First-Trimester Normotension Is a Weak Indicator of Normal Maternal Cardiovascular Function

Abstract

BACKGROUND: As by definition, mean arterial pressure equals the product of cardiac output (CO) and total vascular resistance (TPR), we hypothesized that, irrespective of thresholds to define hypertension, a CO-TPR imbalance might exist in first-trimester normotensive pregnancies with altered risks for adverse gestational outcomes. METHODS: A standard protocol was used for automated blood pressure measurement combined with impedance cardiography assessment of CO and TPR (NICCOMO). First-trimester normotensive pregnant women were categorized into 3 groups relative to the reference 75th percentile (P75) of CO and TPR: (1) normal CO and TPR, (2) high CO, and (3) high TPR. These subgroups were compared at blood pressure thresholds 140/90, 130/85, and 130/80 mmHg. The gestational outcome was categorized after birth according to International Society for Studies of Hypertension in Pregnancy criteria. RESULTS: Compared with pregnancies with normal CO and TPR (≤P75), women with high TPR at blood pressure <140/90 mmHg are at risk for developing gestational hypertension (odds ratio, 3.795 [1.321–10.904]; P <0.010), late-onset preeclampsia (odds ratio, 3.137 [1.060–9.287]; P <0.050), and neonates small for gestational age (odds ratio, 1.780 [1.056–2.998]; P <0.050). CONCLUSIONS: Cardiovascular imbalance can present in normotensive women in the first trimester and is associated with increased risks for adverse gestational outcomes. This study illustrates the relevance of CO and TPR assessments as an adjunct to blood pressure measurement and invites for further exploring their value in screening algorithms for gestational hypertensive disorders and/or small for gestational age.

Mechanisms of leptin-induced endothelial dysfunction

“…Endothelial dysfunction is a hallmark of preeclamptic pregnancy [42]. Recent clinical data shows that high total vascular peripheral resistance score, but not cardiac output, predicts hypertension and adverse fetal outcomes in hypertensive pregnancy patients more so than blood pressure measure alone [43], indicating that increased vascular resistance because of endothelial dysfunction may play a very significant role in adverse outcomes of preeclampsia patients. Several mechanisms have been proposed to mediate endothelial dysfunction in preeclampsia, including inappropriate RAAS activation, reduced NO bioavailability and increases in the production of the vasoconstrictor endothelin-1 [42].…”