Cardiac failure caused by severe pre‐eclampsia with placental abruption, and its treatment with anti‐hypertensive drugs

Aoyama, Kazufumi; Suzuki, Yukiko; Satô, Takeshi; Yamamoto, Taro; Kojima, Kazuhisa; Usami, Takeshi; Ohte, Nobuyuki; Suzumori, Kaoru

doi:10.1046/j.1341-8076.2003.00125.x

Cited by 13 publications

(8 citation statements)

References 6 publications

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“…Local generation of thrombin would be expected to be far greater in "preeclamptic" decidua, given the high incidence of underlying decidual hemorrhage as manifested by hemosiderin deposition as an indicator of occult bleeding, 23 intrauterine hematoma formation, 24 and the overt hemorrhage of abruption. 25,26 Thus, Salafia and colleagues 23 evaluated 462 consecutive placentas of patients delivered at Ͻ32 weeks' gestation compared with 108 consecutive term placentas for evidence of prior decidual hemorrhage as manifested by hemosiderin deposition in the decidua basalis. Decidual hemosiderin was significantly more common in patients with preterm preeclampsia (45/76, 60%) compared with term controls (1/108, 0.8%).…”

Section: Discussionmentioning

confidence: 99%

“…18 The effects of tumor necrosis factor-␣ (TNF␣) and interleukin-1␤ (IL-1␤) were assessed on sFlt-1 expression, since these proinflammatory cytokines are implicated in the early pathogenesis of preeclampsia including inhibition of trophoblast invasion of the decidua. 19 -22 Preeclampsia is also associated with underlying decidual hemorrhage, [23][24][25][26] which generates thrombin when circulating factor VII binds to decidual cell-expressed tissue factor. 27,28 Therefore, the effects of this hemostatic factor were also evaluated on sFlt-1 expression in the decidual cell monolayers.…”

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confidence: 99%

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Thrombin Regulates Soluble fms-Like Tyrosine Kinase-1 (sFlt-1) Expression in First Trimester Decidua

Lockwood

Toti

Arcuri

et al. 2007

The American Journal of Pathology

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The primary placental defect in preeclampsia is shallow trophoblast invasion of the decidua leading to incomplete vascular transformation and inadequate uteroplacental perfusion. Soluble fms-like tyrosine kinase-1 (sFlt-1) seems to interfere with these events by inhibiting local angiogenesis and/or by impeding trophoblast invasion. Preeclampsia is also associated with maternal thrombophilias and decidual hemorrhage, which form thrombin from decidual cell-expressed tissue factor. Although sFlt-1 is highly expressed by trophoblasts, sFlt-1 expression has not been studied in decidual cells, which are the predominant cell type encountered by invading trophoblasts. Here, we demonstrate that isolated decidual cells express sFlt-1 mRNA, suggesting that they can synthesize sFlt-1. Moreover, in first trimester decidual cells, thrombin enhanced sFlt-1 mRNA levels, as measured by quantitative reverse transcriptase-polymerase chain reaction, and levels of secreted sFlt-1 protein, as measured by enzyme-linked immunosorbent assay. The thrombin antagonist hirudin blocked this effect, demonstrating that active thrombin is required. Emphasizing the specificity of the thrombin response, neither interleukin-1beta nor tumor necrosis factor-alpha affected sFlt-1 expression in the decidual cells. In contrast to first trimester decidual cells, thrombin did not affect sFlt-1 levels in cultured term decidual cells. In early pregnancy, thrombin may act as an autocrine/paracrine enhancer of sFlt-1 expression by decidual cells to promote pre-eclampsia by interfering with local vascular transformation.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Thrombin Regulates Soluble fms-Like Tyrosine Kinase-1 (sFlt-1) Expression in First Trimester Decidua

Lockwood

Toti

Arcuri

et al. 2007

The American Journal of Pathology

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“…In vitro studies indicate that macrophage-derived tumor necrosis factor (TNF) a inhibits cytotrophoblast invasion by causing them to undergo apoptosis 31 and by inducing expression of plasminogen activator inhibitor-1 to inhibit urokinase-type plasminogen activator mediated protease activity at the leading edge of trophoblast invasion. 32 A significant subset of P-EC cases are associated with underlying decidual hemorrhage (abruption) [33][34][35] and potentially maternal thrombophilias (reviewed in Sibai et al 27 ). These conditions generate excess thrombin when circulating FVII binds to decidual cell-expressed TF as indicated by augmented circulating levels of the thrombin-antithrombin complex.…”

