1st Division of Cardiology, Division of Neurology, Azienda Ospedaliera-Universitaria "Maggiore della Carità", Eastern Piedmont University, Novara, Italy.
Nutr Metab Cardiovasc Dis. 2012 May;22(5):426-33. doi: 10.1016/j.numecd.2010.08.005. Epub 2010 Dec 24.
Hyperuricemia may be involved in the atherosclerotic process due to endothelial dysfunction and facilitation of smooth muscle cell proliferation. However, debates still exist on the independent role of hyperuricemia, due to its association with several cardiovascular risk factors, such as hypertension, hyperlipidemia, obesity and insulin resistance. Thus, the aim of the current study was to investigate in a consecutive cohort of patients undergoing coronary angiography whether hyperuricemia is associated with the extent of coronary artery disease.
Our population is represented by a total of 1901 consecutive patients undergoing coronary angiography between May 2007 and January 2010 at the Azienda Ospedaliera "Maggiore della Carità", Novara, Italy. We additionally evaluated platelet aggregation by PFA-100 (Collagen/Epinefrine) and Multiplate. Quantitative coronary angiography and analysis of IMT were performed by experienced cardiologists who had no knowledge of the patients' clinical information. Higher uric acid was associated with advanced age, larger prevalence of male gender, diabetes, renal insufficiency, hypertension, previous CABG and MI, but with a lower prevalence of family history of CAD. Patients with high uric acid were more often on calcium antagonists, ace-inhibitors, angiotensin receptor antagonists, and, as expected, on diuretics. A significant relationship was observed between uric acid and the prevalence (OR [95% CI] = 1.18 [1.04-1.32], p = 0.01) and severity of CAD (OR [95% CI] = 1.17 [1.03-1.33], p = 0.014). However, the relationship disappeared after correction for baseline confounding factors for both prevalence (OR [95% CI] = 1.06 [0.93-1.21], p = 0.35) and extent of CAD (OR [95% CI] = 1.0 [0.87-1.15], p = 0.96). No relationship was observed between acid uric and IMT (p = 0.73) analyzed in 359 consecutive patients. Finally, there was no relationship between uric acid and platelet aggregation in patients with or without aspirin therapy, as measured by PFA-100 and Multiplate.
Our study showed that uric acid is not associated with platelet aggregation, the extent of coronary artery disease and IMT. Thus, waiting for the results of additional large studies, uric acid may not be considered as a risk factor for coronary artery disease, and its reduction by specific therapies may not be recommended to prevent coronary artery disease and atherosclerosis.
高尿酸血症可能通过内皮功能障碍和促进平滑肌细胞增殖而参与动脉粥样硬化过程。然而，由于其与高血压、高血脂、肥胖和胰岛素抵抗等多种心血管危险因素相关，高尿酸血症的独立作用仍存在争议。因此，本研究旨在通过连续接受冠状动脉造影的患者队列来研究高尿酸血症与冠状动脉疾病严重程度的关系。
我们的研究人群包括 2007 年 5 月至 2010 年 1 月在意大利诺瓦拉的“Maggiore della Carità”医院接受冠状动脉造影的 1901 例连续患者。我们还通过 PFA-100（胶原/肾上腺素）和 Multiplate 评估了血小板聚集。定量冠状动脉造影和 IMT 分析由不了解患者临床信息的经验丰富的心脏病专家进行。尿酸水平较高与年龄较大、男性比例较大、糖尿病、肾功能不全、高血压、既往 CABG 和 MI 有关，但家族性 CAD 病史的发生率较低。高尿酸血症患者更常使用钙拮抗剂、ACE 抑制剂、血管紧张素受体拮抗剂，并且，如预期的那样，利尿剂的使用也更多。尿酸与 CAD 的发生率（OR[95%CI]=1.18[1.04-1.32]，p=0.01）和严重程度（OR[95%CI]=1.17[1.03-1.33]，p=0.014）呈显著正相关。然而，在对两种发生率（OR[95%CI]=1.06[0.93-1.21]，p=0.35）和 CAD 严重程度（OR[95%CI]=1.0[0.87-1.15]，p=0.96）的基线混杂因素进行校正后，这种相关性消失。在 359 例连续患者中，尿酸与 IMT 之间（p=0.73）也没有关系。最后，在有或没有阿司匹林治疗的患者中，尿酸与 PFA-100 和 Multiplate 测量的血小板聚集之间没有关系。
我们的研究表明，尿酸与血小板聚集、冠状动脉疾病严重程度和 IMT 无关。因此，在等待更多大型研究结果的同时，尿酸可能不能被视为冠状动脉疾病的危险因素，并且通过特定治疗降低尿酸可能不被推荐用于预防冠状动脉疾病和动脉粥样硬化。
