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  1. Article: Coronary Microvascular Function Following Severe Preeclampsia.

    Honigberg, Michael C / Economy, Katherine E / Pabón, Maria A / Wang, Xiaowen / Castro, Claire / Brown, Jenifer M / Divakaran, Sanjay / Weber, Brittany N / Barrett, Leanne / Perillo, Anna / Sun, Anina Y / Antoine, Tajmara / Farrohi, Faranak / Docktor, Brenda / Lau, Emily S / Yeh, Doreen DeFaria / Natarajan, Pradeep / Sarma, Amy A / Weisbrod, Robert M /
    Hamburg, Naomi M / Ho, Jennifer E / Roh, Jason D / Wood, Malissa J / Scott, Nandita S / Carli, Marcelo F Di

    medRxiv : the preprint server for health sciences

    2024  

    Abstract: Background: Preeclampsia is a pregnancy-specific hypertensive disorder associated with an imbalance in circulating pro- and anti-angiogenic proteins. Preclinical evidence implicates microvascular dysfunction as a potential mediator of preeclampsia- ... ...

    Abstract Background: Preeclampsia is a pregnancy-specific hypertensive disorder associated with an imbalance in circulating pro- and anti-angiogenic proteins. Preclinical evidence implicates microvascular dysfunction as a potential mediator of preeclampsia-associated cardiovascular risk.
    Methods: Women with singleton pregnancies complicated by severe antepartum-onset preeclampsia and a comparator group with normotensive deliveries underwent cardiac positron emission tomography (PET) within 4 weeks of delivery. A control group of pre-menopausal, non-postpartum women was also included. Myocardial flow reserve (MFR), myocardial blood flow (MBF), and coronary vascular resistance (CVR) were compared across groups. Soluble fms-like tyrosine kinase receptor-1 (sFlt-1) and placental growth factor (PlGF) were measured at imaging.
    Results: The primary cohort included 19 women with severe preeclampsia (imaged at a mean 16.0 days postpartum), 5 with normotensive pregnancy (mean 14.4 days postpartum), and 13 non-postpartum female controls. Preeclampsia was associated with lower MFR (
    Conclusions: In this exploratory study, we observed reduced coronary microvascular function in the early postpartum period following severe preeclampsia, suggesting that systemic microvascular dysfunction in preeclampsia involves the coronary microcirculation. Further research is needed to establish interventions to mitigate risk of preeclampsia-associated cardiovascular disease.
    Language English
    Publishing date 2024-03-05
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.03.04.24303728
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Coronary Microvascular Function Following Severe Preeclampsia.

    Honigberg, Michael C / Economy, Katherine E / Pabón, Maria A / Wang, Xiaowen / Castro, Claire / Brown, Jenifer M / Divakaran, Sanjay / Weber, Brittany N / Barrett, Leanne / Perillo, Anna / Sun, Anina Y / Antoine, Tajmara / Farrohi, Faranak / Docktor, Brenda / Lau, Emily S / DeFaria Yeh, Doreen / Natarajan, Pradeep / Sarma, Amy A / Weisbrod, Robert M /
    Hamburg, Naomi M / Ho, Jennifer E / Roh, Jason D / Wood, Malissa J / Scott, Nandita S / Di Carli, Marcelo F

    Hypertension (Dallas, Tex. : 1979)

    2024  

    Abstract: Background: Preeclampsia is a pregnancy-specific hypertensive disorder associated with an imbalance in circulating proangiogenic and antiangiogenic proteins. Preclinical evidence implicates microvascular dysfunction as a potential mediator of ... ...