Section: Thrombin and Inflammatory Cytokines May Inhibit Decidual Extmentioning

confidence: 99%

Decidual Hemostasis, Inflammation, and Angiogenesis in Pre-Eclampsia

Lockwood

Huang²,

Krikun³

et al. 2011

Semin Thromb Hemost

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Invasion of the decidua by extravascular trophoblasts (EVTs) is accompanied by thrombin generation from decidual cell (DC) -expressed tissue factor (TF). This TF protects against hemorrhage as EVTs breach capillaries and subsequently invade and remodel spiral arteries and arterioles. Pre-eclampsia (P-EC) is the world’s leading cause of fetal and maternal morbidity and mortality. It is associated with decidual hemorrhage and maternal thrombophilias, which form excess thrombin from DCs, and with maternal infections and other inflammatory conditions that are associated with excess expression of the pro-inflammatory cytokines, interleukin-1 beta (IL-1b) and tumor necrosis factor –alpha (TNF-a). In human first trimester leukocyte-free DCs: 1) thrombin enhances expression of soluble fms-like tyrosine kinase-1 (sFlt-1), a potent inhibitor of angiogenesis; 2) thrombin, IL-1b and TNF-a increase monocyte-recruiting chemokine expression leqading to a macrophage excess in the pre-eclamptic decidua. The pathogenesis of P-EC likely stems from shallow EVT invasion leading to impaired decidual vascular remodeling. The resulting reduced uteroplacental blood flow is associated with a hypoxic placenta, which appears to secrete excess sFlt-1 into the maternal plasma. A regulatory role for DCs in vascular remodeling is indicated since impaired decidual vascular remodeling could stem from an aberrant local anti-angiogenic milieu elicited by excess sFlt-1 and/or macrophage inhibited EVT decidual invasion.

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“…Peripartum cardiomyopathy (PPCM) and hypertensive disorders of pregnancy (HDP) are two major cardiovascular complications of pregnancy and have been reported to share a common underlying pathophysiology in animal studies(9-11). PPCM is characterized by the sudden onset of maternal heart failure presenting either in the last month of pregnancy or in the first five months postpartum.…”

Section: Introductionmentioning

confidence: 99%

Peripartum cardiomyopathy and hypertensive disorders of pregnancy and cardiovascular events among 1.6 million California pregnancies

Arnaout

Nah

Marcus

et al. 2018

Preprint

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1Background-Cardiovascular complications during and soon after pregnancy present an 2 opportunity to assess risk for subsequent cardiovascular disease. We sought to determine 3 whether peripartum cardiomyopathy and hypertensive disorder of pregnancy subtypes predict 4 future myocardial infarction, heart failure, or stroke independent of one another and independent 5 of other risks like gestational diabetes, preterm birth, and intrauterine growth restriction. 6Methods and Results-The California Healthcare Cost and Utilization Project database was 7 used to identify all hospitalized pregnancies from 2005-2009, with follow-up through 2011, for a 8 retrospective cohort study. Pregnancies, exposures, covariates and outcomes were defined by 9 ICD-9 codes. Among 1.6 million pregnancies (mean age 28y; median follow-up time to event 10 2.7y), 558 cases of peripartum cardiomyopathy, 123,603 cases of hypertensive disorders of 11 pregnancy, 107,636 cases of gestational diabetes, 116,768 preterm births, and 23,504 cases of 12 intrauterine growth restriction were observed. Using multivariable Cox proportional hazards 13 models, peripartum cardiomyopathy was independently associated with a 13.0-fold increase in 14 myocardial infarction [95%CI, 4.1-40.9], a 39.2-fold increase in heart failure [95%CI, 30.0-15 51.9], and a 7.7-fold increase in stroke [95%CI, 2.4-24.0]. Hypertensive disorders of pregnancy 16 were associated with a 1.4 [95%CI, 1.0-2.0] to 7.6 [95%CI, 5.4-10.7] fold higher risk of 17 myocardial infarction, heart failure, and stroke. Gestational diabetes, preterm birth, and 18 intrauterine growth restriction had more modest associations with CVD. 19Conclusions-These findings support close monitoring of women with cardiovascular 20 pregnancy complications for prevention of early subsequent cardiovascular events and further 21 study of mechanisms underlying their development.Key Words: peripartum cardiomyopathy, hypertensive disorders of pregnancy, cardiovascular 1 disease, women 2

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Cardiac failure caused by severe pre‐eclampsia with placental abruption, and its treatment with anti‐hypertensive drugs

Cited by 13 publications

References 6 publications

Thrombin Regulates Soluble fms-Like Tyrosine Kinase-1 (sFlt-1) Expression in First Trimester Decidua

Thrombin Regulates Soluble fms-Like Tyrosine Kinase-1 (sFlt-1) Expression in First Trimester Decidua

Decidual Hemostasis, Inflammation, and Angiogenesis in Pre-Eclampsia

Peripartum cardiomyopathy and hypertensive disorders of pregnancy and cardiovascular events among 1.6 million California pregnancies

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