OBJECTIVE To explore incidence and progression of coronary atherosclerosis and identify determinants in patients with rheumatoid arthritis (RA). We specifically evaluated the impact of inflammation, cardiac risk factors, duration of medication exposure, and their interactions on coronary plaque progression. METHODS One hundred one participants with baseline coronary computed tomography angiography findings underwent follow-up assessment a mean ± SD of 83 ± 3.6 months after baseline. Plaque burden was reported as the segment involvement score (describing the number of coronary segments with plaque) and the segment stenosis score (characterizing the cumulative plaque stenosis over all evaluable segments). Plaque composition was classified as noncalcified, mixed, or calcified. Coronary artery calcium (CAC) was quantified using the Agatston method. RESULTS Total plaque increased in 48% of patients, and progression was predicted by older age, higher cumulative inflammation, and total prednisone dose (P < 0.05). CAC progressors were older, more obese, hypertensive, and had higher cumulative inflammation compared to nonprogressors (P < 0.05). Longer exposure to biologics was associated with lower likelihood of noncalcified plaque progression, lesion remodeling, and constrained CAC change in patients without baseline calcification, independent of inflammation, prednisone dose, or statin exposure (all P < 0.05). Longer statin treatment further restricted noncalcified plaque progression and attenuated the effect of inflammation on increased plaque and CAC (P < 0.05). Stringent systolic blood pressure (BP) control further weakened the effect of inflammation on total plaque progression. CONCLUSION Inflammation was a consistent and independent predictor of coronary atherosclerosis progression in RA. It should therefore be specifically targeted toward mitigating cardiovascular risk. Biologic disease-modifying antirheumatic drugs, statins, and BP control may further constrain plaque progression directly or indirectly.

中文翻译：

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累积炎症，心脏危险因素和药物暴露对类风湿关节炎冠状动脉粥样硬化进展的影响。

目的探讨类风湿关节炎（RA）患者的冠状动脉粥样硬化的发生率和进展，并确定其决定因素。我们专门评估了炎症，心脏危险因素，药物暴露持续时间及其相互作用对冠状动脉斑块进展的影响。方法一百零一例具有基线冠状动脉计算机断层扫描血管造影结果的参与者接受了随访评估，基线后的平均±SD为83±3.6个月。斑块负荷报告为节段受累评分（描述冠状动脉斑块的数量）和节段狭窄评分（表征所有可评估节段的累积斑块狭窄）。牙菌斑组成分类为未钙化，混合或钙化。使用Agatston方法定量冠状动脉钙（CAC）。结果48％的患者总斑块增加，其进展由年龄大，累积炎症增加和泼尼松总剂量预测（P <0.05）。与非进展者相比，CAC进展者年龄更大，肥胖，高血压且累积炎症更高（P <0.05）。在没有基线钙化的患者中，更长的生物制剂暴露时间与未钙化斑块进展，病变重塑和受约束的CAC变化的可能性较低相关，而与炎症，泼尼松剂量或他汀类药物暴露无关（所有P <0.05）。他汀类药物的长期治疗进一步限制了非钙化斑块的进程，并减弱了炎症对斑块和CAC升高的影响（P <0.05）。严格的收缩压（BP）控制进一步减弱了炎症对总斑块进展的影响。结论炎症是RA中冠状动脉粥样硬化进展的一致且独立的预测因子。因此，它应专门针对减轻心血管疾病的风险。改善生物疾病的抗风湿药，他汀类药物和BP控制可能会进一步直接或间接限制斑块进展。