    Abstract Background: Preeclampsia is a pregnancy-specific hypertensive disorder associated with an imbalance in circulating proangiogenic and antiangiogenic proteins. Preclinical evidence implicates microvascular dysfunction as a potential mediator of preeclampsia-associated cardiovascular risk.
    Methods: Women with singleton pregnancies complicated by severe antepartum-onset preeclampsia and a comparator group with normotensive deliveries underwent cardiac positron emission tomography within 4 weeks of delivery. A control group of premenopausal, nonpostpartum women was also included. Myocardial flow reserve, myocardial blood flow, and coronary vascular resistance were compared across groups. sFlt-1 (soluble fms-like tyrosine kinase receptor-1) and PlGF (placental growth factor) were measured at imaging.
    Results: The primary cohort included 19 women with severe preeclampsia (imaged at a mean of 15.3 days postpartum), 5 with normotensive pregnancy (mean, 14.4 days postpartum), and 13 nonpostpartum female controls. Preeclampsia was associated with lower myocardial flow reserve (β, -0.67 [95% CI, -1.21 to -0.13];
    Conclusions: In this exploratory cross-sectional study, we observed reduced coronary microvascular function in the early postpartum period following preeclampsia, suggesting that systemic microvascular dysfunction in preeclampsia involves coronary microcirculation. Further research is needed to establish interventions to mitigate the risk of preeclampsia-associated cardiovascular disease.
    Language English
    Publishing date 2024-04-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.124.22905
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1488: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  3. Article ; Online: Subtle abnormalities in contractile function are an early manifestation of sarcomere mutations in dilated cardiomyopathy.

    Lakdawala, Neal K / Thune, Jens J / Colan, Steven D / Cirino, Allison L / Farrohi, Faranak / Rivero, Jose / McDonough, Barbara / Sparks, Elizabeth / Orav, E J / Seidman, J G / Seidman, Christine E / Ho, Carolyn Y

    Circulation. Cardiovascular genetics

    2012  Volume 5, Issue 5, Page(s) 503–510

    Abstract: Background: Sarcomere mutations cause both dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM); however, the steps leading from mutation to disease are not well described. By studying mutation carriers before a clinical diagnosis develops, ...

    Abstract Background: Sarcomere mutations cause both dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM); however, the steps leading from mutation to disease are not well described. By studying mutation carriers before a clinical diagnosis develops, we characterize the early manifestations of sarcomere mutations in DCM and investigate how these manifestations differ from sarcomere mutations associated with HCM.
    Methods and results: Sixty-two genotyped individuals in families with sarcomeric DCM underwent clinical evaluation including strain echocardiography. The group included 12 subclinical DCM mutation carriers with normal cardiac dimensions and left ventricular ejection fraction (LVEF ≥55%), 21 overt DCM subjects, and 29 related mutation (-) normal controls. Results were compared with a previously characterized cohort of 60 subclinical HCM subjects (sarcomere mutation carriers without left ventricular hypertrophy). Systolic myocardial tissue velocity, longitudinal, circumferential, and radial strain, and longitudinal and radial strain rate were reduced by 10%-23% in subclinical DCM mutation carriers compared with controls (P<0.001 for all comparisons), after adjusting for age and family relations. No significant differences in diastolic parameters were identified comparing the subclinical and control cohorts. The opposite pattern of contractile abnormalities with reduced diastolic but preserved systolic function was seen in subclinical HCM.
    Conclusions: Subtle abnormalities in systolic function are present in subclinical DCM mutation carriers, despite normal left ventricular size and ejection fraction. In contrast, impaired relaxation and preserved systolic function appear to be the predominant early manifestations of sarcomere mutations that lead to HCM. These findings support the theory that the mutation's intrinsic impact on sarcomere function influences whether a dilated or hypertrophic phenotype develops.
    MeSH term(s) Adolescent ; Adult ; Aged ; Cardiomyopathy, Dilated/genetics ; Cardiomyopathy, Dilated/physiopathology ; Cardiomyopathy, Hypertrophic/genetics ; Cardiomyopathy, Hypertrophic/physiopathology ; Child ; Child, Preschool ; Cohort Studies ; Echocardiography ; Female ; Genotype ; Heart Rate/physiology ; Humans ; Male ; Middle Aged ; Myocardial Contraction/physiology ; Phenotype ; Sarcomeres/genetics ; Sarcomeres/physiology ; Ventricular Function, Left/physiology ; Young Adult
    Language English
    Publishing date 2012-09-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2477394-3
    ISSN 1942-3268 ; 1942-325X
    ISSN (online) 1942-3268
    ISSN 1942-325X
    DOI 10.1161/CIRCGENETICS.112.962761
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6731: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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  4. Article ; Online: Echocardiographic strain imaging to assess early and late consequences of sarcomere mutations in hypertrophic cardiomyopathy.

