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Title: | Gestational hypertensive disorders show unique patterns of circulatory deterioration with ongoing pregnancy | Authors: | GYSELAERS, Wilfried VONCK, Sharona STAELENS, Anneleen LANSSENS, Dorien TOMSIN, Kathleen OBEN, Jolien DREESEN, Pauline BRUCKERS, Liesbeth |
Issue Date: | 2019 | Publisher: | AMER PHYSIOLOGICAL SOC | Source: | AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 316(3), p. R210-R221 | Abstract: | A combined assessment of heart, arteries, veins, and body fluid content throughout pregnancy has not yet been reported. We hypothesized that a gradual aggravation of circulatory dysfunction exists from the latent to the clinical phase of gestational hypertensive disease (GHD), and that pathways are unique for preeclampsia with early onset < 34 wk (EPE) and late onset >= 34 wk (LPE), and gestational hypertension (GH). Women with singleton pregnancy and no known diseases were invited for a prospective, observational study and had standardized sphygmomanometric blood pressure measurement, bioimpedance body water spectrum analysis, impedance cardiography for cardiac and arterial assessment, and combined Doppler-ECG of hepatic and renal interlobar veins and uterine arteries. Outcome was categorized as uncomplicated (UP, n = 1,700), EPE (n = 87), LPE (n = 218), or GH (n = 188). A linear mixed model for repeated measurements, corrected for age, parity, and body mass index, was employed in SAS 9.4 to analyze trimestral changes within and between groups. From the first to the third trimester, body water increased in all groups, and an increasing number of abnormal parameters relative to UP occurred in all GHD. First-trimester blood pressure and peripheral resistance were higher in GHD than UP, together with increased uterine flow resistance and extracellular water in EPE, and with lower heart rate and aorta flow velocity in LPE. An overall gestational rise of body water volumes coexists with a gradual worsening of cardiovascular dysfunction in GHD, of which pathophysiological pathways are unique for EPE, LPE, and GH, respectively. | Notes: | [Gyselaers, Wilfried; Vonck, Sharon; Lanssens, Dorien; Dreesen, Pauline] Hasselt Univ, Fac Med & Life Sci, Diepenbeek, Belgium. [Gyselaers, Wilfried; Vonck, Sharon; Staelens, Anneleen Simone; Lanssens, Dorien; Tomsin, Kathleen; Oben, Jolien; Dreesen, Pauline] Ziekenhuis Oost Limburg, Dept Obstet & Gynaecol, Schiepse Bos 6, B-3600 Genk, Belgium. [Gyselaers, Wilfried] Hasselt Univ, Dept Physiol, Diepenbeek, Belgium. [Bruckers, Liesbeth] Hasselt Univ, Interuniv Inst Biostat & Stat Bioinformat, Diepenbeek, Belgium. | Keywords: | Maternal hemodynamics;gestational hypertensive disease;gestational hypertension;preeclampsia;pathophysiology | Document URI: | http://hdl.handle.net/1942/30226 | ISSN: | 0363-6119 | e-ISSN: | 1522-1490 | DOI: | 10.1152/ajpregu.00075.2018 | ISI #: | 000461194600004 | Rights: | 2019 the American Physiological Society | Category: | A1 | Type: | Journal Contribution | Validations: | ecoom 2020 |
Appears in Collections: | Research publications |
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gyselaers2019.pdf | Peer-reviewed author version | 2.17 MB | Adobe PDF | View/Open |
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