The effect of iron deficiency on cardiac resynchronization therapy: results from the RIDE‐CRT Study

Abstract Aims Cardiac resynchronization therapy (CRT) improves functional status, induces reverse left ventricular remodelling, and reduces hospitalization and mortality in patients with symptomatic heart failure, left ventricular systolic dysfunction, and QRS prolongation. However, the impact of ir...

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Main Authors: Philipp Lacour, Phi Long Dang, Daniel Armando Morris, Abdul Shokor Parwani, Wolfram Doehner, Franziska Schuessler, Felix Hohendanner, Frank R. Heinzel, Andrea Stroux, Carsten Tschoepe, Wilhelm Haverkamp, Leif‐Hendrik Boldt, Burkert Pieske, Florian Blaschke
Format: Article
Language:English
Published: Wiley 2020-06-01
Series:ESC Heart Failure
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Online Access:https://doi.org/10.1002/ehf2.12675
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author Philipp Lacour
Phi Long Dang
Daniel Armando Morris
Abdul Shokor Parwani
Wolfram Doehner
Franziska Schuessler
Felix Hohendanner
Frank R. Heinzel
Andrea Stroux
Carsten Tschoepe
Wilhelm Haverkamp
Leif‐Hendrik Boldt
Burkert Pieske
Florian Blaschke
author_facet Philipp Lacour
Phi Long Dang
Daniel Armando Morris
Abdul Shokor Parwani
Wolfram Doehner
Franziska Schuessler
Felix Hohendanner
Frank R. Heinzel
Andrea Stroux
Carsten Tschoepe
Wilhelm Haverkamp
Leif‐Hendrik Boldt
Burkert Pieske
Florian Blaschke
author_sort Philipp Lacour
collection DOAJ
description Abstract Aims Cardiac resynchronization therapy (CRT) improves functional status, induces reverse left ventricular remodelling, and reduces hospitalization and mortality in patients with symptomatic heart failure, left ventricular systolic dysfunction, and QRS prolongation. However, the impact of iron deficiency on CRT response remains largely unclear. The purpose of the study was to assess the effect of functional and absolute iron deficiency on reverse cardiac remodelling, clinical response, and outcome after CRT implantation. Methods and results The relation of iron deficiency and cardiac resynchronization therapy response (RIDE‐CRT) study is a prospective observational study. We enrolled 77 consecutive CRT recipients (mean age 71.3 ± 10.2 years) with short‐term follow‐up of 3.3 ± 1.9 months and long‐term follow‐up of 13.0 ± 3.2 months. Primary endpoints were reverse cardiac remodelling on echocardiography and clinical CRT response, assessed by change in New York Heart Association classification. Echocardiographic CRT response was defined as relative improvement of left ventricular ejection fraction ≥ 20% or left ventricular global longitudinal strain ≥ 20%. Secondary endpoints were hospitalization for heart failure and all‐cause mortality (mean follow‐up of 29.0 ± 8.4 months). At multivariate analysis, iron deficiency was identified as independent predictor of echocardiographic (hazard ratio 4.97; 95% confidence interval 1.15–21.51; P = 0.03) and clinical non‐response to CRT (hazard ratio 4.79; 95% confidence interval 1.30–17.72, P = 0.02). We found a significant linear‐by‐linear association between CRT response and type of iron deficiency (P = 0.004 for left ventricular ejection fraction improvement, P = 0.02 for left ventricular global longitudinal strain improvement, and P = 0.003 for New York Heart Association response). Iron deficiency was also significantly associated with an increase in all‐cause mortality (P = 0.045) but not with heart failure hospitalization. Conclusions Iron deficiency is a negative predictor of effective CRT therapy as assessed by reverse cardiac remodelling and clinical response. Assessment of iron substitution might be a relevant treatment target to increase CRT response and outcome in chronic heart failure patients.
