scholarly journals First-trimester screening with specific algorithms for early- and late-onset fetal growth restriction

2016 ◽  
Vol 48 (3) ◽  
pp. 340-348 ◽  
Author(s):  
F. Crovetto ◽  
S. Triunfo ◽  
F. Crispi ◽  
V. Rodriguez-Sureda ◽  
E. Roma ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Late Onset ◽  
First Trimester ◽  
Growth Restriction ◽  
First Trimester Screening ◽  
Trimester Screening

scholarly journals OC10.04: The role of angiogenic factors for first-trimester screening of fetal growth restriction

2014 ◽  
Vol 44 (S1) ◽  
pp. 26-26
Author(s):  
F. Crovetto ◽  
S. Triunfo ◽  
F. Crispi ◽  
V. Rodriguez-Sureda ◽  
C. Dominguez ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
First Trimester ◽  
Angiogenic Factors ◽  
Growth Restriction ◽  
First Trimester Screening ◽  
Trimester Screening

scholarly journals Fetal Growth Restriction: Does an Integrated Maternal Hemodynamic-Placental Model Fit Better?

2020 ◽  
Author(s):  
F. Mecacci ◽  
L. Avagliano ◽  
F. Lisi ◽  
S. Clemenza ◽  
Caterina Serena ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Early Onset ◽  
Late Onset ◽  
First Trimester ◽  
Growth Restriction ◽  
System A ◽  
Adverse Pregnancy ◽  
Therapeutic Tools ◽  
Flat Profile

AbstractIn recent years, a growing interest has arisen regarding the possible relationship between adverse pregnancy outcomes (APOs) and inadequate maternal hemodynamic adaptations to the pregnancy. A possible association between “placental syndromes,” such as preeclampsia (PE) and fetal growth restriction (FGR), and subsequent maternal cardiovascular diseases (CVD) later in life has been reported. The two subtypes of FGR show different pathogenetic and clinical features. Defective placentation, due to a poor trophoblastic invasion of the maternal spiral arteries, is believed to play a central role in the pathogenesis of early-onset PE and FGR. Since placental functioning is dependent on the maternal cardiovascular system, a pre-existent or subsequent cardiovascular impairment may play a key role in the pathogenesis of early-onset FGR. Late FGR does not seem to be determined by a primary abnormal placentation in the first trimester. The pathological pathway of late-onset FGR may be due to a primary maternal cardiovascular maladaptation: CV system shows a flat profile and remains similar to those of non-pregnant women. Since the second trimester, when the placenta is already developed and increases its functional request, a hypovolemic state could lead to placental hypoperfusion and to an altered maturation of the placental villous tree and therefore to an altered fetal growth. Thus, this review focalizes on the possible relationship between maternal cardiac function and placentation in the development of both early and late-onset FGR. A better understanding of maternal hemodynamics in pregnancies complicated by FGR could bring various benefits in clinical practice, improving screening and therapeutic tools.

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