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We report an unexpected death of a 22-year-old primigravida who was admitted to the hospital with sudden abdominal pain two days before a scheduled delivery. During an emergency caesarean section due to intrauterine asphyxia, intraabdominal bleeding was observed with no apparent source of bleeding. Newly formed blood clots in the subdiaphragmatic space and arterial bleeding near the splenic hilum required a surgery on the next day. Hemorrhagic shock led to multiple organ failure on the fourth day of admission. The autopsy revealed ruptured splenic artery at the pancreatic tail and near the splenic hilum. Microscopically, different stages of segmental arterial mediolysis were observed in partially thinned and aneurysmatic artery., Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)

Chronic venous disease (CVD) comprises a spectrum of morphofunctional disorders affecting the venous system, affecting approximately 1 in 3 women during gestation. Emerging evidence highlights diverse maternofetal implications stemming from CVD, particularly impacting the placenta. While systemic inflammation has been associated with pregnancy-related CVD, preliminary findings suggest a potential link between this condition and exacerbated inflammation in the placental tissue. Inflammasomes are major orchestrators of immune responses and inflammation in different organs and systems. Notwithstanding the relevance of inflammasomes, specifically the NLRP3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3)- which has been demonstrated in the placentas of women with different obstetric complications, the precise involvement of this component in the placentas of women with CVD remains to be explored. This study employs immunohistochemistry and real-time PCR (RT-qPCR) to examine the gene and protein expression of key components in both canonical and non-canonical pathways of the NLRP3 inflammasome (NLRP3, ASC-apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain-caspase 1, caspase 5, caspase 8, and interleukin 1β) within the placental tissue of women affected by CVD. Our findings reveal a substantial upregulation of these components in CVD-affected placentas, indicating a potential pathophysiological role of the NLRP3 inflammasome in the development of this condition. Subsequent investigations should focus on assessing translational interventions addressing this dysregulation in affected patient populations.

Aims: Hypertensive pregnancy is associated with increased risks of developing a range of vascular disorders in later life. Understanding when hypertensive target organ damage first emerges could guide optimal timing of preventive interventions. This review identifies evidence of hypertensive target organ damage across cardiac, vascular, cerebral, and renal systems at different time points from pregnancy to postpartum., Methods and Results: Systematic review of Ovid/MEDLINE, EMBASE, and ClinicalTrials.gov up to and including February 2023 including review of reference lists. Identified articles underwent evaluation via a synthesis without meta-analysis using a vote-counting approach based on direction of effect, regardless of statistical significance. Risk of bias was assessed for each outcome domain, and only higher quality studies were used for final analysis. From 7644 articles, 76 studies, including data from 1 742 698 pregnancies, were identified of high quality that reported either blood pressure trajectories or target organ damage during or after a hypertensive pregnancy. Left ventricular hypertrophy, white matter lesions, proteinuria, and retinal microvasculature changes were first evident in women during a hypertensive pregnancy. Cardiac, cerebral, and retinal changes were also reported in studies performed during the early and late post-partum period despite reduction in blood pressure early postpartum. Cognitive dysfunction was first reported late postpartum., Conclusion: The majority of target organ damage reported during a hypertensive pregnancy remains evident throughout the early and late post-partum period despite variation in blood pressure. Early peri-partum strategies may be required to prevent or reverse target organ damage in women who have had a hypertensive pregnancy., Competing Interests: Conflict of interest: None declared., (© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Background: Hypertension has been known to increase the risk of obstetric complications. Recently, the American College of Cardiology endorsed lower thresholds for hypertension as systolic blood pressure of 130-139 mmHg or diastolic blood pressure 80-89 mmHg. However, there is a paucity of information regarding the impact of pre-pregnancy blood pressure on pregnancy outcomes. We aimed to evaluate the effect of pre-pregnancy blood pressure on maternal and neonatal complications., Methods: In this nationwide, population based study, pregnant women without history of hypertension and pre-pregnancy blood pressure < 140/90 mmHg were enrolled. The primary outcome of composite morbidity was defined as any of the followings: preeclampsia, placental abruption, stillbirth, preterm birth, or low birth weight., Results: A total of 375,305 pregnant women were included. After adjusting for covariates, the risk of composite morbidity was greater in those with stage I hypertension in comparison with the normotensive group (systolic blood pressure, odds ratio = 1.68, 95% CI: 1.59 - 1.78; diastolic blood pressure, odds ratio = 1.56, 95% CI: 1.42 - 1.72). There was a linear association between pre-pregnancy blood pressure and the primary outcome, with risk maximizing at newly defined stage I hypertension and with risk decreasing at lower blood pressure ranges., Conclusions: 'The lower, the better' phenomenon was still valid for both maternal and neonatal outcomes. Our results suggest that the recent changes in diagnostic thresholds for hypertension may also apply to pregnant women. Therefore, women with stage I hypertension prior to pregnancy should be carefully observed for adverse outcomes., (© 2022. The Author(s).)

Background: Coronavirus Disease 2019 (COVID-19) is predominately known as a respiratory disease associated with pneumonia, acute respiratory distress syndrome and multiorgan failure. However, extra-pulmonary complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are increasingly being recognized. In this regard, some studies implied the hemostatic and vascular involvements in patients with SARS-CoV-2 infection., Case Presentation: We describe a case of spontaneous Intracerebral Hemorrhage (ICH) in a pregnant patient with COVID-19 and history of cesarean section a week before the occurrence of ICH. The patient underwent emergent craniotomy with acceptable outcome. Hemorrhagic events, including ICH, may happen during COVID-19 infection with several possible mechanisms., Conclusion: COVID-19 patients, especially high-risk groups, are at a risk of intracranial hemorrhage. Therefore, close follow-up must be maintained and hemorrhagic events must be kept in mind in these cases., (© 2021. The Author(s).)

Procoagulant extracellular vesicles (EV) and platelet activation have been associated with gestational vascular complications. EV-induced platelet-mediated placental inflammasome activation has been shown to cause preeclampsia-like symptoms in mice. However, the effect of EV-mediated placental thrombo-inflammation on trophoblast differentiation remains unknown. Here, we identify that the EV-induced thrombo-inflammatory pathway modulates trophoblast morphology and differentiation. EVs and platelets reduce syncytiotrophoblast differentiation while increasing giant trophoblast and spongiotrophoblast including the glycogen-rich cells. These effects are platelet-dependent and mediated by the NLRP3 inflammasome. In humans, inflammasome activation was negatively correlated with trophoblast differentiation marker GCM1 and positively correlated with blood pressure. These data identify a crucial role of EV-induced placental thrombo-inflammation on altering trophoblast differentiation and suggest platelet activation or inflammasome activation as a therapeutic target in order to achieve successful placentation.

