Clinical and Biomarker Predictors of Adverse Left Ventricular Remodeling After First STEMI: Insights into Phenotype...

Background: Adverse left ventricular remodeling (ALVR) remains an important complication after ST-segment elevation myocardial infarction (STEMI) despite timely reperfusion therapy. Early circulating biomarkers reflecting thromboinflammatory and eicosanoid-related pathways may improve identification of patients at risk of unfavorable remodeling. Objectives: To investigate whether platelet count, 20-hydroxyeicosatetraenoic acid (20-HETE), 15(S)-hydroxyeicosatetraenoic acid [15(S)-HETE], and NETosis activity measured on the morning after reperfusion therapy are associated with serial cardiac magnetic resonance (CMR)-defined ALVR after first STEMI. Methods: In this prospective single-center study, 93 patients with first STEMI treated with reperfusion therapy, including primary percutaneous coronary intervention (PCI) in 87 patients and thrombolysis followed by PCI underwent baseline CMR at a median of 4 days after PCI and repeat CMR at 6 months. ALVR was defined as a ≥12% increase in both left ventricular end-diastolic volume and left ventricular end-systolic volume at follow-up. Fasting blood samples obtained on the morning after PCI were used to measure platelet count, 20-HETE, 15(S)-HETE, and NETosis activity. Univariable and multivariable logistic regression and receiver operating characteristic analyses were performed. A secondary exploratory analysis evaluated predictors of absolute improvement in left ventricular ejection fraction (LVEF) of ≥10%. Results: ALVR occurred in 19 of 93 patients (20.4%). Patients with ALVR had lower platelet count and lower 20-HETE levels at baseline. In the multivariable model, lower platelet count (OR 0.981, 95% CI 0.965-0.996; p = 0.015) and lower 20-HETE (OR 0.985, 95% CI 0.970-1.000; p = 0.047) were independently associated with ALVR, whereas urea was not significant. In receiver operating characteristic analysis, 20-HETE showed the highest discriminatory ability for ALVR (AUC 0.713, 95% CI 0.594-0.833; p < 0.001), followed by platelet count (AUC 0.670, 95% CI 0.546-0.794; p = 0.007). By contrast, 15(S)-HETE and NETosis activity were not significant discriminators in the primary analyses. Overall LV function improved during follow-up, with LVEF increasing from 49.0% to 56.0% (p < 0.001). In secondary exploratory analysis, higher HDL was independently associated with LVEF improvement of ≥10% (OR 7.84, 95% CI 1.26-48.99; p = 0.028). Conclusions: Lower platelet count and lower 20-HETE measured on the morning after PCI were independently associated with subsequent CMR-defined ALVR after first STEMI. Platelet count may serve as a simple, clinically accessible marker of risk, while 20-HETE suggests a potential role of eicosanoid-related pathways in remodeling process.