Neutrophil‐to‐lymphocyte ratio and outcomes in patients with new‐onset or worsening heart failure with reduced and preserved ejection fraction
Abstract Aims Inflammation is thought to play a role in heart failure (HF) pathophysiology. Neutrophil‐to‐lymphocyte ratio (NLR) is a simple, routinely available measure of inflammation. Its relationship with other inflammatory biomarkers and its association with clinical outcomes in addition to oth...
| Main Authors: | , , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2021-08-01
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| Series: | ESC Heart Failure |
| Subjects: | |
| Online Access: | https://doi.org/10.1002/ehf2.13424 |
| _version_ | 1819138938365804544 |
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| author | Fraser M. Curran U Bhalraam Mohapradeep Mohan Jagdeep S. Singh Stefan D. Anker Kenneth Dickstein Alexander S. Doney Gerasimos Filippatos Jacob George Marco Metra Leong L. Ng Colin N. Palmer Nilesh J. Samani Dirk J. vanVeldhuisen Adriaan A. Voors Chim C. Lang Ify R. Mordi |
| author_facet | Fraser M. Curran U Bhalraam Mohapradeep Mohan Jagdeep S. Singh Stefan D. Anker Kenneth Dickstein Alexander S. Doney Gerasimos Filippatos Jacob George Marco Metra Leong L. Ng Colin N. Palmer Nilesh J. Samani Dirk J. vanVeldhuisen Adriaan A. Voors Chim C. Lang Ify R. Mordi |
| author_sort | Fraser M. Curran |
| collection | DOAJ |
| description | Abstract Aims Inflammation is thought to play a role in heart failure (HF) pathophysiology. Neutrophil‐to‐lymphocyte ratio (NLR) is a simple, routinely available measure of inflammation. Its relationship with other inflammatory biomarkers and its association with clinical outcomes in addition to other risk markers have not been comprehensively evaluated in HF patients. Methods We evaluated patients with worsening or new‐onset HF from the BIOlogy Study to Tailored Treatment in Chronic Heart Failure (BIOSTAT‐CHF) study who had available NLR at baseline. The primary outcome was time to all‐cause mortality or HF hospitalization. Outcomes were validated in a separate HF population. Results 1622 patients were evaluated (including 523 ventricular ejection fraction [LVEF] < 40% and 662 LVEF ≥ 40%). NLR was significantly correlated with biomarkers related to inflammation as well as NT‐proBNP. NLR was significantly associated with the primary outcome in patients irrespective of LVEF (hazard ratio [HR] 1.18 per standard deviation increase; 95% confidence interval [CI] 1.11–1.26, P < 0.001). Patients with NLR in the highest tertile had significantly worse outcome than those in the lowest independent of LVEF (<40%: HR 2.75; 95% CI 1.84–4.09, P < 0.001; LVEF ≥ 40%: HR 1.51; 95% CI 1.05–2.16, P = 0.026). When NLR was added to the BIOSTAT‐CHF risk score, there were improvements in integrated discrimination index (IDI) and net reclassification index (NRI) for occurrence of the primary outcome (IDI + 0.009; 95% CI 0.00–0.019, P = 0.030; continuous NRI + 0.112, 95% CI 0.012–0.176, P = 0.040). Elevated NLR was similarly associated with adverse outcome in the validation cohort. Decrease in NLR at 6 months was associated with reduced incidence of the primary outcome (HR 0.75; 95% CI 0.57–0.98, P = 0.036). Conclusions Elevated NLR is significantly associated with elevated markers of inflammation in HF patients and is associated with worse outcome. Elevated NLR might potentially be useful in identifying high‐risk HF patients and may represent a treatment target. |
| first_indexed | 2024-12-22T11:14:43Z |
| format | Article |
| id | doaj.art-e06e4af85cf54a3b99495e00918f7b92 |
| institution | Directory Open Access Journal |
| issn | 2055-5822 |
| language | English |
| last_indexed | 2024-12-22T11:14:43Z |
| publishDate | 2021-08-01 |
| publisher | Wiley |
| record_format | Article |
| series | ESC Heart Failure |
| spelling | doaj.art-e06e4af85cf54a3b99495e00918f7b922022-12-21T18:28:04ZengWileyESC Heart Failure2055-58222021-08-01843168317910.1002/ehf2.13424Neutrophil‐to‐lymphocyte ratio and outcomes in patients with new‐onset or worsening heart failure with reduced and preserved ejection fractionFraser M. Curran0U Bhalraam1Mohapradeep Mohan2Jagdeep S. Singh3Stefan D. Anker4Kenneth Dickstein5Alexander S. Doney6Gerasimos Filippatos7Jacob George8Marco Metra9Leong L. Ng10Colin N. Palmer11Nilesh J. Samani12Dirk J. vanVeldhuisen13Adriaan A. Voors14Chim C. Lang15Ify R. Mordi16School of Medicine University of Dundee Dundee UKSchool of Medicine University of Dundee Dundee UKDivision of Molecular and Clinical Medicine University of Dundee Dundee UKDivision of Molecular and Clinical Medicine University of Dundee Dundee UKDepartment of Cardiology (CVK); and Berlin Institute of Health Center for Regenerative Therapies (BCRT); German Centre for Cardiovascular Research (DZHK) partner site Berlin Charité Universitätsmedizin Berlin Berlin GermanyUniversity of Bergen Stavanger University Hospital Stavanger NorwayDivision of Population