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Background: There is limited data on the association between inflammation and the formation of early left ventricular thrombus (LVT) following ST‐elevation myocardial infarction (STEMI). This study aimed to explore the predictive value of several inflammatory biomarkers for LVT formation following STEMI. Methods and Results: Our cohort included 2534 consecutive patients admitted to the cardiac intensive care unit (CICU) with STEMI. The final analysis included 51 patients with LVT and 102 patients without LVT, matched for age, sex, anterior infarct and ejection fraction. Upon admission, patients with LVT had higher white blood cell counts (WBC) (12.8 ± 7 vs. 12.4 ± 4 ×103/µL, p = 0.01), higher absolute neutrophil counts (10.5 ± 4 vs. 8.6 ± 4 ×103/µL, p = 0.003), neutrophil‐to‐lymphocyte ratio (8.2 ± 6 vs. 4.8 ± 4, p = 0.04), and C‐reactive protein (CRP) levels (35.9 ± 62 vs. 18.6 ± 40 mg/L, p = 0.04). Peak values for WBC and CRP were also higher in the LVT group (17.8 ± 8 vs. 14.6 ± 5 ×103/µL, p = 0.003 and 95.8 ± 82 vs. 64.2 ± 76 mg/L, p = 0.02, respectively). In univariate regression analysis, WBC upon admission (OR: 1.12, 95% CI: 1.02–1.21, p = 0.02), peak WBC (OR: 1.09, 95% CI: 1.02–1.17, p = 0.009), neutrophil count upon admission (OR: 1.15, 95% CI: 1.04–1.26, p = 0.004), and peak CRP (OR: 1.01, 95% CI: 1–1.01, p = 0.03) predicted LVT formation, which was also evident in multivariate regression models. Conclusion: WBC and neutrophil counts upon admission, as well as peak WBC and CRP, have additional predictive value for LVT formation following STEMI, beyond classical risk factors. [ABSTRACT FROM AUTHOR]

Background: Acute kidney injury (AKI) is a common and serious complication of ST‐elevation myocardial infarction (STEMI). AKI and chronic kidney disease (CKD) are highly heterogeneous, leaving a wide gap between them. Therefore, the term acute kidney disease (AKD) was implemented, describing prolonged renal injury between 7 and 90 days. We aimed to evaluate the prevalence and predictors of AKD among STEMI patients. Methods: This retrospective observational study included 2940 consecutive patients admitted with STEMI between 2008 and 2022. Renal function was assessed upon admission and routinely thereafter. Renal outcomes were evaluated according to KDIGO criteria, with AKD defined as persistent renal injury of between 7 and 90 days. Results: Two hundred and fifty‐two subjects with STEMI and AKI were included; of them, 117 (46%) developed AKD. Among baseline CKD patients, higher rates of AKD were observed (60% vs. 46%). KDIGO index ≥ 2 was an independent predictor for AKD in in subjects without baseline CKD (AOR 2.63, 95% CI 1.07−6.53). In subjects with baseline CKD, older age and higher creatinine were independent predictors for AKD. Subjects with AKD had a higher 1‐year mortality rate (HR 3.39, 95% CI 1.71−6.72, p < 0.01). This trend was mainly driven by the CKD subpopulation where higher mortality rates for AKD on CKD were observed (HR 5.26, 95% CI 1.83−15.1, p < 0.01). Conclusion: AKD is common among STEMI patients with AKI. The presence of CKD and higher KDIGO stage should prompt strict monitoring for early diagnosis, treatment, and prevention of renal function deterioration. [ABSTRACT FROM AUTHOR]

Background and Aims: The diagnosis of acute kidney injury (AKI) is of importance among patients with ST segment elevation (STEMI) undergoing primary coronary intervention (PCI). It is often delayed given the need in serial measurements of creatinine or other serum markers. Neutrophil gelatinase‐associated lipocalin (NGAL) is a proven marker for AKI, although its role as an early predictor in this setting was scarcely addressed before and was the aim of our study. Methods: Prospective observational study including 133 patients with STEMI treated with PCI. Plasma NGAL was drawn immediately before PCI (NGAL‐0) and 24 h after (NGAL‐24). Similar analysis of C‐reactive protein (CRP) was performed for additional comparison. Results: Mean age was 62 ± 13 years, 78% were men, and 20 (15%) developed AKI after admission. Patients with AKI after admission demonstrated higher levels of NGAL‐0 (164 vs. 95 ng/mL; p < 0.001) and NGAL‐24 (142 vs. 93 ng/mL; p < 0.001). Levels of NGAL‐0 and NGAL‐24 were similar within the AKI and non‐AKI groups. Using ROC curve analysis, NGAL‐0 had best predictive ability for AKI development (AUC 0.841, 95% CI 0.80–0.96), compared with NGAL‐24 (0.783, 95% CI 0.74–0.85), CRP‐0 (0.701, 95% CI 0.58–0.83), and CRP‐24 (0.781, 95% CI 0.66–0.90). The optimal NGAL‐0 cutoff for AKI prediction was 125 ng/mL, with 70% sensitivity, 84% specificity, and 94% negative predictive value. Conclusions: Among STEMI patients, NGAL measurement upon admission are associated with AKI and may serve as a reliable marker for early AKI detection. Future studies may direct risk stratification using this single test can direct personalized evaluations during the admission, and focused interventions to prevent AKI. [ABSTRACT FROM AUTHOR]