    Ho, Carolyn Y / Carlsen, Christian / Thune, Jens Jakob / Havndrup, Ole / Bundgaard, Henning / Farrohi, Faranak / Rivero, Jose / Cirino, Allison L / Andersen, Paal Skytt / Christiansen, Michael / Maron, Barry J / Orav, E John / Køber, Lars

    Circulation. Cardiovascular genetics

    2009  Volume 2, Issue 4, Page(s) 314–321

    Abstract: Background: Genetic testing identifies sarcomere mutation carriers (G+) before clinical diagnosis of hypertrophic cardiomyopathy (HCM), allowing characterization of initial disease manifestations. Previous studies demonstrated that impaired relaxation ... ...

    Abstract Background: Genetic testing identifies sarcomere mutation carriers (G+) before clinical diagnosis of hypertrophic cardiomyopathy (HCM), allowing characterization of initial disease manifestations. Previous studies demonstrated that impaired relaxation develops before left ventricular hypertrophy (LVH). The precise impact of sarcomere mutations on systolic function in early and late disease is unclear.
    Methods and results: Comprehensive echocardiography with strain imaging was performed on 146 genotyped individuals with mutations in 5 sarcomere genes. Contractile parameters were compared in 68 preclinical (G+/LVH-), 40 overt (G+/LVH+) subjects with HCM, and 38 mutation (-) normal control relatives. All subjects had normal left ventricular ejection fraction. In preclinical HCM, global and regional peak systolic strain (epsilon(sys)) and longitudinal systolic strain rate were not significantly different from controls, but early diastolic mitral annular velocity (Ea) was reduced by 13%. In overt HCM, there was a significant 27% and 14% decrease in global longitudinal epsilon(sys) and systolic strain rate, respectively, compared with both preclinical HCM and controls (P<0.013 for all comparisons), and a 33% reduction in Ea.
    Conclusions: Sarcomere mutations have disparate initial effects on diastolic and systolic functions. Preclinical HCM is characterized by impaired relaxation but preserved systolic strain. In contrast, both diastolic and longitudinal systolic abnormalities are present in overt disease despite normal ejection fraction. We propose that diastolic dysfunction is an early consequence of sarcomere mutations, whereas systolic dysfunction results from mutations combined with subsequent pathological remodeling. Identifying mechanistic pathways triggered by these mutations may begin to reshape the clinical paradigm for treatment, based on early diagnosis and disease prevention.
    MeSH term(s) Adolescent ; Adult ; Aged ; Cardiomyopathy, Hypertrophic/diagnostic imaging ; Cardiomyopathy, Hypertrophic/genetics ; Carrier Proteins/genetics ; Child ; Cohort Studies ; Diastole ; Echocardiography, Doppler ; Female ; Genotype ; Humans ; Hypertrophy, Left Ventricular/diagnostic imaging ; Hypertrophy, Left Ventricular/genetics ; Male ; Middle Aged ; Mutation ; Sarcomeres/genetics ; Systole ; Tropomyosin/genetics ; Troponin I/genetics ; Troponin T/genetics ; Ventricular Myosins/genetics
    Chemical Substances Carrier Proteins ; TNNT2 protein, human ; Tropomyosin ; Troponin I ; Troponin T ; myosin-binding protein C ; Ventricular Myosins (EC 3.6.1.-)
    Language English
    Publishing date 2009-06-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2477394-3
    ISSN 1942-3268 ; 1942-325X
    ISSN (online) 1942-3268
    ISSN 1942-325X
    DOI 10.1161/CIRCGENETICS.109.862128
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6731: Show issues Location:
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