Health and Genomics University of Dundee Dundee UKHeart Failure Unit, Department of Cardiology, School of Medicine National and Kopodistrian University of Athens, Athens University Hospital Attikon Athens GreeceDivision of Molecular and Clinical Medicine University of Dundee Dundee UKInstitute of Cardiology, Department of Medical and Surgical Specialties, Radiological Sciences and Public Health University of Brescia Brescia ItalyDepartment of Cardiovascular Sciences University of Leicester and NIHR Leicester Biomedical Research Centre Leicester UKDivision of Population Health and Genomics University of Dundee Dundee UKDepartment of Cardiovascular Sciences University of Leicester and NIHR Leicester Biomedical Research Centre Leicester UKDepartment of Cardiology, University Medical Center Groningen University of Groningen Groningen The NetherlandsDepartment of Cardiology, University Medical Center Groningen University of Groningen Groningen The NetherlandsDivision of Molecular and Clinical Medicine University of Dundee Dundee UKDivision of Molecular and Clinical Medicine University of Dundee Dundee UKAbstract Aims Inflammation is thought to play a role in heart failure (HF) pathophysiology. Neutrophil‐to‐lymphocyte ratio (NLR) is a simple, routinely available measure of inflammation. Its relationship with other inflammatory biomarkers and its association with clinical outcomes in addition to other risk markers have not been comprehensively evaluated in HF patients. Methods We evaluated patients with worsening or new‐onset HF from the BIOlogy Study to Tailored Treatment in Chronic Heart Failure (BIOSTAT‐CHF) study who had available NLR at baseline. The primary outcome was time to all‐cause mortality or HF hospitalization. Outcomes were validated in a separate HF population. Results 1622 patients were evaluated (including 523 ventricular ejection fraction [LVEF] < 40% and 662 LVEF ≥ 40%). NLR was significantly correlated with biomarkers related to inflammation as well as NT‐proBNP. NLR was significantly associated with the primary outcome in patients irrespective of LVEF (hazard ratio [HR] 1.18 per standard deviation increase; 95% confidence interval [CI] 1.11–1.26, P < 0.001). Patients with NLR in the highest tertile had significantly worse outcome than those in the lowest independent of LVEF (<40%: HR 2.75; 95% CI 1.84–4.09, P < 0.001; LVEF ≥ 40%: HR 1.51; 95% CI 1.05–2.16, P = 0.026). When NLR was added to the BIOSTAT‐CHF risk score, there were improvements in integrated discrimination index (IDI) and net reclassification index (NRI) for occurrence of the primary outcome (IDI + 0.009; 95% CI 0.00–0.019, P = 0.030; continuous NRI + 0.112, 95% CI 0.012–0.176, P = 0.040). Elevated NLR was similarly associated with adverse outcome in the validation cohort. Decrease in NLR at 6 months was associated with reduced incidence of the primary outcome (HR 0.75; 95% CI 0.57–0.98, P = 0.036). Conclusions Elevated NLR is significantly associated with elevated markers of inflammation in HF patients and is associated with worse outcome. Elevated NLR might potentially be useful in identifying high‐risk HF patients and may represent a treatment target.https://doi.org/10.1002/ehf2.13424Heart failureNeutrophil‐to‐lymphocyte ratioInflammationBiomarkersOutcome |
| spellingShingle | Fraser M. Curran U Bhalraam Mohapradeep Mohan Jagdeep S. Singh Stefan D. Anker Kenneth Dickstein Alexander S. Doney Gerasimos Filippatos Jacob George Marco Metra Leong L. Ng Colin N. Palmer Nilesh J. Samani Dirk J. vanVeldhuisen Adriaan A. Voors Chim C. Lang Ify R. Mordi Neutrophil‐to‐lymphocyte ratio and outcomes in patients with new‐onset or worsening heart failure with reduced and preserved ejection fraction ESC Heart Failure Heart failure Neutrophil‐to‐lymphocyte ratio Inflammation Biomarkers Outcome |
| title | Neutrophil‐to‐lymphocyte ratio and outcomes in patients with new‐onset or worsening heart failure with reduced and preserved ejection fraction |
| title_full | Neutrophil‐to‐lymphocyte ratio and outcomes in patients with new‐onset or worsening heart failure with reduced and preserved ejection fraction |
| title_fullStr | Neutrophil‐to‐lymphocyte ratio and outcomes in patients with new‐onset or worsening heart failure with reduced and preserved ejection fraction |
| title_full_unstemmed | Neutrophil‐to‐lymphocyte ratio and outcomes in patients with new‐onset or worsening heart failure with reduced and preserved ejection fraction |
| title_short | Neutrophil‐to‐lymphocyte ratio and outcomes in patients with new‐onset or worsening heart failure with reduced and preserved ejection fraction |
| title_sort | neutrophil to lymphocyte ratio and outcomes in patients with new onset or worsening heart failure with reduced and preserved ejection fraction |
| topic | Heart failure Neutrophil‐to‐lymphocyte ratio Inflammation Biomarkers Outcome |
| url | https://doi.org/10.1002/ehf2.13424 |
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