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spelling doaj.art-4131d89ce4b9477a841eb24c3e453b992022-12-21T20:08:50ZengWileyESC Heart Failure2055-58222020-06-01731072108410.1002/ehf2.12675The effect of iron deficiency on cardiac resynchronization therapy: results from the RIDE‐CRT StudyPhilipp Lacour0Phi Long Dang1Daniel Armando Morris2Abdul Shokor Parwani3Wolfram Doehner4Franziska Schuessler5Felix Hohendanner6Frank R. Heinzel7Andrea Stroux8Carsten Tschoepe9Wilhelm Haverkamp10Leif‐Hendrik Boldt11Burkert Pieske12Florian Blaschke13Department of Cardiology Charité—Universitaetsmedizin Berlin, Campus Virchow‐Klinikum Augustenburger Platz 1 Berlin 13353 GermanyDepartment of Cardiology Charité—Universitaetsmedizin Berlin, Campus Virchow‐Klinikum Augustenburger Platz 1 Berlin 13353 GermanyDepartment of Cardiology Charité—Universitaetsmedizin Berlin, Campus Virchow‐Klinikum Augustenburger Platz 1 Berlin 13353 GermanyDepartment of Cardiology Charité—Universitaetsmedizin Berlin, Campus Virchow‐Klinikum Augustenburger Platz 1 Berlin 13353 GermanyDepartment of Cardiology Charité—Universitaetsmedizin Berlin, Campus Virchow‐Klinikum Augustenburger Platz 1 Berlin 13353 GermanyDepartment of Cardiology Charité—Universitaetsmedizin Berlin, Campus Virchow‐Klinikum Augustenburger Platz 1 Berlin 13353 GermanyDepartment of Cardiology Charité—Universitaetsmedizin Berlin, Campus Virchow‐Klinikum Augustenburger Platz 1 Berlin 13353 GermanyDepartment of Cardiology Charité—Universitaetsmedizin Berlin, Campus Virchow‐Klinikum Augustenburger Platz 1 Berlin 13353 GermanyInstitute of Biometry and Clinical Epidemiology Charité—Universitätsmedizin Berlin, Campus Benjamin Franklin Hindenburgdamm 30 Berlin 12203 GermanyDepartment of Cardiology Charité—Universitaetsmedizin Berlin, Campus Virchow‐Klinikum Augustenburger Platz 1 Berlin 13353 GermanyDepartment of Cardiology Charité—Universitaetsmedizin Berlin, Campus Virchow‐Klinikum Augustenburger Platz 1 Berlin 13353 GermanyDepartment of Cardiology Charité—Universitaetsmedizin Berlin, Campus Virchow‐Klinikum Augustenburger Platz 1 Berlin 13353 GermanyDepartment of Cardiology Charité—Universitaetsmedizin Berlin, Campus Virchow‐Klinikum Augustenburger Platz 1 Berlin 13353 GermanyDepartment of Cardiology Charité—Universitaetsmedizin Berlin, Campus Virchow‐Klinikum Augustenburger Platz 1 Berlin 13353 GermanyAbstract Aims Cardiac resynchronization therapy (CRT) improves functional status, induces reverse left ventricular remodelling, and reduces hospitalization and mortality in patients with symptomatic heart failure, left ventricular systolic dysfunction, and QRS prolongation. However, the impact of iron deficiency on CRT response remains largely unclear. The purpose of the study was to assess the effect of functional and absolute iron deficiency on reverse cardiac remodelling, clinical response, and outcome after CRT implantation. Methods and results The relation of iron deficiency and cardiac resynchronization therapy response (RIDE‐CRT) study is a prospective observational study. We enrolled 77 consecutive CRT recipients (mean age 71.3 ± 10.2 years) with short‐term follow‐up of 3.3 ± 1.9 months and long‐term follow‐up of 13.0 ± 3.2 months. Primary endpoints were reverse cardiac remodelling on echocardiography and clinical CRT response, assessed by change in New York Heart Association classification. Echocardiographic CRT response was defined as relative improvement of left ventricular ejection fraction ≥ 20% or left ventricular global longitudinal strain ≥ 20%. Secondary endpoints were hospitalization for heart failure and all‐cause mortality (mean follow‐up of 29.0 ± 8.4 months). At multivariate analysis, iron deficiency was identified as independent predictor of echocardiographic (hazard ratio 4.97; 95% confidence interval 1.15–21.51; P = 0.03) and clinical non‐response to CRT (hazard ratio 4.79; 95% confidence interval 1.30–17.72, P = 0.02). We found a significant linear‐by‐linear association between CRT response and type of iron deficiency (P = 0.004 for left ventricular ejection fraction improvement, P = 0.02 for left ventricular global longitudinal strain improvement, and P = 0.003 for New York Heart Association response). Iron deficiency was also significantly associated with an increase in all‐cause mortality (P = 0.045) but not with heart failure hospitalization. Conclusions Iron deficiency is a negative predictor of effective CRT therapy as assessed by reverse cardiac remodelling and clinical response. Assessment of iron substitution might be a relevant treatment target to increase CRT response and outcome in chronic heart failure patients.https://doi.org/10.1002/ehf2.12675Iron deficiencyCardiac resynchronization therapyHeart failure
spellingShingle Philipp Lacour
Phi Long Dang
Daniel Armando Morris
Abdul Shokor Parwani
Wolfram Doehner
Franziska Schuessler
Felix Hohendanner
Frank R. Heinzel
Andrea Stroux
Carsten Tschoepe
Wilhelm Haverkamp
Leif‐Hendrik Boldt
Burkert Pieske
Florian Blaschke
The effect of iron deficiency on cardiac resynchronization therapy: results from the RIDE‐CRT Study
ESC Heart Failure
Iron deficiency
Cardiac resynchronization therapy
Heart failure
title The effect of iron deficiency on cardiac resynchronization therapy: results from the RIDE‐CRT Study
title_full The effect of iron deficiency on cardiac resynchronization therapy: results from the RIDE‐CRT Study
title_fullStr The effect of iron deficiency on cardiac resynchronization therapy: results from the RIDE‐CRT Study
title_full_unstemmed The effect of iron deficiency on cardiac resynchronization therapy: results from the RIDE‐CRT Study
title_short The effect of iron deficiency on cardiac resynchronization therapy: results from the RIDE‐CRT Study
title_sort effect of iron deficiency on cardiac resynchronization therapy results from the ride crt study
topic Iron deficiency
Cardiac resynchronization therapy
Heart failure
url https://doi.org/10.1002/ehf2.12675
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