Impaired maternal hemodynamics in morbidly obese women: a case–control study

  1. Gutierrez, J. 12
  2. Vinayagam, D. 12
  3. Binder, J. 12
  4. Mantovani, E. 12
  5. Thilaganathan, B. 12
  6. Khalil, A. 12
  1. 1 Fetal Medicine Unit St George's University of London London UK
  2. 2 St George's University Hospitals NHS Foundation Trust Molecular and Clinical Sciences Research Institute London UK
Aldizkaria:
Ultrasound in Obstetrics & amp; Gynecology

ISSN: 0960-7692 1469-0705

Argitalpen urtea: 2017

Alea: 50

Zenbakia: 6

Orrialdeak: 761-765

Mota: Artikulua

DOI: 10.1002/UOG.17428 GOOGLE SCHOLAR lock_openSarbide irekia editor

Beste argitalpen batzuk: Ultrasound in Obstetrics & amp; Gynecology

Laburpena

Objective: Maternal obesity is associated with significant pregnancy complications and is a risk factor for the development of hypertensive disorders of pregnancy as well as other adverse outcomes. There are few data regarding the hemodynamic aberrations observed in maternal obesity. The aim of this study was to investigate maternal hemodynamics in morbidly obese women.Methods: This was a prospective, case–control study of morbidly obese women (body mass index (BMI) ≥ 40 kg/m2) and controls (BMI 20–29.9 kg/m2).The control population was matched for maternal age and gestational age. BMI was calculated based on maternal height and weight at the time of recruitment to the study, which occurred on the same day as the hemodynamic assessment. Pregnant women in the second or third trimester of pregnancy were included. Women who were found to be hypertensive at any time were excluded from the study. A USCOM-1A® device was used to assess hemodynamic parameters (heart rate, stroke volume (SV),cardiac output and systemic vascular resistance (SVR)). The parameters were corrected for body surface area (BSA) to provide the SV index (SVI), cardiac index (CI) and SVR index (SVRI). Mann–Whitney U-test was used to compare the medians of the hemodynamic variables between the two groups.Results: In total, 23 morbidly obese women and 327 controls were included in the analysis. There was no difference in maternal (P = 0.506) or gestational (P = 0.693) age at recruitment between the groups. Mean arterial pressure was higher both at pregnancy booking(90 vs 80 mmHg, P < 0.001) and study recruitment (91 vs 85 mmHg, P < 0.001) in the obese group compared with the controls. Heart rate was higher in the obese group (P = 0.003), but there was no difference in SV (P = 0.271), cardiac output (P = 0.238) or SVR (P = 0.635). Following correction of these parameters for BSA, compared with the control group, SVI (34 vs 45 mL/m2, P < 0.001) and CI (2.96 vs 3.64 L/min/m2, P < 0.001) were significantly reduced in the obese group, whereas SVRI was significantly higher (2354 vs 1840 dynes × s/cm5, P < 0.001).Conclusions: The findings of our study suggest that cardiac function is significantly altered in morbidly obese pregnant women. In order to make appropriate comparisons between individuals, it is imperative that hemodynamic parameters are indexed for BSA, as isstandard practice in pediatric cardiology. The novel finding of reduced CI in morbidly obese pregnant women may explain the predisposition to pre-eclampsia and other adverse outcomes in this population and warrants further investigation. Copyright © 2017 ISUOG. Published by John Wiley & Sons Ltd

Erreferentzia bibliografikoak

  • Lu GC, Rouse DJ, DuBard M, Cliver S, Kimberlin D, Hauth JC. The effect of the increasing prevalence of maternal obesity on perinatal morbidity. Am J Obstet Gynecol 2001; 185: 845 – 849.
  • Vinayagam D, Chandraharan E. The adverse impact of maternal obesity on intrapartum and perinatal outcomes. ISRN Obstet Gynecol 2012; 939 762. https:// doi.org/10.5402/2012/939762.
  • Oyebode O, Mindell J. Use of data from the Health Survey for England in obesity policy making and monitoring. Obes Rev 2013; 14: 463 – 476.
  • Marchi J, Berg M, Dencker A, Olander E, Begley C. Risks associated with obesity in pregnancy, for the mother and baby: a systematic review of reviews. Obes Rev 2015; 16: 621 – 638.
  • Knight M, Kurinczuk JJ, Spark P, Brocklehurst P. Extreme obesity in pregnancy in the United Kingdom. Obstet Gynecol 2010; 115: 989 – 997.
  • Knight M, Kenyon K, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ. Saving lives, improving mothers’ care. Lessons learned to inform future maternity care from the UK and Ireland confidential enquiries into maternal deaths and morbidity 2009 – 2012. MBRRACE-UK Report, 2014. https://www.npeu.ox.ac.uk/mbrrace-uk/ reports
  • Sanghavi M, Rutherford JD. Cardiovascular physiology of pregnancy. Circulation 2014; 130: 1003 – 1008.
  • Veille J-C, Hanson R. Obesity, pregnancy, and left ventricular functioning during the third trimester. Am J Obstet Gynecol 1994; 171: 980 – 983.
  • Dennis A, Castro J, Ong M, Carr C. Haemodynamics in obese pregnant women. Int J Obstet Anesth 2012; 21: 129 – 134.
  • Tranquilli AL, Dekker G, Magee L, Roberts J, Sibai BM, Steyn W, Zeeman GG, Brown MA. The classification, diagnosis and management of the hypertensive disorders of pregnancy: a revised statement from the ISSHP. Pregnancy Hypertens 2014; 4: 97 – 104.
  • Vinayagam D, Thilaganathan B, Stirrup O, Mantovani E, Khalil A. Maternal hemodynamics in normal pregnancies: reference ranges and the role of maternal characteristics. Ultrasound Obstet Gynecol (2017). https://doi.org/10.1002/uog.17504.
  • Magriples U, Boynton MH, Kershaw TS, Rising SS, Ickovics JR. Blood pressure changes during pregnancy: impact of race, body mass index, and weight gain. Am J Perinatol 2013; 30: 415.
  • Carson M, Powrie R, Rosene-Montella K. The effect of obesity and position on heart rate in pregnancy. J Matern Fetal Neonat Med 2002; 11: 40 – 45.
  • Vinayagam D, Patey O, Thilaganathan B, Khalil A. Cardiac output assessment in pregnancy: comparison of two automated monitors with echocardiography. Ultrasound Obstet Gynecol 2017; 49: 32 – 38.
  • Verlohren S, Melchiorre K, Khalil A, Thilaganathan B. Uterine artery Doppler, birth weight and timing of onset of pre-eclampsia: providing insights into the dual etiology of late-onset pre-eclampsia. Ultrasound Obstet Gynecol 2014; 44: 293 – 298.
  • Melchiorre K, Sharma R, Khalil A, Thilaganathan B. Maternal cardiovascular function in normal pregnancy evidence of maladaptation to chronic volume overload. Hypertension 2016; 67: 754 – 762.
  • Melchiorre K, Sharma R, Thilaganathan B. Cardiovascular implications in preeclampsia: an overview. Circulation 2014; 130: 703 – 714.