Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.
Division of Cardiology, Department of Internal Medicine, National Taiwan University Hospital Yun-Lin, Yun-Lin, Taiwan.
J Thromb Haemost. 2017 Aug;15(8):1541-1546. doi: 10.1111/jth.13735. Epub 2017 Jul 14.
Essentials We studied the C-reactive protein (CRP) gene on stroke risk in atrial fibrillation (AF) patients. 725 patients with CRP triallelic polymorphism genotype were followed-up for more than 10 years. Patients with the A-390/T-390 allele of the CRP gene were more likely to get ischemic stroke. The triallelic polymorphism of the CRP is related to ischemic stroke in AF patients.
Background Little evidence is available regarding the impact of genetic polymorphisms on the risk of thromboembolic stroke in patients with atrial fibrillation (AF). An increasing body of evidence is demonstrating that inflammatory responses play an important role in the pathophysiology of AF. Objectives To investigate the effect of genetic polymorphisms of the C-reactive protein (CRP) gene on the incidence of thromboembolic stroke in patients with AF. Methods A total of 725 AF patients were longitudinally followed up for > 10 years; this is the largest and longest AF follow-up cohort with genetic data. CRP promoter triallelic polymorphisms (C-390A and C-390T) were genotyped, and CRP levels were divided into four quartiles. Results Patients with higher CRP levels were more likely to develop thromboembolic stroke than those with lower CRP levels (P<0.001, log-rank test for comparison of four quartiles). After adjustment for conventional risk factors, patients with higher CRP levels were more likely to develop thromboembolic stroke than those in the lowest CRP quartile (hazard ratio [HR] 2.27, 95% confidence interval [CI] 1.08-4.81; the lowest CRP quartile was the reference group). Patients carrying the A-390 or T-390 allele had higher CRP levels (3.35 ± 2.71 mg L versus 2.43 ± 2.00 mg L ), and were more likely to develop thromboembolic stroke, even after adjustment for conventional risk factors (HR 2.07, 95% CI 1.23-3.48). Conclusion The CRP triallelic polymorphism and the CRP level are associated with the risk of incident thromboembolic stroke in patients with AF.
关于遗传多态性对房颤（AF）患者血栓栓塞性卒中风险的影响，目前仅有少量证据。越来越多的证据表明，炎症反应在 AF 的病理生理学中起着重要作用。目的：研究 C 反应蛋白（CRP）基因的遗传多态性对 AF 患者血栓栓塞性卒中发生率的影响。方法：共对 725 例 AF 患者进行了 >10 年的纵向随访；这是最大和最长的具有遗传数据的 AF 随访队列。对 CRP 启动子三核苷酸多态性（C-390A 和 C-390T）进行了基因分型，并将 CRP 水平分为四等份。结果：CRP 水平较高的患者发生血栓栓塞性卒中的可能性高于 CRP 水平较低的患者（P<0.001，对数秩检验比较四等份）。在调整了常规危险因素后，CRP 水平较高的患者发生血栓栓塞性卒中的可能性高于 CRP 水平最低四分位数的患者（危险比 [HR]2.27，95%置信区间 [CI]1.08-4.81；最低 CRP 四分位数为参考组）。携带 A-390 或 T-390 等位基因的患者 CRP 水平较高（3.35±2.71mg/L 比 2.43±2.00mg/L），且即使在调整了常规危险因素后，发生血栓栓塞性卒中的可能性也更高（HR 2.07，95%CI 1.23-3.48）。结论：CRP 三核苷酸多态性和 CRP 水平与 AF 患者发生首发血栓栓塞性卒中的风险相关。
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