医学
内科学
心脏病学
接收机工作特性
生物标志物
尿酸
心肌梗塞
曲线下面积
逻辑回归
病理生理学
溶栓
脂蛋白(a)
冠状动脉造影
冠状动脉疾病
脂蛋白
胆固醇
经皮冠状动脉介入治疗
冠状动脉
冠状动脉粥样硬化
试验预测值
预测值
动脉
甘油三酯
诊断试验中的似然比
血栓
作者
Ramazan Astan,Eyyüp Erkiz,Erdoğan İlkay
出处
期刊:PubMed
[National Institutes of Health]
日期:2026-05-14
标识
DOI:10.14744/anatoljcardiol.2026.6173
摘要
BACKGROUND: Coronary slow flow (CSF) is an angiographic finding characterized by delayed distal vessel opacification despite normal epicardial coronary arteries. Its pathophysiology is multifactorial and involves microvascular dysfunction, endothelial impairment, and chronic inflammation. The uric acid-to-high-density lipoprotein (HDL) cholesterol ratio (UHR) has recently emerged as a novel composite biomarker reflecting both pro-oxidant and anti-inflammatory balance. This study aimed to evaluate the relationship between UHR and CSF. METHODS: In this retrospective cross-sectional study, 218 patients with normal or near-normal coronary arteries on angiography were analyzed. Patients were divided into 2 groups according to the presence of CSF based on thrombolysis in myocardial infarction (TIMI) frame count. Demographic, clinical, and laboratory parameters were compared between groups. Receiver operating characteristic (ROC) analysis was used to determine the discriminatory performance of UHR, and multiple logistic regression was performed to identify independent predictors of CSF. RESULTS: The mean UHR value was significantly higher in the CSF group compared with the control group (0.13 ± 0.04 vs. 0.09 ± 0.04, P < .001). Receiver operating characteristic analysis demonstrated that a UHR cut-off >0.107 predicted CSF with moderate discriminatory ability (area under the curve (AUC) = 0.733, 95% CI: 0.66-0.79, P < .001), with 73.5% sensitivity and 76.2% specificity. Multiple analyses suggested that UHR was independently associated with CSF (OR 1.20 per 0.01-unit increase, 95% CI 1.09-1.31, P < .001). CONCLUSION: Elevated UHR was independently associated with CSF and may represent a readily available biomarker reflecting the metabolic-inflammatory balance contributing to coronary microvascular dysfunction. These findings should be interpreted as associative and hypothesis-generating.
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