Clinical characterization and outcomes of preeclampsia with normal angiogenic profile

Rana, Sarosh; Schnettler, William T.; Powe, Camille E.; Wenger, Julia; Salahuddin, Saira; Cerdeira, Ana Sofia; Verlohren, Stefan; Perschel, F. H.; Arany, Zoltàn; Lim, Kee-Hak; Thadhani, Ravi; Karumanchi, S. Ananth

doi:10.3109/10641955.2013.784788

Cited by 142 publications

(114 citation statements)

References 33 publications

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“…The observation of low and high PlGF levels 56) and, similarly a high sFlt-1/PlGF ratio ≥ 85 (angiogenic preeclampsia) and a low sFlt-1/PlGF ratio < 85 (nonangiogenic preeclampsia), 57) across pregnancy among women who develop preeclampsia may be an important finding in relation to the pathophysiology and study of preeclampsia. Perhaps these different patterns of PlGF indicate that half of the preeclampsia cases result from insufficient angiogenic signaling (low PlGF), whereas the other half result from insensitivity to angiogenic signaling (high PlGF) or are determined by a different pathogenic factor.…”

Section: R E T R a C T E Dmentioning

confidence: 99%

Retraction: Etiopathology of preeclampsia — Recent progress from the perspective of a poor/ischemic placenta

Hidaka¹,

Nakamoto

2014

Hypertens Res Pregnancy

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Section: R E T R a C T E Dmentioning

confidence: 99%

Retraction: Etiopathology of preeclampsia — Recent progress from the perspective of a poor/ischemic placenta

Hidaka¹,

Nakamoto

2014

Hypertens Res Pregnancy

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“…8,[11][12][13][14][15][16] Few adverse outcomes occur in the absence of angiogenic factor abnormalities. 17,18 Although previous studies have detected changes in myocardial function in HDP, 19,20 a direct association between preeclampsia biomarkers, including sFlt1 and sEng, has not been described. In other abnormal cardiovascular states such as congestive heart failure, increased circulating levels of antiangiogenic proteins have been associated with development of endothelial vascular dysfunction, myocardial dysfunction, and adverse cardiovascular outcomes.…”

mentioning

confidence: 97%

Circulating Antiangiogenic Factors and Myocardial Dysfunction in Hypertensive Disorders of Pregnancy

et al. 2016

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H ypertensive disorders of pregnancy (HDP) affect 5% to 10% of pregnant women, 1 are the most common medical complication of pregnancy in developed countries, 2 and are a leading cause of maternal and fetal death worldwide. 3 HDP include preeclampsia, gestational hypertension, chronic hypertension, and superimposed preeclampsia. Preeclampsia targets the vascular endothelium causing widespread maternal vascular endothelial dysfunction. Antiangiogenic proteins have been implicated as being pathogenic in the development of the observed vascular endothelial dysfunction. 4Overexpression of soluble fms-like tyrosine kinase-1 (sFlt1), an endogenous vascular endothelial growth factor inhibitor, is associated with preeclampsia-like phenotypes in a rodent model and symptoms diminish with the addition of vascular endothelial growth factor or placental growth factor. [5][6][7] Multiple human clinical studies have established that levels of the sFlt1 and soluble endoglin (sEng) increase in the circulation of pregnant women with preeclampsia. 4,6,[8][9][10] sFlt1 and sEng levels are elevated weeks before the clinical onset of preeclampsia, and the degree of elevation correlates with adverse maternal and fetal outcomes. 8,[11][12][13][14][15][16] Few adverse outcomes occur in the absence of angiogenic factor abnormalities. 17,18 Although previous studies have detected changes in myocardial function in HDP, 19,20 a direct association between preeclampsia biomarkers, including sFlt1 and sEng, has not been described. In other abnormal cardiovascular states such as congestive heart failure, increased circulating levels of antiangiogenic proteins have been associated with development of endothelial vascular dysfunction, myocardial dysfunction, and adverse cardiovascular outcomes. 21Women with HDP have abnormalities in both systolic and diastolic cardiac function that seem before clinical symptoms.19,22 Despite preservation of left ventricular ejection fraction (LVEF), 23 longitudinal muscle fiber shortening is decreased, suggesting the presence of subclinical left ventricular systolic dysfunction. 20 This finding suggests a Abstract-Hypertensive disorders of pregnancy (HDP) are associated with subclinical changes in cardiac function. Although the mechanism underlying this finding is unknown, elevated levels of soluble antiangiogenic proteins such as soluble fms-like tyrosine kinase-1 (sFlt1) and soluble endoglin (sEng) are associated with myocardial dysfunction and may play a role. We hypothesized that these antiangiogenic proteins may contribute to the development of cardiac dysfunction in HDP. We prospectively studied 207 pregnant women with HDP and nonhypertensive controls and evaluated whether changes in global longitudinal strain (GLS) observed on echocardiography is specific for HDP and whether these changes correlate with HDP biomarkers, sFlt1 and sEng. A total of 62 (30%) patients were diagnosed with preeclampsia (group A), 105 (51%) did not have an HDP (group B), and 40 (19%) were diagnosed with chronic or gestational hype...

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“…Verlohren et al (2012) also assessed the value of serum sFlt-1/PlGF as prognostic markers, showing an increased risk of imminent delivery in preeclamptic women with high sFlt-1/PLGF ratios. In addition, Rana et al (2013) showed that women diagnosed with preeclampsia, but with a normal plasma angiogenic profile, are not at risk for adverse maternal or fetal outcomes. Chappell et al (2013) formance of plasma PlGF alone for prediction of delivery for preeclampsia within 14 d in women at ,35 wk with suspected preeclampsia.…”

Section: Angiogenic Factors As Biomarkersmentioning

confidence: 99%

Molecular Mechanisms of Preeclampsia

Cerdeira

2015

Cold Spring Harb Perspect Med

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Preeclampsia is a pregnancy-specific disease characterized by new onset hypertension and proteinuria after 20 wk of gestation. It is a leading cause of maternal and fetal morbidity and mortality worldwide. Exciting discoveries in the last decade have contributed to a better understanding of the molecular basis of this disease. Epidemiological, experimental, and therapeutic studies from several laboratories have provided compelling evidence that an antiangiogenic state owing to alterations in circulating angiogenic factors leads to preeclampsia. In this review, we highlight the role of key circulating antiangiogenic factors as pathogenic biomarkers and in the development of novel therapies for preeclampsia.

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Clinical characterization and outcomes of preeclampsia with normal angiogenic profile

Cited by 142 publications

References 33 publications

Retraction: Etiopathology of preeclampsia — Recent progress from the perspective of a poor/ischemic placenta

Retraction: Etiopathology of preeclampsia — Recent progress from the perspective of a poor/ischemic placenta

Circulating Antiangiogenic Factors and Myocardial Dysfunction in Hypertensive Disorders of Pregnancy

Molecular Mechanisms of Preeclampsia

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