Interleukin-34 as a Robust Predictor of No-Reflow Phenomenon in ST-Elevation Myocardial Infarction: Insights into Inflammatory Mechanisms and Clinical Implications

IL-34 to Predict NRP

Authors

  • Mehdi Karasu Department of Cardiology, Elazığ Fethi Sekin City Hospital, Türkiye
  • Hasan Ata Bolayır Department of Cardiology, Malatya Turgut Özal University Faculty of Medicine, Malatya, Türkiye
  • İbrahim Aktaş Department of Cardiology, Malatya Turgut Özal University Faculty of Medicine, Malatya, Türkiye

Keywords:

İnterleukin-34, ST-elevation myocardial infarction, No-reflow phenomenon

Abstract

Background: ST-elevation myocardial infarction (STEMI) poses a significant challenge despite advances in reperfusion strategies. The "no-reflow" phenomenon, characterized by inadequate microvascular blood flow restoration following successful revascularization, remains poorly understood. Inflammation, particularly interleukin-34 (IL-34), is implicated in cardiovascular disease, prompting investigation into its role in no-reflow.

Methods: This observational study included 182 STEMI patients (32 with no-reflow, 150 without) and 100 controls. Clinical and angiographic data were analyzed, and IL-34 levels were measured. Logistic regression and ROC analysis assessed IL-34's predictive value for no-reflow.

Results: Patients with no-reflow exhibited elevated IL-34 levels compared to controls and those without no-reflow. Logistic regression identified IL-34 as an independent predictor of no-reflow (OR = 1.020, p < 0.001). ROC analysis showed IL-34's significant predictive value (AUC = 0.972, p < 0.001).

Conclusion: IL-34 emerges as a robust predictor of no-reflow in STEMI, potentially reflecting its role in macrophage activation and the inflammatory response. This finding suggests a novel avenue for understanding and mitigating no-reflow in STEMI, paving the way for targeted therapies. Early identification of high-risk patients could inform tailored interventions, ultimately improving STEMI outcomes. Further research is warranted to elucidate IL-34's mechanistic involvement and validate its predictive value in larger cohorts.

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Published

11.10.2024

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Section

Original Research