High neutrophil-to-lymphocyte ratio as an early sign of cardiotoxicity in breast cancer patients treated with anthracycline.
NLR
cardio-oncology
cardiotoxicity
echocardiography
strain
Journal
Clinical cardiology
ISSN: 1932-8737
Titre abrégé: Clin Cardiol
Pays: United States
ID NLM: 7903272
Informations de publication
Date de publication:
Mar 2023
Mar 2023
Historique:
revised:
14
12
2022
received:
21
10
2022
accepted:
19
12
2022
pubmed:
21
1
2023
medline:
21
3
2023
entrez:
20
1
2023
Statut:
ppublish
Résumé
Cardiotoxicity, defined mainly as left ventricle (LV) dysfunction, is a significant side effect of anthracyclines (ANT) therapy. The need for an early simple marker to identify patients at risk is crucial. A high neutrophil-to-lymphocyte ratio (NLR) has been associated with poor prognosis in cancer patients; however, its role as a predictor for cardiotoxicity development is unknown. Evaluating whether elevated NLR, during ANT exposure, plays a predictive role in the development of cardiotoxicity as defined by LV global longitudinal strain (LV GLS) relative reduction (≥10%). Data were prospectively collected as part of the Israel Cardio-Oncology Registry. A total of 74 female patients with breast cancer, scheduled for ANT therapy were included. NLR levels were assessed at baseline (T1) and during ANT therapy (T2). All patients underwent serial echocardiography at baseline (T1) and after the completion of ANT therapy (T3). NLR ≥ 2.58 at T2 was found to be the optimal predictive cutoff for LV GLS deterioration. A relative LV GLS reduction ≥10% was significantly more common among patients with high NLR (50% vs. 20%, p = .009). NLR ≥ 2.58 at T2 increases the risk for LV GLS reduction by fourfold (odds ratio [OR]: 4.63, 95% confidence interval [CI]: 1.29-16.5, p = .02), with each increase of 1-point NLR adding an additional 15% risk (OR: 1.15, 95% CI: 1.01-1.32, p = .046). Our study provides novel data that high NLR levels, during ANT exposure, have an independent association with the development of LV dysfunction. Routine surveillance of NLR may be an effective means of risk-stratifying.
Sections du résumé
BACKGROUND
BACKGROUND
Cardiotoxicity, defined mainly as left ventricle (LV) dysfunction, is a significant side effect of anthracyclines (ANT) therapy. The need for an early simple marker to identify patients at risk is crucial. A high neutrophil-to-lymphocyte ratio (NLR) has been associated with poor prognosis in cancer patients; however, its role as a predictor for cardiotoxicity development is unknown.
OBJECTIVE
OBJECTIVE
Evaluating whether elevated NLR, during ANT exposure, plays a predictive role in the development of cardiotoxicity as defined by LV global longitudinal strain (LV GLS) relative reduction (≥10%).
METHODS AND RESULTS
RESULTS
Data were prospectively collected as part of the Israel Cardio-Oncology Registry. A total of 74 female patients with breast cancer, scheduled for ANT therapy were included. NLR levels were assessed at baseline (T1) and during ANT therapy (T2). All patients underwent serial echocardiography at baseline (T1) and after the completion of ANT therapy (T3). NLR ≥ 2.58 at T2 was found to be the optimal predictive cutoff for LV GLS deterioration. A relative LV GLS reduction ≥10% was significantly more common among patients with high NLR (50% vs. 20%, p = .009). NLR ≥ 2.58 at T2 increases the risk for LV GLS reduction by fourfold (odds ratio [OR]: 4.63, 95% confidence interval [CI]: 1.29-16.5, p = .02), with each increase of 1-point NLR adding an additional 15% risk (OR: 1.15, 95% CI: 1.01-1.32, p = .046).
CONCLUSIONS
CONCLUSIONS
Our study provides novel data that high NLR levels, during ANT exposure, have an independent association with the development of LV dysfunction. Routine surveillance of NLR may be an effective means of risk-stratifying.
Identifiants
pubmed: 36660883
doi: 10.1002/clc.23966
pmc: PMC10018102
doi:
Substances chimiques
Anthracyclines
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
328-335Subventions
Organisme : Pfizer
Informations de copyright
© 2023 The Authors. Clinical Cardiology published by Wiley Periodicals, LLC.
Références
J Immunol. 1987 Oct 1;139(7):2406-13
pubmed: 2821114
Ann Surg Oncol. 2009 Mar;16(3):614-22
pubmed: 19130139
J Am Coll Cardiol. 2014 Jul 1;63(25 Pt A):2751-68
pubmed: 24703918
J Am Coll Cardiol. 2014 Sep 2;64(9):938-45
pubmed: 25169180
Circ Heart Fail. 2016 Jan;9(1):e002661
pubmed: 26747861
Can J Cardiol. 2014 Oct;30(10):1177-82
pubmed: 25154806
Clin Cancer Res. 2004 Aug 1;10(15):4895-900
pubmed: 15297389
CA Cancer J Clin. 2012 Jul-Aug;62(4):220-41
pubmed: 22700443
Cancer Manag Res. 2021 Jul 28;13:5889-5898
pubmed: 34349562
Eur J Surg Oncol. 2001 Jun;27(4):396-403
pubmed: 11417987
Eur Heart J Cardiovasc Imaging. 2014 Oct;15(10):1063-93
pubmed: 25239940
Breast Cancer Res. 2017 Jan 5;19(1):2
pubmed: 28057046
J Am Heart Assoc. 2020 Dec;9(23):e018306
pubmed: 33190570
Eur Heart J Cardiovasc Imaging. 2017 May 01;18(8):930-936
pubmed: 28379383
Echocardiography. 2018 Feb;35(2):234-240
pubmed: 29106752
Eur Heart J Cardiovasc Imaging. 2017 Apr 01;18(4):392-401
pubmed: 28064155
J Am Soc Echocardiogr. 2008 Dec;21(12):1290-2
pubmed: 19041570
Eur Heart J. 2016 Sep 21;37(36):2768-2801
pubmed: 27567406
Eur J Prev Cardiol. 2022 Mar 25;29(3):463-472
pubmed: 33693524
Eur J Echocardiogr. 2006 Mar;7(2):79-108
pubmed: 16458610
Eur J Cancer. 2013 Apr;49(6):1374-403
pubmed: 23485231
Curr Opin Cardiol. 2019 May;34(3):289-295
pubmed: 30973398
Echocardiography. 2019 Mar;36(3):495-502
pubmed: 30636342
Int J Cardiol. 2013 Sep 30;168(2):1154-9
pubmed: 23219132
Clin Cardiol. 2023 Mar;46(3):328-335
pubmed: 36660883
J Am Soc Echocardiogr. 2012 Jul;25(7):733-40
pubmed: 22578518