Importance: Peripartum cardiomyopathy is a rare form of heart failure due to left ventricular systolic dysfunction that affects women late in pregnancy and the postpartum period. A diagnosis of exclusion, peripartum cardiomyopathy can be difficult to diagnose in the context of the normal physiologic changes of pregnancy and requires a high index of suspicion., Evidence Acquisition: Original research articles, review articles, and guidelines on peripartum cardiomyopathy were reviewed., Results: The etiology of peripartum cardiomyopathy remains poorly defined, but theories include genetic predisposition, as well as myocardial inflammation and angiogenic dysregulation. Risk factors for this condition include hypertensive disorders of pregnancy, Black race, and maternal age older than 30 years. Patients with peripartum cardiomyopathy are at increased risk of acute clinical decompensation, cardiac arrhythmias, thromboembolic complications, and death. Primary treatment modalities include initiation of a medication regimen aimed at the optimization of preload and reduction of afterload. Maternal clinical status is the primary determinant for timing of delivery., Conclusions: Prompt diagnosis and medical management by an interdisciplinary care team are vital for improving outcomes in patients with peripartum cardiomyopathy.

Lower limbs venous insufficiency refers to a wide variety of venous disorders grouped by the term of chronic venous disease (CVD). Hemodynamic and hormonal changes related to pregnancy period, may promote the development of CVD affecting approximately 1 in 3 women. It has been shown that the presence of this condition is associated with damage and placental suffering. Thus, taking IGF-1/PAPP-A/STC-2, inflammatory cytokines production, PI3K/Akt and Wnt/ β-catenin pathways as a part of the alterations that occurs in the placenta due to CVD, the aim of this study will be to examine the main components of these pathways. Genic and protein expression of PAPP-A, STC-2, IGF-1, IRS-4 Wnt-1, β-catenin, c-myc, Cyclin D1, IL-4/IL-6 and PI3K/Akt/mTOR pathway will be analysed through RT-qPCR and immunohistochemical techniques in women with CVD (n=62) and pregnant women without this condition (HC) (n=52). PAPP-A, IGF-1, IL-4, IL-6, IRS-4, PI3K, Akt, mTOR, Wnt-1, β-catenin, c-myc and Cyclin D1 expression were found to be increased in women with CVD, whereas STC-2 were decreased in this group, compared to non-affected women. Our study has demonstrated that IGF-1/PAPP-A/STC-2 axis, PI3K/Akt and Wnt/β-catenin pathways, along with c-myc, Cyclin D1 and inflammatory cytokines are altered in placenta women with CVD. These results extent the knowledge that CVD is associated to a placenta damage with abnormal tissue environment and cellular regulation., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

Normal cardiac contractile and relaxation functions are critically dependent on a continuous energy supply. Accordingly, metabolic perturbations and impaired mitochondrial bioenergetics with subsequent disruption of ATP production underpin a wide variety of cardiac diseases, including diabetic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, anthracycline cardiomyopathy, peripartum cardiomyopathy, and mitochondrial cardiomyopathies. Crucially, there are no specific treatments for preventing the onset or progression of these cardiomyopathies to heart failure, one of the leading causes of death and disability worldwide. Therefore, new treatments are needed to target the metabolic disturbances and impaired mitochondrial bioenergetics underlying these cardiomyopathies in order to improve health outcomes in these patients. However, investigation of the underlying mechanisms and the identification of novel therapeutic targets have been hampered by the lack of appropriate animal disease models. Furthermore, interspecies variation precludes the use of animal models for studying certain disorders, whereas patient-derived primary cell lines have limited lifespan and availability. Fortunately, the discovery of human-induced pluripotent stem cells has provided a promising tool for modelling cardiomyopathies via human heart tissue in a dish. In this review article, we highlight the use of patient-derived iPSCs for studying the pathogenesis underlying cardiomyopathies associated with metabolic perturbations and impaired mitochondrial bioenergetics, as the ability of iPSCs for self-renewal and differentiation makes them an ideal platform for investigating disease pathogenesis in a controlled in vitro environment. Continuing progress will help elucidate novel mechanistic pathways, and discover novel therapies for preventing the onset and progression of heart failure, thereby advancing a new era of personalized therapeutics for improving health outcomes in patients with cardiomyopathy., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email: journals.permissions@oup.com.)

Clinical manifestations of coronavirus disease 2019 (COVID-19) in pregnant women are diverse, and little is known of the impact of the disease on placental physiology. Severe acute respiratory syndrome coronavirus (SARS-CoV-2) has been detected in the human placenta, and its binding receptor ACE2 is present in a variety of placental cells, including endothelium. Here, we analyze the impact of COVID-19 in placental endothelium, studying by immunofluorescence the expression of von Willebrand factor (vWf), claudin-5, and vascular endothelial (VE) cadherin in the decidua and chorionic villi of placentas from women with mild and severe COVID-19 in comparison to healthy controls. Our results indicate that: (1) vWf expression increases in the endothelium of decidua and chorionic villi of placentas derived from women with COVID-19, being higher in severe cases; (2) Claudin-5 and VE-cadherin expression decrease in the decidua and chorionic villus of placentas from women with severe COVID-19 but not in those with mild disease. Placental histological analysis reveals thrombosis, infarcts, and vascular wall remodeling, confirming the deleterious effect of COVID-19 on placental vessels. Together, these results suggest that placentas from women with COVID-19 have a condition of leaky endothelium and thrombosis, which is sensitive to disease severity.

Thrombotic thrombocytopenic purpura (TTP) is an acute, life-threatening thrombotic microangiopathy (TMA) caused by acquired or congenital severe deficiency of ADAMTS13. Pregnancy is a recognized risk factor for precipitating acute (first or recurrent) episodes of TTP. Differential diagnosis with other TMAs is particularly difficult when the first TTP event occurs during pregnancy; a high index of suspicion and prompt recognition of TTP are essential for achieving a good maternal and fetal outcome. An accurate distinction between congenital and acquired cases of pregnancy-related TTP is mandatory for safe subsequent pregnancy planning. In this article, we summarize the current knowledge on pregnancy-associated TTP and describe how we manage TTP during pregnancy in our clinical practice., (© 2020 by The American Society of Hematology.)

