Inflammatory Profile and Risk of Post-Intervention Infection in Relation to Myocardial Necrosis Markers

<b>Background:</b> Post-procedural infection worsens outcomes in acute coronary syndrome (ACS). High-sensitivity cardiac troponin (hs-cTn) reflects myocardial injury, but its utility for infection risk prediction after percutaneous coronary intervention (PCI) is uncertain. Objective: This study aimed to evaluate whether high-sensitivity troponin (hs-cTn) levels are associated with the risk of infection and systemic inflammation. <b>Methods:</b> We performed an exploratory pilot study of consecutive ACS patients undergoing PCI (<i>n</i> = 181) at a tertiary interventional cardiology unit in Romania. Herein, hs-cTn was measured at 24- and 48-h post-PCI. The primary outcome was in-hospital infection (clinical and/or microbiological documentation), with the acknowledgment that nearly half were clinically diagnosed without microbiological confirmation. We assessed discrimination for hs-cTn48h using ROC analysis and explored associations with systemic markers (CRP, ESR, and leukocytes) and NT-proBNP using Spearman correlations. <b>Results:</b> Infections occurred in 9/181 patients (5.0%; 95% CI, 2.6-9.2). Notably, hs-cTn48h showed AUC = 0.49 (approx. 95% CI, 0.30-0.68) for infection discrimination. Correlations between hs-cTn48h and inflammatory markers were weak and non-significant (CRP ρ = 0.126, <i>p</i> = 0.091; ESR ρ = 0.119, <i>p</i> = 0.111; fibrinogen ρ = 0.134, <i>p</i> = 0.073), whereas hs-cTn48h correlated modestly with NT-proBNP (ρ = 0.232, <i>p</i> = 0.002). <b>Conclusions:</b> In this cohort, hs-cTn48h did not predict in-hospital infection after PCI in ACS. These negative findings highlight that troponin should be interpreted primarily as a marker of myocardial necrosis, not infectious risk. Larger multicenter studies with microbiological adjudication and broader biomarker panels are warranted.