The effect of iron deficiency on cardiac resynchronization therapy: results from the RIDE-CRT Study
Philipp Lacour1,2, Phi Long Dang1, Daniel Armando Morris1
1Department of Cardiology, Charité-Universitaetsmedizin Berlin, Campus Virchow-Klinikum, Augustenburger Platz 1, Berlin, 13353, Germany.
Insights
Iron deficiency negatively impacts cardiac resynchronization therapy (CRT) effectiveness, predicting poorer outcomes in heart failure patients. Addressing iron deficiency may improve CRT response and patient results.
Area of Science:
- Cardiology
- Heart Failure Management
- Medical Diagnostics
Background:
- Cardiac resynchronization therapy (CRT) is a standard treatment for heart failure patients with specific criteria.
- While CRT improves outcomes, patient response varies, and factors influencing effectiveness require further investigation.
- The role of iron deficiency, a common comorbidity, in CRT response is not well-established.
Purpose of the Study:
- To investigate the impact of functional and absolute iron deficiency on reverse cardiac remodeling after CRT implantation.
- To assess the effect of iron deficiency on clinical response to CRT.
- To determine the association between iron deficiency and long-term outcomes, including mortality, in CRT recipients.
Main Methods:
- Prospective observational study (RIDE-CRT) including 77 CRT recipients.
- Short-term and long-term follow-up assessing echocardiographic parameters and clinical status (New York Heart Association classification).
- Multivariate analysis to identify predictors of CRT response and outcomes, with specific attention to iron deficiency status.
Main Results:
- Iron deficiency was identified as an independent predictor of both echocardiographic and clinical non-response to CRT.
- A significant association was found between the type of iron deficiency and improvements in left ventricular ejection fraction, global longitudinal strain, and New York Heart Association classification.
- Iron deficiency was significantly associated with increased all-cause mortality but not with heart failure hospitalization.
Conclusions:
- Iron deficiency is a negative predictor of CRT effectiveness, impacting reverse cardiac remodeling and clinical response.
- Iron substitution therapy should be considered as a potential treatment target to enhance CRT response and improve outcomes in heart failure patients.
- Further research into iron management strategies in CRT candidates is warranted.
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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