One to 2 pregnant women in 1000 will experience venous thromboembolism (VTE) during pregnancy or postpartum. Pulmonary embolism (PE) is a leading cause of maternal mortality, and deep vein thrombosis leads to maternal morbidity, with postthrombotic syndrome potentially diminishing quality of life for a woman's lifetime. However, the evidence base for pregnancy-related VTE management remains weak. Evidence-based guideline recommendations are often extrapolated from nonpregnant women and thus weak or conditional, resulting in wide variation of practice. In women with suspected PE, the pregnancy-adapted YEARS algorithm is safe and efficient, rendering computed tomographic pulmonary angiography to rule out PE unnecessary in 39%. Low molecular weight heparin (LMWH) in therapeutic doses is the treatment of choice during pregnancy, and anticoagulation (LMWH or vitamin K antagonists [VKAs]) should be continued until 6 weeks after delivery, with a 3-month minimum total duration. LMWH or VKA use does not preclude breastfeeding. Postpartum, direct oral anticoagulants are an option if a woman does not breastfeed and long-term use is intended. Management of delivery, including type of analgesia, requires a multidisciplinary approach and depends on local preferences and patient-specific conditions. Several options are possible, including waiting for spontaneous delivery with temporary LMWH interruption. Prophylaxis for recurrent VTE prevention in subsequent pregnancies is indicated in most women with a history of VTE., (© 2020 by The American Society of Hematology.)

Pregnancy leads to adaptations for maternal and fetal energy needs. The cardiovascular system bears the brunt of the adaptations as the heart and vessels enable nutrient supply to maternal organs facilitated by the placenta to the fetus. The components of the cardiovascular system are critical in the balance between maternal homeostatic and fetus driven homeorhetic regulation. Since lipids intersect maternal cardiovascular function and fetal needs with growth and in stress, factors affecting lipid deposition and mobilization impact risk outcomes. Here, the cardiovascular components and functional derangements associated with cardiovascular pathology in pregnancy, vis-à-vis lipid deposition, mobilization and maternal and/or cardiac and fetal energy needs are detailed. Most reports on the components and associated pathology in pregnancy, are on derangements affecting the extracellular matrix and epicardial fat, followed by the endothelium, vascular smooth muscle, pericytes and myocytes. Targeted studies on all cardiovascular components and pathological outcomes in pregnancy will enhance targeted interventions., (Copyright © 2020 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Background: Chronic venous disease (CVD) is a prevalent lower limb venous pathology that especially affects women, who also show an increased risk of this disease during pregnancy. Studies have shown significant structural changes in the placentas of women with CVD and several markers of tissue damage have been also described. Patients and Methods: To try to understand the different placental pathologies, research efforts have focused on examining metabolomic profiles as indicators of the repercussions of these vascular disorders. This study examines changes produced in the metabolomic profiles of chorionic villi in the placentas of women with CVD. In a study population of 12 pregnant women, 6 with and 6 without CVD, we compared through mass spectroscopy coupled to ultra-high performance liquid chromatography (UHPLC-MS), 240 metabolites in chorionic villus samples. Results: This study is the first to detect in the placental villi of pregnant women with CVD, modifications in lysophosphatidylcholines and amino acids along with diminished levels of other lipids such as triglycerides, sphingomyelins, and non-esterified omega 9 fatty acids, suggesting a role of these abnormalities in the pathogenesis of CVD. Conclusions: Our findings are a starting point for future studies designed to examine the impacts of CVD on maternal and fetal well-being., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

Assessment of the plasma concentrations of natriuretic peptides (NPs) is widely used to diagnose and evaluate the progression of cardiac failure, and their potential as markers of preeclampsia (PE) has been examined in recent years. It has been established that plasma concentrations of NPs do not change in the course of normal pregnancy. However, elevated levels of these peptides may have a prognostic value in patients with PE. This study presents information about the relevance of NPs assessment in the evaluation of physiological pregnancy, as well as in pregnancy complicated with arterial hypertension. The most commonly examined NPs is the N-terminal fragment of the brain natriuretic peptide (NT-proBNP), and it may be prognostic marker of PE and other complications of pregnancy.

Background: Peripartum cardiomyopathy (PPCM) is life-threatening heart disease. However, the causes and pathogenesis of PPCM remain unclear. Previous studies found that β1 adrenoceptor antibodies (β1AA) had possible involvement in the development of PPCM. In the present study, we determined the potential relationship between PPCM and β1AA, including the mechanism of β1AA leading to PPCM., Methods: We extracted the β1AA from the postpartum Wistar rats that were injected by the antigen peptide segment of the β1 adrenoceptor to produce PPCM. We tested the effects of β1AA on H9C2 cell line by CCK-8, LDH, TUNEL, SA-ELISA, qRT-PCR, and western blot methods. Furthermore, PGC-1α was overexpressed to rescue the effect of β1AA on H9C2 cells., Results: We found that the extracted β1AA induced apoptosis of cardiac myocytes of H9C2 cell line. Moreover, the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), which is a master regulator of mitochondrial metabolism, and its downstream transcript vascular endothelial growth factor (VEGF) got decreased in H9C2 cells after β1AA treatment. In addition, the effect of β1AA could be inhibited by atenolol, the antagonist of β1 adrenoceptors (β1AR) and imitated by isoprenaline, the agonist of β1AR. Furthermore, overexpression of PGC-1α in the H9C2 cells rescued the apoptosis of cells and inhibitory expression of VEGF induced by β1AA., Conclusions: Our results suggest that the symptoms of PPCM due to myocardial cell apoptosis induced by β1AA inhibiting the PGC-1α-related pathway impairs mitochondrial energy metabolism. Therefore, our results uncover a previously unknown role of the β1AA pathway in the etiology of PPCM and provide a novel potential target for the treatment of PPCM.

