ETD

• cardiac magnetic resonance
• epicardial adipose tissue
• inflammatory biomarkers
• left ventricular remodeling
• ST-elevation myocardial infarction

Background: Left ventricular remodelling (LVR) after ST-elevation myocardial infarction (STEMI) remains a major determinant of prognosis. Yet, even among patients with similar clinical, angiographic, and therapeutic profiles, LVR may vary markedly. The mechanisms of such difference remain unclear.
Although several clinical, biochemical, and imaging predictors of LVR have been proposed, a comprehensive understanding of the interplay between systemic inflammation, conventional biomarkers, and advanced cardiac magnetic resonance (CMR) parameters is lacking.
Purpose: To identify predictors of adverse and reverse (positive) ventricular remodeling after STEMI by integrating clinical data, systemic inflammatory markers, epicardial adipose tissue (EAT) thickness, and multiparametric cardiac magnetic resonance (CMR) parameters.
Methods: Consecutive STEMI patients undergoing successful primary percutaneous coronary intervention (pPCI) and early CMR were prospectively enrolled. Biomarkers included high-sensitivity troponin, NT-proBNP, C-reactive protein (CRP), and neutrophil-to-lymphocyte ratio (NLR). EAT thickness was measured by echocardiography. CMR parameters include infarct size (IS), microvascular obstruction (MVO), intramyocardial hemorrhage (IMH), area at risk (AAR), and myocardial salvage index. Remodeling was assessed at 12 ± 1.4 months. Univariate and multivariate logistic regression analyses were performed.
Results: A total of 78 patients were included. At 12 months, 18 (23%) developed adverse remodelling, 24 (31%) exhibited positive remodelling, and 36 (46%) showed no remodelling. Adverse remodeling was significantly associated with higher CRP levels (OR 1.10, 95% CI 1.02–1.18), higher NLR (OR 1.17, 95% CI 0.99–1.38), larger IS (OR 1.06, 95% CI 1.01–1.10), presence of MVO (OR 1.06, 95% CI 1.00–1.10), and reduced salvage index (OR 1.11, 95% CI 1.03–1.21). Positive remodelling was predicted by lower CRP levels (OR 0.89, 95% CI 0.80–0.99), reduced EAT thickness (OR 0.78, 95% CI 0.62–0.98), and higher salvage index (aOR 0.95, 95% CI 0.89–1.00). IMH and AAR, although showing a trend towards an increased risk of adverse remodeling, did not reach statistical significance. Conventional biomarkers (troponin and NT-proBNP) showed no predictive value for remodelling. In multivariable analysis, reduced salvage index and peak CRP independently predicted both adverse and positive remodeling, while EAT thickness remained associated with positive remodelling only.
Conclusions: In patients with STEMI treated by pPCI, the development of ventricular remodelling is best predicted by a combination of CMR-derived markers (salvage index, infarct size, MVO) and systemic inflammation (CRP, NLR), whereas classical biomarkers such as troponin and NT-proBNP lack discriminative power. Importantly, EAT thickness emerged as a relevant marker inversely associated with positive remodelling. These findings support a multiparametric approach that integrates CMR tissue characterization, inflammatory profiling, and EAT assessment to refine post-infarction risk stratification. Larger, multicenter studies are warranted to validate these results and explore whether targeted anti-inflammatory and metabolic interventions can modify remodeling trajectories and improve outcomes.