Sflt-1 in heart failure: relation with disease severity and biomarkers

Gruson, Damien; Hermans, Michel P.; Ferracin, Benjamin; Ahn, Sylvie A.; Rousseau, Michel F.

doi:10.1080/00365513.2016.1190863

Cited by 18 publications

(12 citation statements)

References 29 publications

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“…sFlt-1 is linked to cardiovascular remodeling and was demonstrated to be elevated in patients with heart failure. Additionally, it was suggested as a potential biomarker of cardiovascular risk [ 41 ]. Similar facts have been established for sEng, as it is considered as a reliable candidate for an indicator of hypertension, hypercholesterolemia, endothelial dysfunction and cardiovascular risk [ 42 , 43 ].…”

Section: The Association Between Preeclampsia Pathogenesis and Cardiomentioning

confidence: 99%

Preeclampsia and Related Cardiovascular Risk: Common Genetic Background

2018

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Purpose of ReviewPreeclampsia (PE) is a hypertensive disorder exclusive for pregnancy. It affects women all over the world and poses a great threat to life, both for mother and child. No definitive treatment exists and placenta delivery comprises the only known cure for PE. One of the most severe complications observed in preeclamptic women is the occurrence of cardiovascular diseases (CVDs) later in life.Recent FindingsBoth PE and CVDs share some of their pathogenic pathways and gene variations. Thus far, a number of publications have examined those relationships; however, almost all of them focus only on common risk factors. The precise pathomechanism and genetic basis of PE and its associated cardiovascular complications remain unknown.SummaryTherefore, the aim of this review is to unify and clarify the current state of knowledge and provide direction for future studies, especially those regarding the genetic aspect.

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Section: The Association Between Preeclampsia Pathogenesis and Cardiomentioning

confidence: 99%

Preeclampsia and Related Cardiovascular Risk: Common Genetic Background

2018

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“…Furthermore, sFlt-1 exacerbated mitochondrial reactive oxygen species formation and mitochondrial membrane potential dissipation [45]. As the increased circulatory level of sFlt-1 is associated with cardiovascular complications, such as chronic heart failure [46,47], we sought to investigate whether HO-1 and sFlt-1 play a role in the regulation of cardiac mitochondrial activity using a well-established model of high sFlt-1 environment by the tail-vein injection of adenovirus sFlt-1 in Hmox1 +/− mice. We further tested whether a hydrogen sulfide-releasing molecule, MZe786, could rescue sFlt-1-induced mitochondrial dysfunction in the heart of Hmox1 −/− mice.…”

Section: Introductionmentioning

confidence: 99%

MZe786 Rescues Cardiac Mitochondrial Activity in High sFlt-1 and Low HO-1 Environment

et al. 2020

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Hypertensive disorder in pregnancy is a major cause of maternal and perinatal mortality worldwide. Women who have had preeclampsia are at three to four times higher risk in later life of developing high blood pressure and heart disease. Soluble Flt-1 (sFlt-1) is elevated in preeclampsia and may remain high postpartum in women with a history of preeclampsia. Heme oxygenase-1 (Hmox1/HO-1) exerts protective effects against oxidative stimuli and is compromised in the placenta of pregnant women with preeclampsia. We hypothesized that sFlt-1 inhibits cardiac mitochondrial activity in HO-1 deficient mice. HO-1 haplo-insufficient mice (Hmox1+/−) were injected with adenovirus encoding sFlt-1 (Ad-sFlt-1) or control virus (Ad-CMV). Subsequently, they were treated daily with either placebo or MZe786 for six days, when the heart tissue was harvested to assess cardiac mitochondrial activity. Here, we show that the loss of HO-1 disturbed cardiac mitochondrial respiration and reduced mitochondrial biogenesis. The overexpression of sFlt-1 resulted in the inhibition of the cardiac mitochondrial activity in Hmox1+/− mice. The present study demonstrates that the hydrogen sulfide (H2S) releasing molecule, MZe786, rescues mitochondrial activity by stimulating cardiac mitochondrial biogenesis and antioxidant defense in Hmox1−/− mice and in Hmox1+/− mice exposed to a high sFlt-1 environment.

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“…Furthermore, given that the ratio of serum soluble fms-like tyrosine kinase 1 to placental growth factor has recently been validated as a biochemical predictor of pre-eclampsia, 26 it too can be evaluated as a marker of persistent endothelial dysfunction and risk of cardiovascular disease after pregnancy. 27 28 Regardless, we need better data about whether prenatal biochemical screening offers additive information over that provided by conventional cardiovascular disease risk factors and adverse events in pregnancy, 4 5 6 7 8 such as the maternal placental syndromes or preterm delivery. One approach might be an analysis of risk reclassification, assessing the proportion of women whose level of risk changes if the values of prenatal screening are added to a list of conventional risk factors.…”

Section: Discussionmentioning

confidence: 99%

Prenatal biochemical screening and long term risk of maternal cardiovascular disease: population based cohort study

Ray

Huang

Meschino

et al. 2018

BMJ

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ObjectiveTo examine whether abnormal prenatal biochemical screening results are associated with an increased risk of premature cardiovascular disease after pregnancy.DesignPopulation based cohort study.SettingThe entire province of Ontario, Canada, where healthcare is universally available.ParticipantsWomen aged 12-55 years, without pre-existing cardiovascular disease, who underwent prenatal screening between 1993 and 2011. One pregnancy per woman was randomly selected.ExposuresLow (≤5th centile multiple of the median) serum total chorionic gonadotropin, unconjugated estriol, and pregnancy associated plasma protein A and high (≥95th centile multiple of the median) alphafetoprotein and dimeric inhibin-A.Main outcome measuresComposite of hospital admission or revascularisation for coronary artery, cerebrovascular, or peripheral arterial disease or hospital admission for heart failure or dysrhythmia at least 365 days after pregnancy.ResultsAmong 855 536 pregnancies, and after a median of 11.4 (interquartile range 6.8-17.5) years of follow-up, 6209 women developed the main cardiovascular disease outcome. Abnormal results for each of the five prenatal biochemical screening analytes, especially dimeric inhibin-A, were associated with a higher risk of cardiovascular disease. Women with an abnormally high dimeric inhibin-A (≥95th centile) had the highest rate of cardiovascular disease (30 events or 8.3 per 10 000 person years versus 251 events or 3.8 per 10 000 person years for those <95th centile; multivariable adjusted hazard ratio 2.0, 95% confidence interval 1.4 to 3.0). Compared with women without any abnormal biochemical measure, the hazard ratio for the cardiovascular disease composite outcome was 1.2-1.3 times higher with one abnormal analyte and 1.5-2.0 times higher with two or more abnormal analytes.ConclusionsWomen with abnormal prenatal biochemical screening results, especially for dimeric inhibin-A, may be at higher risk of cardiovascular disease. If these findings are replicated elsewhere, a massive amount of data exists that could aid in identifying women at higher risk of premature cardiovascular disease and that could be conveyed to them or their healthcare providers.

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Sflt-1 in heart failure: relation with disease severity and biomarkers

Cited by 18 publications

References 29 publications

Preeclampsia and Related Cardiovascular Risk: Common Genetic Background

Preeclampsia and Related Cardiovascular Risk: Common Genetic Background

MZe786 Rescues Cardiac Mitochondrial Activity in High sFlt-1 and Low HO-1 Environment

Prenatal biochemical screening and long term risk of maternal cardiovascular disease: population based cohort study

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