University of Oxford Centre for Clinical Magnetic Resonance Research (OCMR), Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, Oxford, UK; Division of Cardiology, Department of Medicine, Groote Schuur Hospital, Cape Town, South Africa.
University of Oxford Centre for Clinical Magnetic Resonance Research (OCMR), Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, Oxford, UK.
Int J Cardiol. 2018 Nov 1;270:253-259. doi: 10.1016/j.ijcard.2018.06.099. Epub 2018 Jun 25.
Rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA) are common disorders associated with increased rates of cardiovascular disease (CVD), but the contribution of cytokine-induced inflammation to impaired cardiovascular function in these conditions remains poorly understood.
We assessed the effect of anti-TNF therapy on myocardial and vascular function, myocardial tissue characteristics and perfusion in inflammatory arthropathy and systemic rheumatic disease (IASRD) patients, using cardiovascular magnetic resonance (CMR).
20 RA patients, 7 AS patients, 5 PsA patients without previously known CVD scheduled to commence anti-TNF therapy and 8 RA patients on standard disease modifying antirheumatic drugs underwent CMR at 1.5 T, including cine, tagging, pulse wave velocity (PWV), T2-weighted, native and postcontrast T1 mapping, ECV quantification, rest and stress perfusion and late gadolinium enhancement (LGE) imaging.
Following anti-TNF therapy, there was significant reversal of baseline subclinical cardiovascular dysfunction, as evidenced by improvement in peak systolic circumferential strain (p < 0.001), peak diastolic circumferential strain rate (p < 0.001), and total aortic PWV, (p < 0.001). This was accompanied by a reduction in myocardial inflammation, as assessed by T2-weighted imaging (p = 0.005), native T1 mapping (p = 0.009) and ECV quantification (p = 0.001), as well as in serum inflammatory markers like CRP (p < 0.001) and ESR (p < 0.001), and clinical measures of disease activity (DAS28-CRP, p = 0.001; BASDAI, p < 0.001). A trend towards improvement in myocardial perfusion was observed (p = 0.07). Focal myocardial fibrosis, as detected by LGE CMR was not altered by anti-TNF therapy (p = 0.92).
Anti-TNF therapy reduces subclinical myocardial inflammation and improves cardiovascular function in RA, AS and PsA. CMR may be used to track disease progression and response to therapy. Future CMR-based studies to demonstrate effect of anti-TNF therapy modulation of vascular structure and function on hard clinical events and outcomes would be useful.
类风湿关节炎（RA）、强直性脊柱炎（AS）和银屑病关节炎（PsA）是常见的与心血管疾病（CVD）发生率增加相关的疾病，但细胞因子诱导的炎症对这些疾病中心血管功能受损的影响仍知之甚少。
我们使用心血管磁共振（CMR）评估抗 TNF 治疗对炎症性关节炎和系统性风湿病（IASRD）患者心肌和血管功能、心肌组织特征和灌注的影响。
20 例 RA 患者、7 例 AS 患者、5 例无先前已知 CVD 的 PsA 患者计划开始接受抗 TNF 治疗，8 例 RA 患者接受标准疾病修饰抗风湿药物治疗，在 1.5T 上进行 CMR，包括电影、标记、脉搏波速度（PWV）、T2 加权、原始和对比后 T1 映射、ECV 定量、静息和应激灌注和晚期钆增强（LGE）成像。
抗 TNF 治疗后，基线亚临床心血管功能障碍得到显著逆转，表现为峰值收缩周向应变（p<0.001）、峰值舒张周向应变率（p<0.001）和总主动脉 PWV（p<0.001）改善。这伴随着心肌炎症的减少，通过 T2 加权成像（p=0.005）、原始 T1 映射（p=0.009）和 ECV 定量（p=0.001）评估，以及血清炎症标志物如 CRP（p<0.001）和 ESR（p<0.001），以及疾病活动的临床指标（DAS28-CRP，p=0.001；BASDAI，p<0.001）。观察到心肌灌注的改善趋势（p=0.07）。LGE CMR 检测到的局灶性心肌纤维化未因抗 TNF 治疗而改变（p=0.92）。
抗 TNF 治疗可降低 RA、AS 和 PsA 患者的亚临床心肌炎症并改善心血管功能。CMR 可用于跟踪疾病进展和治疗反应。未来基于 CMR 的研究，以证明抗 TNF 治疗对血管结构和功能的调节对硬临床事件和结局的影响将是有用的。
