Figure 2 - uploaded by Roger McMaster-Fay
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Placental bed spiral artery normal mid-trimester development (of a low resistance circulation-green), maldevelopment (blue) and disease (red)
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![Figure 1. From Wigglesworth [21]](profile/Roger-Mcmaster-Fay/publication/328354352/figure/fig1/AS:703859588624385@1544824611552/From-Wigglesworth-21_Q320.jpg)
The maldevelopment of the spiral arteries in the placental bed reduces uteroplacental blood flow and results in diseases later in the pregnancy. These diseases are here called the uteroplacental vascular syndromes. These syndromes have serious consequence for both the infant and the mother. These pregnancies with a maldeveloped uteroplacental circu...
Context in source publication
Context 1
... the third trimester, in some pregnancies these maldeveloped spiral arteries may further undergo disease changes similar to atherosclerosis. This of atherotic disease process was termed 'acute atherosis' [22], which results in further restriction of blood flow and even complete vascular occlusion causing placental ischemia and infarction ( Figure 2). ...
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Citations
... We previously speculated that these two peaks in cffDNA are most likely indicative of trophoblast injury and coincide in the first peak, with the failure of trophoblast invasion ('physiological change') of the spiral arteries in the placental bed and in the second peak, with the development of acute atherosis of those vessels. 7 Aspirin's main effects in prophylaxis against the Uteroplacental Vascular Syndromes 7 is most likely through its anti-platelet activity: firstly by minimising / preventing the formation of intervillous thrombi forming because of trophoblast / villous injury caused by the shear effect ('jet turbulence') of the increased blood flow through the undilated spiral arteries; 8 and secondly by the maintenance of blood flow through these diseased vessels when they develop acute atherosis. 3 ...
We read with interest the recent article on the effects of aspirin on utero-placental hemodynamics,1 as this has been an area of interest to us since presenting our findings on this subject five years ago,2 although our conclusions2,3 were the opposite to those of your publication. Two recent publications had similar findings to ours.4,5 It is not difficult to see where the difference arises.
... Dr Roger McMaster-Fay, 9 and illustrates how maldevelopment of the spiral arteries can lead to subsequent narrowing and occlusion in the presence of acute atherosis, a lesion described by Dr Arthur Hertig, 10 Professor of Pathology at Harvard Medical School. The name of the lesion was chosen because of its resemblance to the images observed in atheromas. ...
... We propose an analysis of the nuMoM2b data to calculate the predictive ability of this BWt/HC ratio for PFGR [11]. ...
... Further away from term, before the development of muscle and viscera and the laying down of fat, growth restriction is more general and hence the more symmetric (rather than the asymmetric).] Uteroplacental vascular insufficiency is the cause of PFGR [3] and as such is one of the Uteroplacental Vascular Syndromes (UPVS) [11]. ...
The subject of intrauterine growth restriction has and continues to be in confusion because academic journals continue to publish articles that define the outcome of this disease as low birthweight or small for gestational age. This fault has been recently addressed with the recent publication of Fetal-Placental Growth Restriction: a series of 28 articles in 7 sections by 56 recognised authors. But even in this publication no alternative to low birthweight is clearly defined as an alternative to describe the outcome of this disease. As the name of this publication implies, this aberrant fetal growth has its origin in the maldevelopment of a normal, low resistance, uteroplacental circulation. It is therefore not surprising the many these cases have been detected preclinically using in mid-pregnancy uteroplacental Doppler flow studies.
Previous studies have shown that an improvement in outcome definition is achieved when it address the asymmetry of growth these infant have. This review concludes that a ratio of birthweight to head circumference would be the simplest and most appropriate definition.
Preeclampsia is one of the “great obstetrical syndromes” in which multiple and sometimes overlapping pathologic processes activate a common pathway consisting of endothelial cell activation, intravascular inflammation, and syncytiotrophoblast stress. This article reviews the potential etiologies of preeclampsia. The role of uteroplacental ischemia is well-established on the basis of a solid body of clinical and experimental evidence. A causal role for microorganisms has gained recognition through the realization that periodontal disease and maternal gut dysbiosis are linked to atherosclerosis, thus possibly to a subset of patients with preeclampsia. The recent reports indicating that SARS-CoV-2 infection might be causally linked to preeclampsia are reviewed along with the potential mechanisms involved. Particular etiologic factors, such as the breakdown of maternal-fetal immune tolerance (thought to account for the excess of preeclampsia in primipaternity and egg donation), may operate, in part, through uteroplacental ischemia, whereas other factors such as placental aging may operate largely through syncytiotrophoblast stress. This article also examines the association between gestational diabetes mellitus and maternal obesity with preeclampsia. The role of autoimmunity, fetal diseases, and endocrine disorders is discussed. A greater understanding of the etiologic factors of preeclampsia is essential to improve treatment and prevention.
