Inflammatory cytokine profiling across acute coronary syndrome subtypes: Comparison of STEMI and NSTE-ACS.
This study aimed to characterize differences in clinical presentation, metabolic parameters and cytokine profiles between STEMI and NSTE-ACS patients and identify potential biomarkers of disease severity and inflammation.
An exploratory study was conducted on 60 ACS patients (30 STEMI, 30 NSTE-ACS) experiencing their first episode. Clinical characteristics, routine laboratory parameters and multiplex cytokine analysis (GM-CSF, IFN-γ, IL-1β, IL-4, IL-6, IL-8, IL-9, IL-10, IL-12P70, IL-18, MCP-1, M-CSF, TNF-α) were compared. Normality was assessed using the Shapiro-Wilk test and statistical comparisons were made using t-tests or Mann-Whitney U tests for continuous variables and chi-square tests for categorical variables. Multivariable logistic regression and Benjamini-Hochberg false-discovery-rate (FDR) correction were applied.
Chest pain was more frequent in STEMI (28/30 [93.3%] vs 15/30 [50.0%]; p = 0.0006) with higher prevalence of diabetes mellitus (24/30 [80.0%] vs 6/30 [20.0%]; p < 0.0001), worse lipid profile and increased inflammation (CRP 126.48 [44.63 - 169.75] mg/L vs 15.98 [3.75 - 39.49] mg/L; p = 0.0001). Cytokine analysis revealed significantly higher levels of IL-6, IL-8, IL-1β, IL-18, and M-CSF in STEMI after FDR correction (all FDR < 0.05). These differences persisted in non-diabetic sensitivity analysis and after multivariable adjustment for diabetes, HbA1c and CRP. The composite cytokine panel showed modest discriminatory capacity (AUC 0.69, 95% CI 0.55 - 0.83).
STEMI is characterized by greater inflammation, dyslipidemia and diabetes burden compared to NSTE-ACS. These differences persist after sensitivity analysis, multivariable adjustment and FDR correction revealing distinct inflammatory profiles that support the hypothesis of subtype-specific immune activation and pathways.
An exploratory study was conducted on 60 ACS patients (30 STEMI, 30 NSTE-ACS) experiencing their first episode. Clinical characteristics, routine laboratory parameters and multiplex cytokine analysis (GM-CSF, IFN-γ, IL-1β, IL-4, IL-6, IL-8, IL-9, IL-10, IL-12P70, IL-18, MCP-1, M-CSF, TNF-α) were compared. Normality was assessed using the Shapiro-Wilk test and statistical comparisons were made using t-tests or Mann-Whitney U tests for continuous variables and chi-square tests for categorical variables. Multivariable logistic regression and Benjamini-Hochberg false-discovery-rate (FDR) correction were applied.
Chest pain was more frequent in STEMI (28/30 [93.3%] vs 15/30 [50.0%]; p = 0.0006) with higher prevalence of diabetes mellitus (24/30 [80.0%] vs 6/30 [20.0%]; p < 0.0001), worse lipid profile and increased inflammation (CRP 126.48 [44.63 - 169.75] mg/L vs 15.98 [3.75 - 39.49] mg/L; p = 0.0001). Cytokine analysis revealed significantly higher levels of IL-6, IL-8, IL-1β, IL-18, and M-CSF in STEMI after FDR correction (all FDR < 0.05). These differences persisted in non-diabetic sensitivity analysis and after multivariable adjustment for diabetes, HbA1c and CRP. The composite cytokine panel showed modest discriminatory capacity (AUC 0.69, 95% CI 0.55 - 0.83).
STEMI is characterized by greater inflammation, dyslipidemia and diabetes burden compared to NSTE-ACS. These differences persist after sensitivity analysis, multivariable adjustment and FDR correction revealing distinct inflammatory profiles that support the hypothesis of subtype-specific immune activation and pathways.
Authors
Mittal Mittal, Singhal Singhal, Batta Batta, Mehrotra Mehrotra, Sharma Sharma
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