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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
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We are analyzing https://link.springer.com/article/10.1007/s00395-020-0782-6.

Title:
Action of iron chelator on intramyocardial hemorrhage and cardiac remodeling following acute myocardial infarction | Basic Research in Cardiology
Description:
Intramyocardial hemorrhage is an independent predictor of adverse outcomes in ST-segment elevation myocardial infarction (STEMI). Iron deposition resulting from ischemia–reperfusion injury (I/R) is pro-inflammatory and has been associated with adverse remodeling. The role of iron chelation in hemorrhagic acute myocardial infarction (AMI) has never been explored. The purpose of this study was to investigate the cardioprotection offered by the iron-chelating agent deferiprone (DFP) in a porcine AMI model by evaluating hemorrhage neutralization and subsequent cardiac remodeling. Two groups of animals underwent a reperfused AMI procedure: control and DFP treated (N = 7 each). A comprehensive MRI examination was performed in healthy state and up to week 4 post-AMI, followed by histological assessment. Infarct size was not significantly different between the two groups; however, the DFP group demonstrated earlier resolution of hemorrhage (by T2* imaging) and edema (by T2 imaging). Additionally, ventricular enlargement and myocardial hypertrophy (wall thickness and mass) were significantly smaller with DFP, suggesting reduced adverse remodeling, compared to control. The histologic results were consistent with the MRI findings. To date, there is no effective targeted therapy for reperfusion hemorrhage. Our proof-of-concept study is the first to identify hemorrhage-derived iron as a therapeutic target in I/R and exploit the cardioprotective properties of an iron-chelating drug candidate in the setting of AMI. Iron chelation could potentially serve as an adjunctive therapy in hemorrhagic AMI.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Non-Profit & Charity

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

The income method remains a mystery to us.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Link.springer.com might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

pubmed, article, google, scholar, myocardial, cas, infarction, central, iron, imaging, acute, hemorrhage, cardiovasc, heart, injury, ghugre, reperfusion, magnetic, coronary, circulation, resonance, microvascular, remodeling, circ, cardiac, wood, infarct, obstruction, med, res, research, patients, intramyocardial, wright, ami, study, deferiprone, magn, reson, toronto, chelation, ventricular, therapy, cardiovascular, left, cardiol, adverse, mri, size, access,

Topics {✒️}

high-dose iron-chelator therapy month download article/chapter st-elevation-myocardial infarction identify hemorrhage-derived iron high-molecular-weight molecules intracerebral convection-enhanced delivery cardiac ischemia-reperfusion injury hsv color space–simplecolordetectionbyhue post-myocardial-infarction setting iron-chelating drug candidate myocardial ischaemia-reperfusion injury cd11/cd18 integrin receptor assess post-infarct myocardium article basic research article behrouzi ugt1a6 genotype-related pharmacokinetics hemorrhage promotes inflammation iron-chelating agent deferiprone ischemia–reperfusion injury ischemia-reperfusion injury full article pdf iron chelation therapy extracellular collagen matrix vivo validation sunnybrook research institute benjamin ej iron-chelating therapy acute myocardial infarction lugo-olivieri ch author information authors ghugre nr cardiovascular magnetic resonance myocardial reperfusion injury reperfused ami procedure week 4 post-ami magnetic resonance imaging privacy choices/manage cookies garcia-dorado subacute myocardial infarction myocardial infarction culminates previous myocardial infarction percutaneous coronary intervention left ventricular remodeling investigators halt-mi stroke statistics-2017 update stroke statistics–2012 update related subjects practical medical applications myocardial infarct size residual myocardial iron

Questions {❓}

  • Dharmakumar R (2016) “Rusty hearts”: is it time to rethink iron chelation therapies in post-myocardial-infarction setting?
  • Heusch P, Nensa F, Heusch G (2015) Is MRI really the gold standard for the quantification of salvage from myocardial infarction?
  • Hinder M, Yi BA, Langenickel TH (2018) Developing drugs for heart failure with reduced ejection fraction: what have we learned from clinical trials?
  • Jugdutt BI (2003) Ventricular remodeling after infarction and the extracellular collagen matrix: when is enough enough?

