Zhong Shan, Wang Siqi, Zhao Peng, Piao Minghui, Jin Cheng, Tian Jinwei
Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin, 150086, China.
Heilongjiang Provincial Key Laboratory of Panvascular Disease, Harbin, China.
Cardiovasc Toxicol. 2025 Apr 17. doi: 10.1007/s12012-025-10000-y.
Despite advances in anti-atherosclerotic therapies, residual risk persists in coronary artery disease (CAD). The uric acid to high-density lipoprotein cholesterol ratio (UHR), a metabolic-inflammatory marker, may predict residual risk, but its association with plaque progression remains unexplored. This study investigates the impact of UHR on atherosclerotic plaque burden in CAD patients after treatment. In this prospective cohort study, 118 patients with newly diagnosed CAD undergoing percutaneous coronary intervention were stratified into quartiles by baseline UHR. Intravascular ultrasound assessed plaque burden and characteristics at baseline and 12-month follow-up. Logistic regression and restricted cubic spline models evaluated associations between UHR and plaque progression, adjusting for cardiovascular risk factors. At baseline, the highest UHR quartile (UHR-4) exhibited higher rates of plaque rupture (19.6% vs. 0-8.7%, P = 0.002) and microchannels (56.5% vs. 33.3-55.3%, P = 0.031) compared to lower quartiles. Baseline percent atheroma volume (PAV) was greater in UHR-4 (52.73% vs. 51.04-52.09%, P = 0.006). At follow-up, UHR-4 had a 3.2-fold increased risk of plaque burden > 70% (adjusted RR 3.237, 95% CI 1.156-9.063, P = 0.025), with a linear UHR-plaque burden relationship (P = 0.015). No associations were observed between UHR and minimal lumen area or positive remodeling. Elevated UHR is independently associated with high atherosclerotic plaque burden (> 70%) in CAD patients under guideline-directed therapy after adjusting for traditional risk factors. UHR may serve as a complementary biomarker to existing risk scores, guiding targeted therapies to mitigate plaque vulnerability.
尽管抗动脉粥样硬化治疗取得了进展，但冠状动脉疾病（CAD）患者仍存在残余风险。尿酸与高密度脂蛋白胆固醇比值（UHR）作为一种代谢炎症标志物，可能预测残余风险，但其与斑块进展的关联仍未得到探索。本研究调查了UHR对CAD患者治疗后动脉粥样硬化斑块负荷的影响。在这项前瞻性队列研究中，118例新诊断为CAD并接受经皮冠状动脉介入治疗的患者按基线UHR分层为四分位数。血管内超声评估了基线和12个月随访时的斑块负荷及特征。逻辑回归和受限立方样条模型评估了UHR与斑块进展之间的关联，并对心血管危险因素进行了校正。在基线时，与较低四分位数相比，最高UHR四分位数（UHR-4）的斑块破裂率（19.6%对0-8.7%，P = 0.002）和微通道率（56.5%对33.3-55.3%，P = 0.031）更高。UHR-4的基线粥样斑块体积百分比（PAV）更大（52.73%对51.04-52.09%，P = 0.006）。在随访时，UHR-4斑块负荷>70%的风险增加了3.2倍（校正RR 3.237，95%CI 1.156-9.063，P = 0.025），存在UHR与斑块负荷的线性关系（P = 0.015）。未观察到UHR与最小管腔面积或正向重构之间的关联。在调整传统危险因素后，UHR升高与接受指南指导治疗的CAD患者中高动脉粥样硬化斑块负荷（>70%）独立相关。UHR可作为现有风险评分的补充生物标志物，指导靶向治疗以降低斑块易损性。