As a common complication of pregnancy, gestational hypoxia has been shown to predispose offspring to vascular dysfunction. Propionate, one of short-chain fatty acids, exerts cardioprotective effects via reducing blood pressure. This study examined whether prenatal hypoxia impaired propionate-stimulated large-conductance Ca 2+ -activated K + (BK) channel activities in vascular smooth muscle cells (VSMCs) of offspring. Pregnant rats were exposed to hypoxia (10.5% oxygen) and normoxia (21% oxygen) from gestational day 7-21. At 6 weeks of age, VSMCs in mesenteric arteries of offspring were analysed for BK channel functions and gene expressions. It was shown firstly that propionate could open significantly BK single channel in VSMCs in a concentration-dependent manner. Antagonists of G protein βγ subunits and inositol trisphosphate receptor could completely suppress the activation of BK by propionate, respectively. Gα i/o and ryanodine receptor were found to participate in the stimulation on BK. Compared to the control, vasodilation and increments of BK NPo (the open probability) evoked by propionate were weakened in the offspring by prenatal hypoxia with down-regulated Gβγ and PLCβ. It was indicated that prenatal hypoxia inhibited propionate-stimulated BK activities in mesenteric VSMCs of offspring via reducing expressions of Gβγ and PLCβ, in which endoplasmic reticulum calcium release might be involved., (© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)

Background: Incidence rates of cardiomyopathies, which are a common cause of heart failure in young people, have increased during the last decades. An association between body weight in adolescence and future cardiomyopathy among men was recently identified. Whether or not this holds true also for women is unknown. The aim was therefore to determine whether for young women being overweight or obese is associated with a higher risk of developing cardiomyopathy., Methods: This was a registry-based national prospective cohort study with data collected from the Swedish Medical Birth Register, 1982 to 2014, with up to 33 years of follow-up. Included women were of childbearing age (18-45 years) during the initial antenatal visit in their first or second pregnancy (n=1 393 346). We obtained baseline data on body mass index (BMI), smoking, education, and previous disorders. After exclusions, mainly because of previous disorders, the final sample was composed of 1 388 571 women. Cardiomyopathy cases were identified by linking the Medical Birth Register to the National Patient and Cause of Death registers., Results: In total, we identified 1699 cases of cardiomyopathy (mean age at diagnosis, 46.2 [SD 9.1] years) during the follow-up with an incidence rate of 5.9 per 100 000 observation years. Of these, 481 were diagnosed with dilated cardiomyopathy, 246 had hypertrophic cardiomyopathy, 61 had alcohol/drug-induced cardiomyopathy, and 509 had other forms. The lowest risk for being diagnosed with a cardiomyopathy was detected at a BMI of 21 kg/m 2 , with a gradual increase in risk with higher BMI, particularly for dilated cardiomyopathy, where a hazard ratio of 4.71 (95% CI, 2.81-7.89) was found for severely obese subjects (BMI ≥35 kg/m 2 ), as compared with BMI 20 to <22.5., Conclusions: Elevated BMI among young women was associated with an increased risk of being diagnosed with a subsequent cardiomyopathy, especially dilated cardiomyopathy, starting already at mildly elevated body weight, whereas severe obesity entailed an almost 5-fold increase in risk. With the increasing numbers of persons who are overweight or obese, higher rates of cardiomyopathy can be expected in the future, along with an altered disease burden related to adiposity.

Objectives: Inferior vena cava syndrome (IVCS) is a heterogenous group of symptoms resulting in obstruction of the main vein inflow . Common reasons are thrombotic changes and tumors. Incidence of inferior vena cava (IVC) anomalies is 0.3% in general population. Iatrogenic IVC lesions caused by catheter insertion play increasing role. Treatment varies depending on the condition., Material and Methods: 32-year old patient was diagnosed with IVC stenosis during infertility related preconception evaluation and informed about increased risk in planned pregnancy. Throughout the well progressing pregnancy patient received low molecular weight heparin., Results: The diagnosis was confirmed intraoperatively during the planned cesarean section. Early postpartum period was normal and patient was discharged with antithrombotic prophylaxis., Conclusions: Isolated IVC stenosis in pregnancy has not been yet reported in medical literature. Even though IVC anomalies may be associated with other congenital changes, in this case the central venous line treatment in infancy seems to be the most likely cause. Malformations are often accidentally diagnosed because patients are usually asymptomatic. CT and MRI are recommended diagnostic tools. Conservative treatment is recommended for asymptomatic patients, as opposed to surgical treatment for symptomatic. However, due to condition's rarity, there is no evidence based approach management.

Objectives: This papers aims to investigate the association between different levels of postpartum weight retention (PPWR) and cardiometabolic risk among the Saudi women 12 months postpartum., Methods: This study is a follow-up of subgroup of cohort from Riyadh mother and baby multicenter cohort study. Clinical data were collected from participants 12 months after delivery and included current Body Mass Index (BMI), waist circumference, hip circumference, and blood pressure. In addition the following blood tests done were fasting blood glucose (FBG), glycosylated haemoglobin (HbA1c) levels, and lipids profile to assess the participants' cardiometabolic risks. The participants were categorized into three groups based on the level of PPWR: weight retention < 3kg; weight retention 3 to < 7kg; and weight retention ≥ 7kg. Subsequently, the prevalence of cardiometabolic risk factors was compared in the three groups to assess the association between different levels of PPWR and cardiometabolic risk factors. Logistic regression was used to test the effect of PPWR in the development of metabolic syndrome and Adjusted Odds Ratio (AOR) was calculated., Results: A total of 115 women participated in this study. Around 35% of the study population retained ≥ 7 kg of weight. The prevalence of cardiometabolic risk factors, including metabolic syndrome (MetS), increases with the increase of PPWR (p<0.01). The prevalence of MetS is 13% with highest frequency in the group with the highest weight retention. The determinants developing MetS were prepregnancy weight; AOR (95% CI); 1.08 (1.02-1.14), P< 0.01, current BMI, AOR (95% CI); 1.30 (1.12-1.51), P< 0.01, and FBG during pregnancy, AOR (95% CI); and 4.82 (1.72-13.48), P < 0.01., Conclusion: Increased weight retention after delivery augments the rate of occurrence of cardiometabolic risk factors. Determinants of the development of MetS in postpartum Saudi women are increased prepregnancy weight, current BMI, and FBG during pregnancy.

Objective: Women have been shown to have a higher risk of cerebral aneurysm formation, growth, and rupture than men. The authors present a review of the recently published neurosurgical literature that studies the role of pregnancy and female sex steroids, to provide a conceptual framework with which to understand the various risk factors associated with cerebral aneurysms in women at different stages in their lives., Methods: The PubMed database was searched for "("intracranial" OR "cerebral") AND "aneurysm" AND ("pregnancy" OR "estrogen" OR "progesterone")" between January 1980 and February 2019. A total of 392 articles were initially identified, and after applying inclusion and exclusion criteria, 20 papers were selected for review and analysis. These papers were then divided into two categories: 1) epidemiological studies about the formation, growth, rupture, and management of cerebral aneurysms in pregnancy; and 2) investigations on female sex steroids and cerebral aneurysms (animal studies and epidemiological studies)., Results: The 20 articles presented in this study include 7 epidemiological articles on pregnancy and cerebral aneurysms, 3 articles reporting case series of cerebral aneurysms treated by endovascular therapies in pregnancy, 3 epidemiological articles reporting the relationship between female sex steroids and cerebral aneurysms through retrospective case-control studies, and 7 experimental studies using animal and/or cell models to understand the relationship between female sex steroids and cerebral aneurysms. The studies in this review report similar risk of aneurysm rupture in pregnant women compared to the general population. Most ruptured aneurysms in pregnancy occur during the 3rd trimester, and most pregnant women who present with cerebral aneurysm have caesarean section deliveries. Endovascular treatment of cerebral aneurysms in pregnancy is shown to provide a new and safe form of therapy for these cases. Epidemiological studies of postmenopausal women show that estrogen hormone therapy and later age at menopause are associated with a lower risk of cerebral aneurysm than in matched controls. Experimental studies in animal models corroborate this epidemiological finding; estrogen deficiency causes endothelial dysfunction and inflammation, which may predispose to the formation and rupture of cerebral aneurysms, while exogenous estrogen treatment in this population may lower this risk., Conclusions: The aim of this work is to equip the neurosurgical and obstetrical/gynecological readership with the tools to better understand, critique, and apply findings from research on sex differences in cerebral aneurysms.

