Interleukin-34 as a Robust Predictor of No-Reflow Phenomenon in ST-Elevation Myocardial Infarction: Insights into Inflammatory Mechanisms and Clinical Implications
Objective: 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...
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| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
Galenos Publishing House
2024-10-01
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| Series: | Gazi Medical Journal |
| Subjects: | |
| Online Access: | https://gazimedj.com/articles/interleukin-34-as-a-robust-predictor-of-no-reflow-phenomenon-in-st-elevation-myocardial-infarction-insights-into-inflammatory-mechanisms-and-clinical-implications/doi/gmj.2024.4054 |
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| Summary: | Objective: 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 patients with STEMI (32 with no-reflow, 150 without) and 100 controls. Clinical and angiographic data were analyzed, and IL-34 levels were measured. Logistic regression and receiver operating characteristic (ROC) analysis assessed IL-34’s predictive value for no-reflow.
Results: Patients with no reflow exhibited elevated IL-34 levels compared with controls and those without no-reflow. Logistic regression identified IL-34 as an independent predictor of no-reflow (odds ratio: 1,020, p<0.001). ROC analysis showed IL-34’s significant predictive value (area under the curve: 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. These findings suggest 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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| ISSN: | 2147-2092 |