Key result
Higher presentation NLR is independently linked to impaired long-term GLS after myocarditis.
Why the study?
The relationship between simple, routinely available inflammatory markers and residual LV functional impairment assessed by 2D global longitudinal strain in patients recovered from myocarditis was not well established.
Is admission neutrophil-to-lymphocyte ratio (NLR) associated with residual impairment of left ventricular global longitudinal strain (GLS) in patients recovered from acute myocarditis?
Cohort (n=154)
No
Is admission neutrophil-to-lymphocyte ratio (NLR) associated with residual impairment of left ventricular global longitudinal strain (GLS) in patients recovered from acute myocarditis?
Answers are grounded in this paper and cite their sources.
An elevated neutrophil-to-lymphocyte ratio at hospital admission for acute myocarditis is an independent predictor of residual subclinical left ventricular dysfunction, as indicated by impaired global longitudinal strain at long-term follow-up.
Objectives: This study aimed to investigate the relationship between simple, routinely available inflammatory markers and residual impairment of left ventricular (LV) function assessed by 2D global longitudinal strain (GLS) in patients recovered from myocarditis. Materials and Methods: This prospective study included patients diagnosed with Myocarditis who were followed in our heart failure clinic. All participants underwent conventional echocardiography and 2D strain analysis at follow-up. Echocardiographic data was compared with age and sex-matched healthy controls. The study group’s bloodwork was analyzed for inflammatory biomarkers, including neutrophil-to-lymphocyte ratio (NLR), at defined time intervals starting from admission. Results: A total of 104 myocarditis patients [22 women, mean age 30.9 ± 8.5 years, baseline LV ejection fraction (LVEF) 56.8 ± 6.8%] were included. At a median follow-up of 78.4 months (IQR: 53.5–99.2), median GLS remained significantly less negative compared with healthy controls [–18.0% (IQR: −18.8 to −17.5) vs −21.4% (IQR: −22.7 to −19.4); P < 0.001]. At presentation, patients showed elevated inflammatory markers (WBC 10.7 ± 3.4 K/µL, NLR 5.53 ± 3.54, C-reactive protein 81.1 ± 67.7 mg/L), with WBC and NLR demonstrating an initial increase followed by significant decline at 72 hours and 6 months ( P < 0.001). Regression analyses confirmed impaired GLS in myocarditis patients compared to controls (crude β = 2.88, 95% CI: 2.21–3.55; adjusted β = 2.54, 95% CI: 1.63–3.44; P < 0.001). Within the myocarditis cohort, admission NLR was independently associated with impaired GLS at follow-up (crude β = 0.190, 95% CI: 0.103–0.277; adjusted β = 0.170, 95% CI: 0.088–0.267; P < 0.001). Sex-stratified analysis showed significance in males (β = 0.179, 95% CI: 0.088–0.270; P < 0.001; R 2 = 0.163) but not in females (β = 0.194, 95% CI: −0.107 to 0.496; P = 0.194; R 2 = 0.083). Conclusion: Elevated inflammatory markers at presentation, particularly NLR, were associated with impaired GLS at follow-up, independent of baseline demographic and clinical covariates. The predictive value of NLR appeared more evident in males, though limited female representation precludes firm sex-specific conclusions. NLR may serve as a simple, cost-effective marker for identifying patients at risk of residual subclinical LV dysfunction after myocarditis, but larger, sex-balanced cohorts are required to confirm these findings.
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Khadija et al. (2025) conducted a cohort in Myocarditis (n=154). Neutrophil-to-lymphocyte ratio (NLR) at admission was evaluated on Global longitudinal strain (GLS) at follow-up (adjusted β = 0.170, 95% CI 0.088-0.267, p=<0.001). Higher neutrophil-to-lymphocyte ratio at presentation was independently associated with impaired global longitudinal strain at long-term follow-up in patients recovering from myocarditis.
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