng/(kg.min) group (P < .05) and by 15 mm Hg in the 30 ng/(kg.min) group (P < .05) at 6 hours. In the same dose groups, right atrial pressure decreased, and dyspnea as reported by patients tended to improve. At 24 hours, 15 and 30 ng/(kg.min) urodilatin infusions decreased N-terminal-pro-brain natriuretic peptide levels by 40% and 45%, respectively, compared with baseline. Between 1 to 12 hours, plasma cyclic guanosine monophosphate levels at 15 and 30 ng/(kg.min) urodilatin were significantly higher than both placebo and the respective baseline after infusion start (P < .05 and .01). Among the different groups, there was no obvious difference regarding total number of patients with adverse events and total number of adverse events. During infusion, 3 transient asymptomatic hypotensions occurred in the urodilatin groups.

Conclusions: Our findings show that urodilatin may be a new agent for the therapy for DHF.
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http://dx.doi.org/10.1016/j.ahj.2005.01.022DOI Listing
December 2005

Isolation and characterization of a novel proopiomelanocortin-derived peptide from hemofiltrate of chronic renal failure patients.

Endocrinology 2005 Apr 13;146(4):2060-8. Epub 2005 Jan 13.

IPF PharmaCeuticals GmbH, Feodor Lynen Strasse 31, D-30625 Hannover, Germany.

We report the isolation of a novel human circulating proopiomelanocortin-derived peptide, VA-beta-MSH, from hemofiltrate and its pharmacological characterization. Screening for lipolytic activity in differentiated 3T3-L1 adipocytes led to the isolation from a hemofiltrate peptide library by alternating reverse phase and cation exchange chromatography. In the course of this isolation, we also identified human beta-MSH-(1-22). We synthesized VA-beta-MSH by the N-(9-fluorenyl)-methoxycarbonyl (F-moc) solid phase method and used synthetic beta-MSH-(1-22) to confirm that both isolated peptides are lipolytically active in a dose-dependent manner in differentiated 3T3-L1 adipocytes in the nanomolar range. Using cAMP ELISA, we demonstrate that stimulation with both peptides caused a strong cAMP elevation in this cell system. Furthermore, we show that the selective inhibitors of cAMP-dependent protein kinase, 8-(4-Chlorophenylthio)adenosine-3',5'-cyclic monophosphorothioate, Rp-isomer (Rp-8-CPT-cAMPS); N-[2-(p-Bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H89), significantly reduce VA-beta-MSH- and beta-MSH-(1-22)-mediated lipolysis. Although isolated after its lipolytic activity on 3T3-L1 cells, this newly identified circulating human melanocortin may serve other functions in human physiology. Moreover, the fact that these peptides have been identified after a functional assay, but have been overseen in large proteomic approaches, underscores the importance of such approaches in identifying previously undescribed circulating bioactive molecules.
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http://dx.doi.org/10.1210/en.2004-1097DOI Listing
April 2005

Cooperative activation of lipolysis by protein kinase A and protein kinase C pathways in 3T3-L1 adipocytes.

Endocrinology 2004 Nov 29;145(11):4940-7. Epub 2004 Jul 29.

IPF PharmaCeuticals GmbH, Feodor-Lynen-Strasse 31, D-30625 Hannover, Germany.

In the present study, we investigate the coherence of signaling pathways leading to lipolysis in 3T3-L1 adipocytes. We observe two linear signaling pathways: one well known, acting via cAMP and protein kinase A (PKA) activation, and a second one induced by phorbol 12-myristate 13-acetate treatment involving protein kinase C (PKC) and MAPK. We demonstrate that both the PKA regulatory subunits RIalpha and RIIbeta are expressed in 3T3-L1 adipocytes and are responsible for the lipolytic effect mediated via the cAMP/PKA pathway. Inhibition of the PKA pathway by the selective PKA inhibitor Rp-8-CPT-cAMPS does not impair lipolysis induced by PKC activation, and neither PD98059 nor U0126, as known MAPK kinase inhibitors, changes the level of glycerol release caused by PKA activation, indicating no cross-talk between these two pathways when only one is activated. However, when both are activated, they act synergistically on glycerol release. Additional experiments focusing on this synergy show no involvement of MAPK phosphorylation and cAMP formation. Phosphorylation of hormone-sensitive lipase is similar upon stimulation of either pathway, but we demonstrate a difference in the ability of both PKA and the PKC pathway activation to phosphorylate perilipin, which in turn may be an explanation for the different maximal lipolytic effect of both pathways.
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http://dx.doi.org/10.1210/en.2004-0803DOI Listing
November 2004

High-performance liquid chromatographic assay with fluorescence detection for the simultaneous measurement of carboxylate and lactone forms of irinotecan and three metabolites in human plasma.

J Chromatogr B Analyt Technol Biomed Life Sci 2003 May;788(1):65-74

Department of Pharmaceutical Sciences, Mail Stop 313, St. Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38105-2794, USA.

Irinotecan (CPT-11), a camptothecin analog, is metabolized to SN-38, an active topoisomerase I inhibitor, and inactive metabolites, including APC and SN-38 glucuronide (SN-38G). A high-performance liquid chromatographic assay method to simultaneously measure the lactone and carboxylate forms of CPT-11, SN-38, SN-38G, and APC in human plasma was developed. Chromatography was accomplished with a reversed-phase C(8) column and fluorescence detection. A gradient mobile phase system was used. The buffer for mobile phase A consisted of 0.75 M ammonium acetate, 5 mM tetrabutylammonium phosphate (pH 6.0), and acetonitrile (86:14, v/v). The buffer for mobile phase B was identical to mobile phase A with the exception of the concentration (50:50, v/v). Precipitation of plasma proteins was performed with cold methanol. The linear range of detection of the lactone and carboxylate forms of SN-38, SN-38G, and APC was 2-25 ng/ml, and 5-300 ng/ml for CPT-11. The limit of quantitation for the analytes ranged from 0.5 to 5 ng/ml. Analysis of patients' plasma samples obtained before and after CPT-11 administration showed that the assay is suitable for measuring lactone and carboxylate forms of CPT-11, SN-38, SN-38G, and APC in clinical studies.
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http://dx.doi.org/10.1016/s1570-0232(02)01016-4DOI Listing
May 2003