Background: Maternal hypertension, type 2 diabetes (T2D) and obesity are associated with an increased risk of having offspring with conotruncal heart defects (CTDs). Prior studies have identified sets of single nucleotide polymorphisms (SNPs) that are associated with risk for each of these three adult phenotypes. We hypothesized that these same SNPs are associated with maternal risk of CTDs in offspring., Methods and Results: We evaluated the parents of children with a CTD ascertained from the Children's Hospital of Philadelphia (n = 466) and by the Pediatric Cardiac Genomic Consortium (n = 255). We used a family-based design to assess the association between CTDs and the maternal genotype for individual hypertension, T2D, and obesity-related SNPs and found no association between CTDs and the maternal genotype for any individual SNP. In addition, we calculated genetic risk scores (GRS) for hypertension, T2D, and obesity using previously published GRS formulas. When comparing the GRS of mothers to fathers, there were no statistically significant differences in the mean for the combined GRS or the GRS for each individual condition. However, when we categorized the mothers and fathers of cases with CTDs as having high (>95th percentile) or low (≤95th percentile) scores, compared to fathers, mothers had almost two times the odds of having a high GRS for hypertension (OR 1.7, 95% CI 1.0, 2.8) and T2D (OR 1.8, 95% CI 1.1, 3.1)., Conclusions: Our results support a link between maternal genetic risk for hypertension/T2D and CTDs in their offspring. These associations might be independent of maternal phenotype at conception., Competing Interests: The authors have declared that no competing interests exist.

Women with Marfan syndrome (MFS) are at high risk for pregnancy-associated aortic dissection. Pathogenic models that singularly invoke hemodynamic stress are difficult to reconcile with predominant postnatal occurrence of aortic tear, often occurring weeks to months after delivery. In consideration of events that peak at term, are sustained after delivery, and might synergize with previously defined signaling pathways implicated in aneurysm progression, we examined the hormone oxytocin, which initiates uterine contraction and milk letdown for the duration of lactation through phosphorylation of extracellular signal-regulated kinase (ERK). In a mouse model of MFS that shows highly penetrant postnatal aortic dissection, risk was strongly attenuated by preventing lactation or use of an oxytocin receptor antagonist. Survival correlated inversely with the extent of ERK activation in the aortic wall, and strong protection was observed upon attenuation of ERK phosphorylation using an inhibitor of ERK kinase (MEK) or the U.S. Food and Drug Administration-approved medication hydralazine, offering potential therapeutic strategies for pregnancy-associated vascular catastrophe in the setting of MFS., (Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)

Aim: The present paper intends in the first place to clarify the confusing terminology for describing the vascular pathology of the placental bed in relation to long-term risk of cardiovascular disease., Methods: Systematic review of relevant topics., Results: The maternal blood supply to the placenta is achieved by some 100 utero-placental spiral arteries with an outside diameter varying between 200 and 600 microns. Defective physiological changes of the myometrial segment of utero-placental spiral arteries and, particularly in preeclampsia associated to hypertensive disease, the presence of atherosclerosis in their proximal segment are a cause of obstructive vascular pathology. On the other hand, basal arteries which supply the inner myometrium and basal decidua are not affected by physiological change and maintain their musculoelastic structure. They can be identified by their external diameter of less than 120 microns. Acute atherosis is an aspecific vascular lesion that occurs in basal as well as spiral arteries inside, as well as outside, the placental bed in association with a variety of obstetrical conditions., Conclusions: An increased risk of future cardiovascular disease, should be linked to atherosis or, at a later stage, atherosclerosis of utero-placental spiral arteries, rather than to that of decidual basal arteries.

The aim of our study was to quantify risk factors for venous thromboembolism (VTE) during the puerperal period. The case-control study was conducted in Women's Hospital, Zhejiang University, China, from January 2006 to December 2016; cases of hospitalized VTE within 1 week after delivery were identified according to International Classification of Diseases, Ninth Revision, Clinical Modification codes. Control postpartum women without VTE were randomly selected, matched on birth day, age, delivery mode, and number of fetus with 4:1 ratio. Clinical risk factors for postpartum VTE and coagulation parameters were analyzed. We found independent variables that were significantly related to postpartum VTE (all P < .05) in a binary logistic regression analysis included preeclampsia/eclampsia (odds ratio [OR], 2.89; 95% confidence interval [CI], 1.56-5.37) and postpartum hemorrhage (OR, 4.6; 95% CI, 1.71-12.40). D-dimer was the only biomarker that statistically significant associated with postpartum VTE in 3 days after delivery (all P < .05). These findings showed preeclampsia/eclampsia and postpartum hemorrhage were important risk factors for early VTE during puerperal period. A higher level of D-dimer was more meaningful than other coagulation parameters to suspect early thrombotic disease after delivery.

Marfan syndrome is a hereditary connective tissue disorder. The main cause of mortality in these patients is due to cardiovascular complications related to dilation of an aneurysm and dissection of the aortic root, a situation that increases their risk due to the physiological changes that occur during pregnancy, childbirth and puerperium. The case is presented of a pregnant woman with Marfan syndrome and aortic root dilatation of 42mm. The issues are discussed, such as the mode of delivery (vaginal delivery vs. caesarean section) depending on the aortic root diameter or the choice of type of anaesthesia (general vs. neuraxial) in these cases., (Copyright © 2018 Sociedad Española de Anestesiología, Reanimación y Terapéutica del Dolor. Publicado por Elsevier España, S.L.U. All rights reserved.)