Schema {🗺️}

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         headline:Action of iron chelator on intramyocardial hemorrhage and cardiac remodeling following acute myocardial infarction
         description:Intramyocardial hemorrhage is an independent predictor of adverse outcomes in ST-segment elevation myocardial infarction (STEMI). Iron deposition resulting from ischemia–reperfusion injury (I/R) is pro-inflammatory and has been associated with adverse remodeling. The role of iron chelation in hemorrhagic acute myocardial infarction (AMI) has never been explored. The purpose of this study was to investigate the cardioprotection offered by the iron-chelating agent deferiprone (DFP) in a porcine AMI model by evaluating hemorrhage neutralization and subsequent cardiac remodeling. Two groups of animals underwent a reperfused AMI procedure: control and DFP treated (N = 7 each). A comprehensive MRI examination was performed in healthy state and up to week 4 post-AMI, followed by histological assessment. Infarct size was not significantly different between the two groups; however, the DFP group demonstrated earlier resolution of hemorrhage (by T2* imaging) and edema (by T2 imaging). Additionally, ventricular enlargement and myocardial hypertrophy (wall thickness and mass) were significantly smaller with DFP, suggesting reduced adverse remodeling, compared to control. The histologic results were consistent with the MRI findings. To date, there is no effective targeted therapy for reperfusion hemorrhage. Our proof-of-concept study is the first to identify hemorrhage-derived iron as a therapeutic target in I/R and exploit the cardioprotective properties of an iron-chelating drug candidate in the setting of AMI. Iron chelation could potentially serve as an adjunctive therapy in hemorrhagic AMI.
         datePublished:2020-03-05T00:00:00Z
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      headline:Action of iron chelator on intramyocardial hemorrhage and cardiac remodeling following acute myocardial infarction
      description:Intramyocardial hemorrhage is an independent predictor of adverse outcomes in ST-segment elevation myocardial infarction (STEMI). Iron deposition resulting from ischemia–reperfusion injury (I/R) is pro-inflammatory and has been associated with adverse remodeling. The role of iron chelation in hemorrhagic acute myocardial infarction (AMI) has never been explored. The purpose of this study was to investigate the cardioprotection offered by the iron-chelating agent deferiprone (DFP) in a porcine AMI model by evaluating hemorrhage neutralization and subsequent cardiac remodeling. Two groups of animals underwent a reperfused AMI procedure: control and DFP treated (N = 7 each). A comprehensive MRI examination was performed in healthy state and up to week 4 post-AMI, followed by histological assessment. Infarct size was not significantly different between the two groups; however, the DFP group demonstrated earlier resolution of hemorrhage (by T2* imaging) and edema (by T2 imaging). Additionally, ventricular enlargement and myocardial hypertrophy (wall thickness and mass) were significantly smaller with DFP, suggesting reduced adverse remodeling, compared to control. The histologic results were consistent with the MRI findings. To date, there is no effective targeted therapy for reperfusion hemorrhage. Our proof-of-concept study is the first to identify hemorrhage-derived iron as a therapeutic target in I/R and exploit the cardioprotective properties of an iron-chelating drug candidate in the setting of AMI. Iron chelation could potentially serve as an adjunctive therapy in hemorrhagic AMI.
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         Myocardial infarction
         Iron chelation
         Hemorrhage
         Inflammation
         Ischemia–reperfusion injury
         Myocardial remodeling
         Cardiology
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                     name:Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Canada
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            name:John C. Wood
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               name:ApoPharma Inc, Toronto, Canada
               type:PostalAddress
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            name:ApoPharma Inc
            address:
               name:ApoPharma Inc, Toronto, Canada
               type:PostalAddress
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            name:ApoPharma Inc
            address:
               name:ApoPharma Inc, Toronto, Canada
               type:PostalAddress
            type:Organization
            name:University of Toronto
            address:
               name:Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Canada
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               name:Schulich Heart Program, Sunnybrook Health Sciences Centre, Toronto, Canada
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            name:University of Toronto
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               name:Department of Medical Biophysics, University of Toronto, Toronto, Canada
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      email:[email protected]
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      name:Physical Sciences Platform, Sunnybrook Research Institute, Toronto, Canada
      name:Physical Sciences Platform, Sunnybrook Research Institute, Toronto, Canada
      name:Physical Sciences Platform, Sunnybrook Research Institute, Toronto, Canada
      name:ApoPharma Inc, Toronto, Canada
      name:ApoPharma Inc, Toronto, Canada
      name:ApoPharma Inc, Toronto, Canada
      name:ApoPharma Inc, Toronto, Canada
      name:Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Canada
      name:Childrens Hospital Los Angeles, University of Southern California, Los Angeles, USA
      name:Schulich Heart Program, Sunnybrook Health Sciences Centre, Toronto, Canada
      name:Physical Sciences Platform, Sunnybrook Research Institute, Toronto, Canada
      name:Schulich Heart Program, Sunnybrook Health Sciences Centre, Toronto, Canada
      name:Department of Medical Biophysics, University of Toronto, Toronto, Canada
      name:Physical Sciences Platform, Sunnybrook Research Institute, Toronto, Canada
      name:Schulich Heart Program, Sunnybrook Health Sciences Centre, Toronto, Canada
      name:Department of Medical Biophysics, University of Toronto, Toronto, Canada
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