Early and Late Preeclampsia

Abstract

Abstract-Because early and late preeclampsia (PE) are thought to be different disease entities, we compared maternal cardiac function at 24 weeks gestation in a group of normotensive asymptomatic patients with subsequent development of early (Ͻ34 weeks gestation) and late (Ն34 weeks gestation) PE (blood pressure Ͼ140/90ϩproteinuria Ͼ300 mg/dL) to detect possible early differences in the hemodynamic state. ; PϽ0.001). Early and late PE appear to develop from different hemodynamic states. Late PE appears to be more frequent in patients with high body mass index and low total vascular resistance; earlier forms of PE appear to be more frequent in patients with lower BMI and with bilateral notching of the uterine artery. These findings support the hypothesis of different hemodynamics and origins for early PE (placental mediated, linked to defective trophoblast invasion with high percentage of altered uterine artery Doppler) and late PE (linked to constitutional factors such as high body mass index). Key Words: preeclampsia/pregnancy Ⅲ hemodynamcs Ⅲ echocardiography P reeclampsia (PE) is associated with maternal perinatal morbidity and mortality 1 and affects 5% to 7% of pregnant patients worldwide. 2 Hemodynamic investigations during the latent phase of PE are scarce and conflicting because of the different classifications 3,4 used in the definition: mild, moderate, and severe, as well as early and late. The concept of early and late PE is more modern, and it is widely accepted that these two entities have different etiologies and should be regarded as different forms of the disease. 3,4 Early-onset PE (before 34 weeks) is commonly associated with abnormal uterine artery Doppler, fetal growth restriction (FGR), and adverse maternal and neonatal outcomes. 1,5 In contrast, late-onset PE (after 34 weeks) is mostly associated with normal or slight increased uterine resistance index, a low rate of fetal involvement, and more favorable perinatal outcomes. 5,6 Early-onset PE and FGR are placenta-mediated diseases that share important similarities as recently demonstrated by Crispi et al, 7,8 who reported placental growth factor (PIGF) as a useful second-trimester screening test for this form of the disease, but not for late-onset PE/FGR. Maternal echocardiography might identify at 24 weeks gestation patients who subsequently develop early severe maternal and fetal complications through the assessment of maternal hemodynamics and left ventricular geometry (elevated maternal total vascular resistance [TVR] and the presence of concentric geometry) 9 -11 suggesting an involvement of the whole cardiovascular system in the placental mediated disorder. Previous data published by Bosio 12 and Easterling 13 on the latent phase of PE are in contrast with this model (describing low TVR and high cardiac output [CO]), although the patients from those series developed late forms of PE.Interestingly, hemodynamics and volume homeostasis in women with previous PE appear to be similar to hypertensive subjects and different from healthy paro...

Phenotypes of Pregnant Women Who Subsequently Develop Hypertension in Pregnancy

“…Women at the highest risk of developing a hypertensive disorder of pregnancy exhibit a distinct cardiovascular, placental and clinical phenotype before the development of hypertension, consistent with previous reports 3, 9, 16, 17. To the best of our knowledge, this is the first analysis to evaluate clinical characteristics in a consolidated manner, rather than individually.…”

“…It is well accepted that the majority of pregnant women who subsequently develop hypertension in pregnancy exhibit abnormalities in maternal hemodynamics before the clinical development of hypertension, with or without aberrations in circulating angiogenic proteins that regulate vascular function early in pregnancy 3, 4, 5. The clinical syndromes of hypertension in pregnancy are distinctly heterogeneous.…”

Additive value of standard ECG for the risk prediction of hypertensive disorders during pregnancy

“…21,22 Although some echocardiographic studies showed that women developing hypertensive complications during pregnancy may have different LA dimensions than controls, [23][24][25][26] the potential link between LA abnormality detected early in pregnancy by echocardiography or ECG and development of hypertensive disorders remains elusive. However, some possible mechanisms are supported by epidemiological data and experimental models.…”

Low molecular weight heparin for the prevention of severe preeclampsia: where next?

“…Early-onset preeclampsia is strongly associated with placental disease characterized by maternal vascular malperfusion, where the abnormal placental villi secrete excessive amounts of antiangiogenic proteins and reduced levels of pro-angiogenic proteins into the maternal circulation [7][8][9]. Women with early-onset disease, typically associated with FGR, develop hypertension earlier in pregnancy that is characterized by increased systemic vascular resistance, reduced cardiac output and stroke volume along with relative bradycardia [5]. In contrast, late-onset preeclampsia is less commonly associated with severe placental disease, and consequently exhibits less dramatic alterations in the circulating levels of placentalderived angiogenic proteins [8,10].…”

“…Only 1% of pregnant women develop early-onset preeclampsia, where both the maternal and fetal implications are substantially greater, typically resulting in FGR and the need for iatrogenic preterm delivery before 34 weeks' gestation [2]. Early-onset preeclampsia is hypothesized to be a direct consequence of the interactions between a dysfunctional placenta and maternal cardiovascular system, while late-onset preeclampsia is hypothesized to be largely triggered by maternal constitutional factors [3][4][5]. Typically, women with early-onset preeclampsia present with an acute, severe syndrome that threatens the life of both the mother and her fetus.…”