# The Neutrophil–Lymphocyte Ratio Is Associated with Cardiac Magnetic Resonance Imaging-Derived Myocardial Fibrosis

**Authors:** Michael Poledniczek, Christina Kronberger, Lena Marie Schmid, Katharina Mascherbauer, Carolina Donà, Matthias Koschutnik, Laura Lunzer, Christian Nitsche, Dietrich Beitzke, Christian Loewe, Christian Hengstenberg, Andreas Anselm Kammerlander

PMC · DOI: 10.3390/jcm15041441 · 2026-02-12

## TL;DR

This study finds that a blood test measuring neutrophil-lymphocyte ratio is linked to signs of heart tissue scarring seen on MRI scans.

## Contribution

The novel contribution is showing that a simple blood test (NLR) correlates with myocardial fibrosis detected via cardiac MRI.

## Key findings

- Higher NLR tertiles correlated with lower ejection fraction and increased right ventricular volume.
- NLR was significantly associated with prolonged myocardial T1 times and increased extracellular volume (ECV).
- CRP showed similar associations with T1 and ECV as NLR, but both explained only a modest portion of variation.

## Abstract

Background: Sub-clinical inflammation is considered a key mechanism in cardiovascular disease and myocardial remodeling. We therefore evaluated whether the neutrophil–lymphocyte ratio (NLR), a simple inflammatory marker derived from a routine full blood count, is associated with myocardial fibrosis. Methods: Consecutive patients from a cardiac magnetic resonance imaging (CMR) registry were included and stratified by the NLR tertile. The association of the NLR and the levels of C-reactive protein (CRP) with CMR-derived myocardial T1 time and the extracellular volume fraction (ECV) were assessed using linear regression analysis and compared using Z-scores. In addition, an association with outcome was tested utilizing the log-rank test. Results: 1152 patients (72.4 years, 53.1% male) constituted the final cohort. The median NLR was 3.11 [interquartile range (IQR): 2.145–4.67]. Tertiles were based on the cut-off values ≤ 2.5, >2.5 and <4.0, and ≥4.0. A higher NLR tertile was associated with lower biventricular ejection fraction, hypertrophy, and increased right ventricular volume. The myocardial native T1 time [tertile 1 vs. 3: 1010 ms (984–1038) vs. 1030 (1001–1059), p < 0.001] and ECV [tertile 1 vs. 3: 26.3% (24.2–28.6) vs. 28.1% (25.5–31.4), p < 0.001] also significantly differed between the NLR tertiles. The NLR’s and the CRP’s association with elevated myocardial T1 time and ECV were comparable; however, the proportion of variation in the target variables explained by either was generally low. Conclusions: In our CMR all-comer cohort, NLR and CRP were significantly associated with prolonged myocardial T1 times and increased ECV. However, only a modest variation observed in both parameters was explained by either variable.

## Full-text entities

- **Genes:** IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}
- **Diseases:** Chronic Kidney Disease (MESH:D051436), insulin resistance (MESH:D007333), myocardial infarction (MESH:D009203), infection (MESH:D007239), hypertrophic or dilated cardiomyopathy (MESH:D002311), cardiovascular disease (MESH:D002318), diabetes (MESH:D003920), hypertrophy (MESH:D006984), valvular heart disease (MESH:D006349), atrial fibrillation (MESH:D001281), cancer (MESH:D009369), hypertension (MESH:D006973), myocardial remodeling (MESH:D064752), dyslipidemia (MESH:D050171), death (MESH:D003643), atherosclerosis (MESH:D050197), injury to (MESH:D014947), Chronic inflammation (MESH:D007249), Myocardial Fibrosis (MESH:D005355), NLR (MESH:D015467), hyperlipidemia (MESH:D006949), Metabolic syndrome (MESH:D024821), myocardial apoptosis (MESH:D065703), abdominal obesity (MESH:D056128), CMR (MESH:C564543), post-ischemic scarring (MESH:D002921), COPD (MESH:D029424), impaired myocardial relaxation (MESH:D009202), systemic (MESH:D015619), coronary artery disease (MESH:D003324), systolic dysfunction (MESH:D006331), cardiac amyloidosis (MESH:D000686), peripheral artery disease (MESH:D058729), atrial and ventricular arrhythmia (MESH:D001145), heart failure (MESH:D006333), obesity (MESH:D009765)
- **Chemicals:** doxorubicin (MESH:D004317), oxygen (MESH:D010100), NT-proBNP (-), canakinumab (MESH:C541220), glucose (MESH:D005947), rosuvastatin (MESH:D000068718), cholesterol (MESH:D002784), reactive oxygen species (MESH:D017382), Colchicine (MESH:D003078), gadolinium (MESH:D005682)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12942423/full.md

---
Source: https://tomesphere.com/paper/PMC12942423