Early inflammation and left ventricular remodeling after acute ST-elevation myocardial infarction: the Neutrophil-to-Lymphocyte Ratio as a predictor of cardiac dysfunction

Inflammation plays a key role in the pathophysiology of acute ST-elevation myocardial infarction (STEMI) and subsequent left ventricular (LV) remodeling. Rapid neutrophil mobilization, followed by monocyte and lymphocyte recruitment, may contribute to adverse remodeling and LV dysfunction,

increasing the risk of heart failure. Early identification of patients at risk of LV dysfunction post-STEMI could optimize therapeutic strategies and improve outcomes. This study evaluates the impact of early inflammatory responses on LV remodeling after STEMI. Specifically, it assesses whether inflammatory

biomarkers, including leukocyte dynamics, predict LV dysfunction in the acute phase, enhancing early risk stratification.

Methods: A prospective, descriptive, analytical, longitudinal study was conducted on patients with STEMI without prior cardiovascular disease between January 2023 and January 2025. Blood samples were collected at primary percutaneous coronary intervention and 12 hours later. Advanced echocardiography was

performed prior to discharge. Leukocyte dynamics and inflammatory parameters were analyzed in relation to adverse LV remodeling, defined as reduced left ventricular ejection fraction (LVEF) or impaired global longitudinal strain (GLS), using IBM SPSS Statistic.

Results: The study included 52 patients (median age 56,6 years, IQR 52-61), with 84,6%male. Cardiovascular risk factors included smoking (84%), hypertension (49%), diabetes (25%), and dyslipidemia (50%). Most patients (92%) were Killip- Kimball class I, the rest were class II. The culprit vessel was the RCA (50%),followed by LAD (38.5%) and LCx (11.5%). Revascularization involved drug- eluting stents in 42 patients (80.7%), 1 bioresorbable stent (1.9%), and 2 balloon angioplasties (3.8%). All patients received AAS and P2Y12 inhibitors, primarily Prasugrel (46%) and Ticagrelor (44%).

Median LVEF was 49.6% (IQR 45-55%), with a mean GLS of -13% ± -3.3% in the acute phase. At 12 hours, the inflammatory response was characterized by leukocytosis (12,707 ± 3,741 cells/μL), predominantly neutrophils (median 9,230, IQR 6,940-11,560). Lymphocytes averaged 2,227 ± 803 cells/μL, and monocytes 985 (IQR 767-1,307). The median neutrophil-to-lymphocyte ratio

(NLR) at 12 hours was 3.7 (IQR 2.8-4.5). Peak C-reactive protein was 61 ± 57 mg/dl. NRL at 12 hours was the principal predictor of both LVEF and GLS, with significant negative correlation coefficients (-0.369, p=0.012; -0.377, p=0.012, respectively). Higher NLR was associated with reduced GLS (<-16%) with a statistically significant difference of -1.04 (-2.05 to -0.02, p=0.045).

Conclusion: A higher neutrophil-to-lymphocyte ratio at 12 hours post-STEMI was associated with lower LVEF and GLS, suggesting its potential as an early predictor of adverse LV remodeling. This biomarker may aid in early risk stratification. Further studies are needed to validate these findings and explore their clinical

implications.