Reduction in the incidence of myocardial infarction in patients with rheumatoid arthritis who respond to anti-tumor necrosis factor alpha therapy: results from the British Society for Rheumatology Biologics Register.
Reduction in the incidence of myocardial infarction in patients with rheumatoid arthritis who respond to anti-tumor necrosis factor alpha therapy: results from the British Society for Rheumatology Biologics Register.
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DOI：
10.1002/art.22809
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发表时间：
2007-09
影响因子：
--
通讯作者：
Symmons, D P M
中科院分区：
文献类型：
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作者：
Dixon, W G;Watson, K D;Lunt, M;Hyrich, K L;Silman, A J;Symmons, D P M
风湿性关节炎（RA）与冠状动脉疾病的风险增加有关，可能通过共同的炎症机制起作用。本研究旨在验证抗肿瘤坏死因子α（anti-TNFα）治疗RA患者的强大抗肿瘤作用可能导致心肌梗死（MI）发生率降低的假设。我们使用英国风湿病学会生物制剂登记处（一项全国性前瞻性观察性研究）的数据，比较了8,670例接受抗TNF α治疗的RA患者和2,170例接受传统疾病缓解抗风湿药物（DMARD）治疗的活动性RA患者的MI发生率。截至2006年7月，抗TNF α队列在13，233人-年随访期间发生了63起MI，DMARD队列在2，893人-年随访期间发生了17起MI，相当于发生率分别为4.8起事件/1，000人-年和5.9起事件/1，000人-年。校正基线风险因素后，与DMARD队列相比，抗TNF α队列的MI发生率未降低（发生率比1.44 [95%置信区间0.56-3.67]）。在对6个月内对治疗有应答的抗TNF α治疗患者与无应答患者的分析中，发现应答者的MI发生率为3.5起事件/1，000人-年，无应答者为9.4起事件/1，000人-年。应答者与非应答者的校正发生率比（95%置信区间）为0.36（0.19-0.69）。这些结果表明，与接受传统DMARD治疗的RA患者相比，接受抗TNF α治疗的RA患者的MI发生率并不低。然而，与无应答者相比，抗TNF α治疗6个月后有应答者的MI风险显著降低。这一发现支持了炎症在MI中起关键作用的观点。
Rheumatoid arthritis (RA) is associated with an increased risk of coronary artery disease, possibly acting via shared mechanisms of inflammation. This study was undertaken to test the hypothesis that the powerful antiinflammatory effect of anti–tumor necrosis α (anti-TNFα) therapy might lead to a reduction in the incidence of myocardial infarction (MI) in patients with RA. Using data from the British Society for Rheumatology Biologics Register, a national prospective observational study, we compared MI rates in 8,670 patients with RA treated with anti-TNFα and 2,170 patients with active RA treated with traditional disease-modifying antirheumatic drugs (DMARDs). Through July 2006, 63 MIs occurred in the anti-TNFα cohort during 13,233 person-years of followup and 17 MIs occurred in the DMARD cohort during 2,893 person-years of followup, equivalent to a rate of 4.8 events per 1,000 person-years and 5.9 events per 1,000 person-years, respectively. After adjustment for baseline risk factors, there was no reduction in the rate of MI in the anti-TNFα cohort compared with the DMARD cohort (incidence rate ratio 1.44 [95% confidence interval 0.56–3.67]). In an analysis of anti-TNFα–treated patients who responded to the treatment within 6 months versus those who did not, MI rates were found to be 3.5 events per 1,000 person-years in responders and 9.4 events per 1,000 person-years in nonresponders. The adjusted incidence rate ratio (95% confidence interval) for responders compared with nonresponders was 0.36 (0.19–0.69). These results indicate that RA patients treated with anti-TNFα do not have a lower incidence of MI compared with RA patients treated with traditional DMARDs. However, the risk of MI is markedly reduced in those who respond to anti-TNFα therapy by 6 months compared with nonresponders. This finding supports the notion that inflammation plays a pivotal role in MI.