Abnormal maternal cardiac function and morphology in pregnancies complicated by intrauterine fetal growth restriction

Vasapollo, B.; Valensise, H.; Novelli, G. P.; Larciprete, G.; Pierro, G. Di; Altomare, F.; Casalino, B.; Galante, Alberto; Arduini, Domenico

doi:10.1046/j.1469-0705.2002.00847.x

Cited by 74 publications

(97 citation statements)

References 31 publications

(43 reference statements)

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“…An increase in BP may allow placental perfusion to be maintained. Reportedly, in PIH patients the mean BP, cardiac output and ejection volume are lower in pregnancies complicated by IUGR [43,44]. In IUGR, the increase in maternal BP may stem from a compensatory mechanism that is jeopardized by anti-hypertensive treatment [45].…”

Section: Discussionmentioning

confidence: 99%

Circadian rhythm of maternal blood pressure and fetal growth

Maggioni¹,

Cornelissen²,

Otsuka³

et al. 2005

Biomedicine & Pharmacotherapy

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This study aimed at examining any relation between the circadian variation in blood pressure (BP) in human pregnancy and fetal growth. A prospective study included 52 pregnant women monitored during the third trimester of pregnancy. There were 33 uncomplicated pregnancies with normal fetal growth (Group 1) and 19 pregnancies complicated by intrauterine growth retardation (IUGR), confirmed at birth (Group 2). Ten women (five in each group) had pregnancy-induced hypertension. All women were hospitalized and followed a similar daily routine. BP was recorded with an automatic wearable device. Measurements were obtained every 20 min for 24 ± 1 h. BP profiles were analyzed by conventional statistical methods and by cosinor, involving the least squares fit of cosine curves with an anticipated period (24 h) to the data. BP parameters, fetal outcome, demographic and obstetric characteristics were compared between the two groups. Logistic regression and multivariate analyses were used to assess factors putatively associated with fetal outcome. The circadian amplitude of diastolic BP was found to be larger in normotensive women with IUGR. As gauged by odds ratios (OR), the circadian amplitude of diastolic BP (OR = 1.7, 95% CI: 1.1-2.8; P = 0.03) and hematocrit (OR = 1.4, 95% CI: 1.0-1.9; P = 0.04) were the only variables positively and independently associated with IUGR. In the presence of maternal hypertension, the circadian amplitude of systolic BP was negatively associated with IUGR (OR = 0.7, 95% CI: 0.5-1.0; P = 0.03). A larger circadian variation in diastolic BP, rather than a difference in the mean value of systolic or diastolic BP, was found to be statistically significantly associated with IUGR. This study adds another condition in which the circadian BP amplitude constitutes a harbinger of elevated risk, apart from an association with a shortened lifespan in the absence or presence of malignant hypertension and with an increased risk of stroke and nephropathy reported earlier.

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Section: Discussionmentioning

confidence: 99%

Circadian rhythm of maternal blood pressure and fetal growth

Maggioni¹,

Cornelissen²,

Otsuka³

et al. 2005

Biomedicine & Pharmacotherapy

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“…Left ventricular end-diastolic and end-systolic diameters and interventricular septum and posterior wall diastolic thicknesses were detected as previously described [25][26][27] according to the recommendation of the American Society of Echocardiography. 28 Left ventricular mass in grams was calculated by the Devereux formula.…”

Section: Echocardiographic Evaluationmentioning

confidence: 99%

Persistent Maternal Cardiac Dysfunction After Preeclampsia Identifies Patients at Risk for Recurrent Preeclampsia

et al. 2016

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Maternal cardiovascular health represents the key point for developing an uneventful pregnancy, and its proper function is important for a normal evolution of pregnancy. Serious pregnancy-related hypertensive disorders such as preeclampsia might entail severe future effects on women's health even after delivery and influence the long-term quality of life as well as the following pregnancy outcomes. A proper maternal cardiovascular adaptation to the pregnancy plays a key role for preventing gestational hypertensive complications, such as preeclampsia. [1][2][3][4][5] Preeclampsia affects the 3% to 8% of pregnancies and represents a cause of increased maternal and perinatal morbidity and mortality. 6,7 According to the different onset time, the origin and hemodynamics, preeclampsia is classified as early (placental mediated, linked to defective trophoblast invasion with high incidence of altered uterine artery Doppler, and lower body mass index [BMI]) and late (related to higher BMI and no alteration of uterine artery Doppler) 8 recurring in 15% of the following pregnancies.9-11 Former preeclamptics have a 7× higher risk of disease recurrence compared with women who have had a normal pregnancy. 12,13Patients with a previous preeclampsia show maternal cardiac dysfunction, and they are more likely to develop systemic hypertension and to die at an early age from cardiovascular disease. [14][15][16][17] In particular, postpartum follow-up of women with a previous preeclampsia showed persistence of altered cardiac geometry and left ventricular dysfunction. 18,19 The latest studies in literature highlight the importance of assessing maternal cardiac function and structure evaluating hemodynamics in terms of total vascular resistance (TVR), left ventricular geometric pattern with regard to the presence of concentric geometry, and diastolic dysfunction. [20][21][22] It is of primary importance to understand how to select and identify those women at increased risk for recurrent preeclampsia. In a recent study, Scholten et al 23 concluded that the risk of recurrent preeclampsia and fetal growth restriction in a subsequent pregnancy is inversely and linearly related to pregnancy plasma volume, and this condition might predispose to abnormal hemodynamic adaptation to pregnancy. In previously early preeclamptic women, given the high incidence of postpartum asymptomatic left ventricular abnormalities, the high See Editorial Commentary, pp 690-692Abstract-The purpose of our study was to assess cardiac function in nonpregnant women with previous early preeclampsia before a second pregnancy to highlight the cardiovascular pattern, which may take a risk for recurrent preeclampsia. Seventy-five normotensive patients with previous preeclampsia and 147 controls with a previous uneventful pregnancy were enrolled in a case-control study and submitted to echocardiographic examination in the nonpregnant state 12 to 18 months after the first delivery. All patients included in the study had pregnancy within 24 months from the echocardiograp...

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“…21,25,26 The following variables were measured: peak flow velocity in early diastole (E wave velocity) and during atrial contraction (A wave velocity); E/A ratio; E and A wave timevelocity integrals; deceleration time of the E-wave (DtE) and duration of the A wave (A wave duration); isovolumetric relaxation time of the left ventricle (IVRT).…”

Section: Diastolic Functionmentioning

confidence: 99%

Early and Late Preeclampsia

Valensise¹,

Vasapollo²,

Gagliardi³

et al. 2008

Hypertension

483

224

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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...

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Abnormal maternal cardiac function and morphology in pregnancies complicated by intrauterine fetal growth restriction

Abstract: The absence of a 'correct' maternal cardiovascular compensatory response to abnormal trophoblastic invasion, might be one of the factors that slowly determine the conditions of reduced placental perfusion and eventually of the development of fetal growth restriction.

Cited by 74 publications

References 31 publications

Circadian rhythm of maternal blood pressure and fetal growth

Circadian rhythm of maternal blood pressure and fetal growth

Persistent Maternal Cardiac Dysfunction After Preeclampsia Identifies Patients at Risk for Recurrent Preeclampsia

Early and Late Preeclampsia

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