Impaired maternal hemodynamics in morbidly obese women: a case-control study.
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 is standard 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.
Fetal Medicine Unit, St George's University of London, London, UK.|St George's University Hospitals NHS Foundation Trust, Molecular and Clinical Sciences Research Institute, London, UK.
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http://orcid.org/0000-0001-9474-6572
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Vinayagam
Fetal Medicine Unit, St George's University of London, London, UK.|St George's University Hospitals NHS Foundation Trust, Molecular and Clinical Sciences Research Institute, London, UK.
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J
Gutierrez
Fetal Medicine Unit, St George's University of London, London, UK.|St George's University Hospitals NHS Foundation Trust, Molecular and Clinical Sciences Research Institute, London, UK.
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Binder
Fetal Medicine Unit, St George's University of London, London, UK.|St George's University Hospitals NHS Foundation Trust, Molecular and Clinical Sciences Research Institute, London, UK.
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Mantovani
Fetal Medicine Unit, St George's University of London, London, UK.|St George's University Hospitals NHS Foundation Trust, Molecular and Clinical Sciences Research Institute, London, UK.
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B
Thilaganathan
Fetal Medicine Unit, St George's University of London, London, UK.|St George's University Hospitals NHS Foundation Trust, Molecular and Clinical Sciences Research Institute, London, UK.
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A
Khalil
D000222:Adaptation, Physiological / Q000502:physiology*; D000328:Adult; D001783:Blood Flow Velocity; D002303:Cardiac Output, Low / Q000209:etiology* / Q000503:physiopathology; D016022:Case-Control Studies; D004452:Echocardiography; D005260:Female; D006439:Hemodynamics; D006801:Humans; D046110:Hypertension, Pregnancy-Induced / Q000209:etiology* / Q000503:physiopathology; D063130:Maternal Death; D008991:Monitoring, Physiologic; D009767:Obesity, Morbid / Q000150:complications* / Q000503:physiopathology; D011247:Pregnancy; D011446:Prospective Studies; D013318:Stroke Volume / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology*
USCOM®; hemodynamics; non-invasive cardiac output monitoring; obesity; pregnancy