Maternal haemodynamic function differs in pre‐eclampsia when it is associated with a small‐for‐gestational‐age newborn: a prospective cohort study

H Perry,J Gutierrez,A Khalil,J Binder,B Thilaganathan

doi:10.1111/1471-0528.16269

Abstract

To describe maternal haemodynamic differences in gestational hypertension with small-for-gestational-age babies (HDP+SGA), gestational hypertension with appropriate-for-gestational-age babies (HDP-only) and control pregnancies. Prospective cohort study. Tertiary Hospital, UK. Women with gestational hypertension and healthy pregnant women. Maternal haemodynamic indices were measured using a non-invasive Ultrasound Cardiac Output Monitor (USCOM-1A® ) and corrected for gestational age and maternal characteristics using device-specific reference ranges. Maternal cardiac output, stroke volume, systemic vascular resistance. We included 114 HDP+SGA, 202 HDP-only and 401 control pregnancies at 26-41weeks of gestation. There was no significant difference in the mean arterial blood pressure (110 versus 107mmHg, P=0.445) between the two HDP groups at presentation. Pregnancies complicated by HDP+SGA had significantly lower median heart rate (76 versus 85bpm versus 83bpm), lower cardiac output (0.85 versus 0.98 versus 0.97MoM) and higher systemic vascular resistance (1.4 versus 1.0 versus 1.2MoM) compared with control and HDP-only pregnancies, respectively (all P<0.05). Women with HDP+SGA present with more severe haemodynamic dysfunction than HDP-only. Even HDP-only pregnancies exhibit impaired haemodynamic indices compared with normal pregnancies, supporting a role of the maternal cardiovascular system in gestational hypertension irrespective of fetal size. Central haemodynamic changes may play a role in the pathogenesis of pre-eclampsia and should be considered alongside placental aetiology. Hypertensive disorders of pregnancy are associated with worse maternal haemodynamic function when associated with small-for-gestational-age birth.

Highlights

There is increasing evidence for the role of the maternal cardiovascular system in the development of gestational hypertension and preeclampsia
Pregnancies complicated by hypertensive disorders of pregnancy (HDP)+SGA had significantly lower median heart rate (76bpm vs 85bpm vs 83bpm), lower cardiac output (0.85MoM vs 0.98MoM vs 0.97MoM) and higher systemic vascular resistance (1.4MoM vs 1.0MoM vs 1.2MoM) compared to control and HDP-only pregnancies, respectively
An alternative explanation to the theory of two separate disease mechanisms, is that gestational hypertension and preeclampsia are a disease-continuum, with its severity related to the degree of underlying maternal hemodynamic dysfunction; notably a lack of increase in maternal cardiac output and decrease in systemic vascular resistance as would be expected in normal pregnancy.[26]

Summary

Introduction

There is increasing evidence for the role of the maternal cardiovascular system in the development of gestational hypertension and preeclampsia. Different classifications of hypertension in pregnancy have been proposed which are differentiated by the development of proteinuria, maternal organ dysfunction or fetal growth restriction in preeclampsia[17] as well as different variations on ‘early’ and ‘lateonset’ preeclampsia. These two conditions have typically been separated at 34 weeks of gestation and have been purported as different disease entities with different pathological mechanisms.[18,19,20] Early-onset preeclampsia is a placenta-mediated disease secondary to a failure of the physiological transformation of the spiral arteries into dilated, non-elastic vessels to allow for maximal maternal-placental blood flow. The resulting narrow vessels impede blood flow leading to placental ischaemia, which results in small for gestational age fetuses in addition to hypertension.[20,21,22,23,24,25] Late-onset disease is thought to be secondary to maternal cardio-metabolic dysfunction, which is less likely to be associated with small for gestational age babies.[18,19,20] An alternative explanation to the theory of two separate disease mechanisms, is that gestational hypertension and preeclampsia are a disease-continuum, with its severity related to the degree of underlying maternal hemodynamic dysfunction; notably a lack of increase in maternal cardiac output and decrease in systemic vascular resistance as would be expected in normal pregnancy.[26]

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Conclusion