Inflamatory index in patients with ST-elevation myocardial infarction: a new pronostic tool for cardiogenic shock

Inflammation plays a significant role in the pathophysiology of cardiovascular diseases, particularly in myocardial infarction; the inflammatory indices have emerged as a potential cost-effective prognostic tool.

Determine that the inflammatory index provided a new tool for the initial evaluation of patients at high risk of developing cardiogenic shock.

We conducted a prospective cohort study at a tertiary care center in our city, including patients above 18 years who presented in 2025 with STEMI and had a complete initial blood count. Exclusion criteria were: other acute diagnoses, malignancy, autoimmune disease, recent infection, or hematologic malignancies such as leukemia. We calculated inflammatory indices, including neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), pan-inflammatory value (PIV), systemic inflammatory index (SII), and systemic inflammatory response index (SIRI). In-hospital outcomes collected included cardiogenic shock and mortality.

A total of 400 patients were included; 84% were male, with a mean age of 60.9 years. Hypertension was present in 51.8% of cases, and cardiogenic shock (CS) occurred in 6% (n = 24). Patients who developed CS exhibited significantly higher inflammatory indices compared with those without CS (p < 0.05 for all). Mean NLR and SII values were markedly elevated in the CS group (8.8 ± 4.2 vs 6.6 ± 5.3, p = 0.001; 2303 ± 1291 vs 1652 ± 1481, p = 0.01, respectively). Similarly, PLR (203 ± 89 vs 167 ± 95, p = 0.02), SIRI (7.1 ± 5.0 vs 5.1 ± 5.3, p = 0.03), and PIV (6.2 ± 5.4 vs 4.5 ± 4.9, p = 0.04) were higher among shock patients. In ROC analysis, NLR and SII demonstrated the best discriminative performance for predicting CS. NLR showed an AUC of 0.69 (95% CI 0.61–0.79). The optimal cutoff by Youden’s index was 4.6, yielding 91% sensitivity and 45% specificity, while a balanced threshold of 7.1 achieved 65% sensitivity and 69% specificity. SII exhibited a similar AUC of 0.70 (95% CI 0.60–0.79), with an optimal cutoff value of 1479, corresponding to 83% sensitivity and 61% specificity. In multivariable analysis, both indices remained independently associated with CS after adjustment for confounding factors. No significant differences were observed in in-hospital mortality between groups.

Inflammatory indices derived from routine blood counts are significantly associated with the development of cardiogenic shock in ACS. Despite their simplicity, these biomarkers demonstrated acceptable discriminative performance and may serve as early, cost-effective tools for bedside risk stratification and clinical decision support.

ROC Curves for Cardiogenic Shock