Maternal lipid profiles during pregnancy are associated with risk for preterm birth. This study investigates the association between maternal dyslipidemia and subsequent preterm birth among pregnant women in the state of California. Births were identified from California birth certificate and hospital discharge records from 2007-2012 (N = 2,865,987). Preterm birth was defined as <37 weeks completed gestation and dyslipidemia was defined by diagnostic codes. Subtypes of preterm birth were classified as preterm premature rupture of membranes (PPROM), spontaneous labor, and medically indicated, according to birth certificate data and diagnostic codes. The association between dyslipidemia and preterm birth was tested with logistic regression. Models were adjusted for maternal age at delivery, race/ethnicity, hypertension, pre-pregnancy body mass index, insurance type, and education. Maternal dyslipidemia was significantly associated with increased odds of preterm birth (adjusted OR: 1.49, 95%CI: 1.39, 1.59). This finding was consistent across all subtypes of preterm birth, including PPROM (adjusted OR: 1.54, 95%CI: 1.34, 1.76), spontaneous (adjusted OR: 1.51, 95%CI: 1.39, 1.65), and medically indicated (adjusted OR: 1.454, 95%CI: 1.282, 1.649). This study suggests that maternal dyslipidemia is associated with increased risk for all types of preterm birth., Competing Interests: The authors have declared that no competing interests exist.

Background: Mesenteric venous thrombosis (MVT) is an infrequent thrombotic event that can cause devastating intestinal hemorrhagic ischemia. The mortality rate among patients with acute MVT ranges from 20 to 50%. Occurrence of MVT in pregnancy is quite rare. In this case report, we describe a pregnant woman who presented with acute MVT at 35 weeks of gestation., Case Presentation: Our case was a 26-year-old primigravid woman at 35 weeks gestation. She presented to Guangzhou First People's Hospital with complaints of abdominal pain, nausea and vomiting. The second day after admission, she complained of more intense abdominal pain, anorexia, vomiting and abdominal distention that were out of proportion to physical signs. An emergency exploratory laparotomy was performed. The entire ileum, part of the jejunum and part of the ascending colon were gangrenous, and thromboembolism was discovered in the corresponding mesenteric veins. The necrotic intestine was resected and an end-to-end jejunum-colon anastomosis was performed. A cesarean section was performed to remove the placenta and fetus, which had expired. Histopathological analysis revealed extensive edema, hemorrhage, inflammatory infiltration and necrosis in the resected bowel, and widespread thrombosis in mesenteric venous lumens., Conclusion: The diagnosis of MVT during pregnancy is very difficult due to its low incidence, and non-characteristic symptoms, signs and laboratory results. MVT may be the underlying cause of severe abdominal pain during pregnancy and should be included in the differential diagnosis of pregnant patients with an acute abdomen.

Pregnancy evokes many challenges on the maternal cardiovascular system that may unmask predispositions for future disease. This is particularly evident for women who develop pregnancy-related disorders, for example, pre-eclampsia and gestational diabetes or hypertension. Such pregnancy-related syndromes increase the risk for cardiovascular disease (CVD) postpartum. As a result, pregnancy has been termed as a cardiovascular stress test and an indicator or marker to predict the development of CVD later in life. In addition, pregnancy-related disorders impact the development of offspring also placing them at a higher risk for disease. Utilizing pregnancy as a physiological stressor, the current investigation sought to determine whether the cardiovascular system of offspring exposed to gestational hypertension in utero would respond adversely to the stress of pregnancy. Heterozygous atrial natriuretic peptide gene-disrupted (ANP +/- ) offspring were generated by either crossing male wildtype ANP +/+ with female knockout ANP -/- to produce ANP +/-KO mice or crossing female wildtype ANP +/+ with male knockout ANP -/- to produce ANP +/-WT mice. To study the cardiovascular stress induced by pregnancy, female ANP +/-WT and ANP +/-KO mice were mated with male wildtype ANP +/+ mice to initiate pregnancy. Cardiac size and molecular expression of the renin-angiotensin (RAS) and natriuretic peptide systems (NPS) were compared between offspring groups. Our data demonstrate that gestational hypertension and lack of maternal ANP did not significantly impact the progression and regression of pregnancy-induced cardiac hypertrophy over gestation and postpartum in ANP +/- offspring. Additionally, the molecular cardiac expression of the RAS and NPS did not differ between offspring groups. Future investigation should assess potential differences in cardiac function and the impact of fetal-programming on offspring cardiovascular adaptations during pregnancy in more severe models of pregnancy-related hypertensive syndrome such as angiotensin II or isoproterenol infusion.

Objective: To assess obstetric and aortic outcomes in women with Marfan Syndrome according to aortic root diameter, in view of recommendations for caesarean delivery when the aortic root diameter is ≥40 mm in the 2010 American guidelines versus >45 mm in the 2011 European guidelines., Study Design: In this retrospective cohort study conducted at Sainte-Justine Mother and Child Tertiary Hospital, 27 pregnancies in 20 women with Marfan Syndrome as defined by the international criteria, were followed prospectively between 1994 and 2017, after excluding women with prior aortic surgery. Obstetric and aortic outcomes were compared in 2 groups according to aortic root diameter: < 40 mm (21 pregnancies) and 40-45 mm (6 pregnancies)., Results: 21/27 women had a vaginal delivery. The caesarean section rate was 23.8% and 16.7% in women with diameter <40 mm and 40-45 mm respectively (p-value = 1), and perinatal outcome was similar across groups. Two women with a prepregnancy aortic root diameter <40 mm developed an acute type B dissection during the third trimester. Both had a family history of aortic dissection., Conclusions: Vaginal delivery with rigorous pain control and avoidance of Valsalva maneuver may be safely considered in women with Marfan Syndrome and an aortic root diameter ≤45 mm. The risk of type B aortic dissection during pregnancy is hard to predict. Other factors such as family history of dissection and descending aorta size may play an important role, and this may modify our counselling., (Copyright © 2018 Elsevier B.V. All rights reserved.)

The prevention and treatment of venous thromboembolism (VTE) poses distinct gender-specific challenges. Women of childbearing age are at an increased risk of VTE secondary to the transient risk factors of combined hormonal contraception (CHC) and pregnancy. Cancers specific to women are associated with a significant burden of VTE; whilst the incidence of VTE in localised breast cancer is 5 per 1000 person-years, more cases are seen due to the prevalence of breast cancer. Treatment of VTE in women can be complicated by abnormal uterine bleeding, now increasingly reported with direct oral anticoagulants (DOACs) as well as vitamin K antagonists. Divergence between international guidelines regarding the use of CHC following an oestrogen-associated VTE and appropriate withdrawal of such contraception requires clarification for clinicians. Additionally, there is uncertainty as to whether to consider such events provoked or unprovoked and, consequently, the optimal duration of treatment in these women remains unclear. During pregnancy and the puerperium, the traditional anticoagulants remain the agents of choice with no further advances in DOAC safety data, and similarly in lactation. Further studies evaluating the safety and optimal treatment strategies in these women are awaited., (© 2018 British Society for Haematology and John Wiley & Sons Ltd.)

