Letter: Comment on STEMI Inflammatory Index: Toward Actionable Risk Stratification

Dear Editor,

We read with great interest the article by Can et al, which evaluated the inflammatory prognostic index (IPI) for predicting contrast-induced nephropathy (CIN) after primary percutaneous coronary intervention (pPCI) in patients with ST-segment elevation myocardial infarction (STEMI). This work is clinically timely. CIN occurred in 15.1% of the cohort; admission IPI remained independently associated with CIN, and its discriminative performance exceeded those of the neutrophil-to-lymphocyte ratio, C-reactive protein-to-albumin ratio, and systemic immune-inflammation index. These findings provide useful evidence that systemic inflammation contributes to renal vulnerability in the acute coronary intervention setting. ¹

An issue merits further consideration. In routine practice, CIN risk after PCI is influenced by age, renal function, diabetes, hemodynamic status, left ventricular ejection fraction, anemia, and procedural complexity.^2,3 Thus, the key clinical question is not simply whether IPI is associated with CIN, but whether it improves risk classification beyond established practical variables. The classic and contemporary Mehran scores were designed to translate such variables into practical risk estimates. Comparing a clinical model alone with the same model plus IPI would clarify any incremental value of this biomarker.^2,3

Similarly, calibration, reclassification indices, and decision curve analysis would strengthen the interpretation. Although a greater area under the curve is encouraging, it does not necessarily mean that a marker will improve bedside decision making. Decision curve analysis could test whether an IPI-guided strategy provides net benefit across clinically plausible thresholds for preventive measures, like intensifying hydration, limiting contrast volume, avoiding nephrotoxic drugs, or monitoring renal function more closely. Such evidence would be particularly useful before recommending IPI for routine risk prediction.^4,5

A second consideration concerns the proposed IPI cut-off of 8.35. This threshold is derived from C-reactive protein, albumin, neutrophil count, and lymphocyte count, all of which may vary by assay platform, sampling time, infarct-related stress, intercurrent infection, and nutritional status. Modeling IPI as a continuous variable, or using restricted cubic splines, could help determine whether the relationship with CIN is linear or threshold dependent. Such modeling may also reduce the risk of overinterpreting a single cut-off before external validation.

Overall, Can et al ¹ provide an important contribution by identifying IPI as an accessible inflammatory marker in a high-risk STEMI population. Future studies demonstrating improved calibration, incremental risk stratification, and clinical net benefit would help move IPI from a statistically robust association toward actionable bedside use.

Kaiwen GeAffiliated Hospital of Nanjing University of Chinese Medicine (Jiangsu Province Hospital of Chinese Medicine), Jiangsu, China Yonggang He, BSDepartment of Critical Care Medicine, Zhejiang University Mingzhou Hospital (Zhejiang University Mingzhou Hospital), Ningbo, Zhejiang, China