A 32-year-old pregnant woman, diagnosed with Behçet's disease 6 months earlier, presented with recent mild hemoptysis and exertional dyspnea. Transthoracic echocardiography showed an enlarged dysfunctional right ventricle. A large hypoechoic triangular-shaped mass was seen attached to the inner right ventricular wall, filling the cavity. No change in the size of the mass was noted after anticoagulant administration, and right heart failure progressed. Surgery was performed to remove the mass and repair the tricuspid valve. This was a very rare presentation of Behçet's disease in pregnancy, which resulted in delivery of a completely healthy baby despite corticosteroid pulse therapy and cyclophosphamide.

Background: Peripartum cardiomyopathy is a life-threatening condition that occurs during the peripartum period in previously healthy women. Cardiovascular magnetic resonance (CMR) T1 mapping permits sensitive detection of tissue edema and fibrosis, and it may be useful in identifying altered myocardial tissue characteristics in peripartum cardiomyopathy. However, left ventricular (LV) volumes and mass increase considerably even in normal pregnancy, and it is not known whether altered tissue characteristics can be found in normal pregnancy. The aim of this study was to investigate whether the LV remodeling observed in normal pregnancy is associated with altered tissue characteristics determined by CMR., Methods: Twelve normal pregnant women and 15 non pregnant women underwent cine CMR and myocardial T1 measurement at 1.5 T. Pregnant women were scanned three times, in the 2nd and 3rd trimesters of pregnancy and at 1 month postpartum. LV volumes, LV mass (LVM), and global longitudinal strain (GLS) were analyzed by cine CMR. Native myocardial T1 was determined using modified Look-Locker inversion recovery (MOLLI) images., Results: LV end-diastolic volume (EDV) was significantly greater in the 3rd trimester (126 ± 22 mL) than in non-pregnant women (108 ± 14 mL, p < 0.05). LVM was significantly greater in the 3rd trimester (88.7 ± 11.8 g) than at 1 month postpartum (70.0 ± 9.8 g, p < 0.05) and in non-pregnant women (66.3 ± 13.9 g, p < 0.05). Myocardial native T1 among the 2nd and 3rd trimesters, 1 month postpartum, and non-pregnant women were similar (1133 ± 55 ms, 1138 ± 86 ms, 1105 ± 45 ms, and 1129 ± 52 ms, respectively, p = 0.59) as were GLS (- 19.5 ± 1.8, - 19.7% ± 2.2, - 19.0% ± 2.0%, and - 19.3% ± 1.9%, respectively, p = 0.66)., Conclusions: LV remodeling during normal pregnancy is associated with myocardial hypertrophy, but not with edema or diffuse fibrosis of the myocardium or LV contractile dysfunction. These results observed in normal pregnancy will serve as an important basis for identifying myocardial abnormalities in patients with peripartum cardiomyopathy and other pregnancy-related myocardial diseases.

Objective: Because the management of cerebral aneurysms during pregnancy remains controversial, the objective of this study was to perform a retrospective review of pregnant women with cerebral aneurysms to determine whether pregnancy is a risk factor for aneurysm rupture., Methods: The change in size of aneurysms during pregnancy was examined by performing repeat magnetic resonance angiography in five pregnant women with cerebral aneurysms between 2005 and 2013. The outcome examined was development of subarachnoid hemorrhage., Results: Among the five pregnancies, there were eight cerebral aneurysms. Subarachnoid hemorrhage did not developed during any pregnancy. In four of the pregnancies, the cerebral aneurysms did not change in size during pregnancy, remaining 2-5 mm. Although in one pregnancy, the aneurysm increased from 6 to 7 mm during the third trimester, it returned to its original size in the postpartum period., Conclusions: We suggest that if the cerebral aneurysm is small (≤ 5 mm), it is likely to remain unchanged despite the increase in circulating blood volume during pregnancy. Cerebral aneurysms greater than 5 mm but without blebs, irregular shape, high-risk location, or increased aspect ratio are also at low risk of rupture and are not likely to change during pregnancy.

Objective: To carry out a retrospective study of the clinical features of patients with intrauterine hematoma in the second and third trimesters, and discuss the risk factors for poor pregnancy outcomes., Methods: A total of 398 patients who underwent routine examination in our hospital from January 2011 to December 2015 were classified into normal pregnancy (NP) group (N = 265) and adverse pregnancy (AP) group (N = 133), according to their pregnancy outcomes. Maternal clinical demographics, gestational age, location of hematoma, volume of hematoma, and accompanying contraction and vaginal bleeding were recorded., Results: The average age of pregnant women in the NP and AP groups was 28.25 ± 4.06 and 29.5 ± 5.06 years, respectively (p = 0.007). Gestational age at first detection of hematoma was 15.11 ± 5.13 weeks in the NP group compared with 21.22 ± 8.25 weeks in the AP group (p < 0.001). In the AP group, the incidence of retroplacental hematoma (54.1%) and palpable contractions (62.8%) was significantly higher than in the NP group (25.7% and 12.1%, respectively; p < 0.01). However, similar maternal parity or history of delivery, volume of hematoma and incidence of vaginal bleeding were found., Conclusion: Intrauterine hematoma in the second and third trimesters is a sign of pathological pregnancy, resulting in adverse outcomes. Maternal age, gestational age at first diagnosis, location of hematoma and accompanying contraction are risk factors for poor pregnancy outcomes.

Obesity has reached epidemic proportions and is a well-recognised risk factor for venous thromboembolism (VTE). This article summarises the current understanding of obesity and debates how obesity induces this increased risk of VTE. Obesity is associated with prothrombotic changes which have been well-characterised and include increased levels of plasminogen activator-1, von Willebrand factor, fibrinogen and evidence of increased coagulation and platelet activation; however, these changes do not seem to account for all the increased risk. Accumulating evidence suggests a significant role for increased tissue factor expression and signalling in this relationship, with increased tissue factor expression present in adipose and possibly systemic tissues, induced by adipose generated cytokines. Lastly, there is a strong suggestion that decreased venous flow due to venous enlargement may play the major role in increased VTE risk with obesity., (© 2017 Elsevier Ltd. All rights reserved.)

Background: Failure of physiologic transformation of spiral arteries has been reported in preeclampsia, fetal growth restriction, fetal death, and spontaneous preterm labor with intact or ruptured membranes. Spiral arteries with failure of physiologic transformation are prone to develop atherosclerotic-like lesions of atherosis. There are striking parallels between preeclampsia and atherosclerotic disease, and between lesions of atherosis and atherosclerosis. Endothelial activation, identified by intercellular adhesion molecule-1 expression, is present in atherosclerotic-like lesions of heart transplantation, and is considered a manifestation of rejection. Similarly, endothelial activation/dysfunction has been implicated in the pathophysiology of atherosclerosis and preeclampsia. Intercellular adhesion molecule-1-overexpressing-activated endothelial cells are more resistant to trophoblast displacement than nonactivated endothelium, and may contribute to shallow spiral artery trophoblastic invasion in obstetrical syndromes having failure of physiologic transformation., Objective: We sought to determine whether failure of spiral artery physiologic transformation was associated with activation of interstitial extravillous trophoblasts and/or spiral artery endothelium and presence of acute atherosis in the placental basal plate., Study Design: A cross-sectional study of 123 placentas (19-42 weeks' gestation) obtained from normal pregnancies (n = 22), preterm prelabor rupture of membranes (n = 26), preterm labor (n = 23), preeclampsia (n = 27), intrauterine fetal death (n = 15), and small for gestational age (n = 10) was performed. Failure of spiral artery physiologic transformation and presence of cell activation was determined using immunohistochemistry of placental basal plates containing a median of 4 (minimum: 1; maximum: 9) vessels per placenta. Endothelial/trophoblast cell activation was defined by the expression of intercellular adhesion molecule-1. Investigators examining microscopic sections were blinded to clinical diagnosis. Pairwise comparisons among placenta groups were performed with Fisher exact test and Wilcoxon rank sum test using a Bonferroni-adjusted level of significance (.025)., Results: We found that 87% (94/108) of placentas having spiral arteries with failure of physiologic transformation (actin-positive and cytokeratin-negative) in the basal plate, and 0% (0/15) of placentas having only spiral arteries with complete physiologic transformation (cytokeratin-positive and actin-negative), had arterial endothelial and/or interstitial extravillous trophoblasts reactive with the intercellular adhesion molecule-1 activation marker (P < .001). A significant correlation (R 2  = 0.84) was found between expression of spiral artery endothelial and interstitial extravillous trophoblast intercellular adhesion molecule-1 (P < .001) in activated placentas. Lesions of atherosis were found in 31.9% (30/94) of placentas with complete and/or partial failure of physiologic transformation of spiral arteries that were intercellular adhesion molecule-1-positive, in none of the 14 placentas with failure of physiologic transformation that were intercellular adhesion molecule-1-negative, and in none of the 15 placentas with complete spiral artery physiologic transformation without failure (P = .001). All placentas (30/30, 100%) with atherosis were identified in placentas having concomitant spiral artery endothelial and interstitial extravillous trophoblast activation., Conclusion: Failure of spiral artery physiologic transformation in the placental basal plate is associated with interstitial extravillous trophoblast and arterial endothelial activation along with increased frequency of spiral artery atherosis. These findings may be used to improve the characterization of different disorders of the placental bed such as in refining the existing tools for the early prediction of risk for preterm, preeclamptic, and other abnormal pregnancies., (Copyright © 2016 Elsevier Inc. All rights reserved.)

We present results of the histopathological workup of a prosthetic aortic valve which was explanted from a 31-year-old woman due to valve thrombosis during early pregnancy. Our images demonstrate nicely thrombotic material directly adherent to the pyrolytic carbon surface in a human specimen., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Activation of the coagulation and inflammatory systems are physiologically occurring during pregnancy. However, excess activation of either system is well documented in gestational vascular diseases (GVD). GVD are placenta-mediated pregnancy complications and a major cause of feto-maternal morbidity and mortality. The causal relevance of excess coagulation and inflammatory responses for GVD remains largely unknown. Deciphering the causal relationship of excess coagulation and inflammation in GVD may allow conceptualizing new therapeutic approaches to combat GVD. Platelet activation and procoagulant extracellular vesicles (EVs) provide a link between coagulation and inflammation and their activation or generation in GVD is well established. As recently shown EVs cause sterile placental inflammation by activating maternal platelets that release ATP and activate purinergic receptor signaling and NLRP3 inflammasome in the embryonic trophoblast. This thrombo-inflammatory mechanism suggests a novel link between coagulation activation and sterile inflammation in GVD. These findings highlight a role of anti-platelet therapies in GVD. In addition, targeting the inflammasome alone or in combination with platelet inhibition may provide a new therapeutic strategy in GVD., (© 2017 Elsevier Ltd. All rights reserved.)

Peripartum cardiomyopathy (PPCM) refers to irreversible cardiomyocyte damage that occurs during the last month of pregnancy, or within 5 months after giving birth. It is characterized by systolic heart failure. This life-threatening condition is relatively uncommon, but the incidence has been climbing up. Because of its high mortality, it is crucial for physicians to have high suspicious for the disease. Studies have been done to search into specific lab test and treatment for PPCM. Therapies like anti-viral, anti-inflammatory and immunosuppression regimen have been explored. New regimen like exosomes has also been explored and revealed promising effects.

The markers of endothelium dysfunction and factors of inflammation in pregnant women with hypertension with hypertension disorders of various genesis were analyzed. The clinical laboratory study was carried out on the basis of sampling of 158 women at pregnancy period of22-3 7 weeks. Out of this sampling 30 women had previously present chronic arterial hypertension, 3 0 women had chronic arterial hypertension and consecutive preeclampsia, 43 women had preeclampsia and 55 women had uncomplicated course of pregnancy without hypertension disorders (control group). It is established that in pregnant women with hypertension disorders of various genesis endothelial dysfunction and inflammation are developed/ This occurrence is confirmed by increasing of in blood of number of circulating desquamated endotheliocytes, C-reactive protein and homocystein in all groups; by increasing of serum level of t-PA, endothelin (1-21), MMP-2, sVCAM-1 and IL-6 under preeclampsia, including one consecutive to chronic arterial hypertension; by increasing of content of IL-6 in blood serum under chronic arterial hypertension with consecutive preeclampsia. The criteria are developed concerning serum content of t-PA, sVCAM-1, endothelin (1-21) and MMP-2 permitting to diagnose differentially previously present hypertension and preeclampsia, including consecutive one to chronic arterial hypertension.