Schwartz Thomas, Sjaastad Ivar, Flatø Berit, Vistnes Maria, Christensen Geir, Sanner Helga
Institute for Experimental Medical Research, Oslo University Hospital-Ullevål, KG Jebsen Cardiac Research Center and Center for Heart Failure Research, Institute for Clinical Medicine, University of Oslo, Department of Cardiology, Oslo University Hospital-Ullevål and Section of Rheumatology, Oslo University Hospital-Rikshospitalet, Oslo, Norway Institute for Experimental Medical Research, Oslo University Hospital-Ullevål, KG Jebsen Cardiac Research Center and Center for Heart Failure Research, Institute for Clinical Medicine, University of Oslo, Department of Cardiology, Oslo University Hospital-Ullevål and Section of Rheumatology, Oslo University Hospital-Rikshospitalet, Oslo, Norway Institute for Experimental Medical Research, Oslo University Hospital-Ullevål, KG Jebsen Cardiac Research Center and Center for Heart Failure Research, Institute for Clinical Medicine, University of Oslo, Department of Cardiology, Oslo University Hospital-Ullevål and Section of Rheumatology, Oslo University Hospital-Rikshospitalet, Oslo, Norway
Institute for Experimental Medical Research, Oslo University Hospital-Ullevål, KG Jebsen Cardiac Research Center and Center for Heart Failure Research, Institute for Clinical Medicine, University of Oslo, Department of Cardiology, Oslo University Hospital-Ullevål and Section of Rheumatology, Oslo University Hospital-Rikshospitalet, Oslo, Norway Institute for Experimental Medical Research, Oslo University Hospital-Ullevål, KG Jebsen Cardiac Research Center and Center for Heart Failure Research, Institute for Clinical Medicine, University of Oslo, Department of Cardiology, Oslo University Hospital-Ullevål and Section of Rheumatology, Oslo University Hospital-Rikshospitalet, Oslo, Norway Institute for Experimental Medical Research, Oslo University Hospital-Ullevål, KG Jebsen Cardiac Research Center and Center for Heart Failure Research, Institute for Clinical Medicine, University of Oslo, Department of Cardiology, Oslo University Hospital-Ullevål and Section of Rheumatology, Oslo University Hospital-Rikshospitalet, Oslo, Norway Institute for Experimental Medical Research, Oslo University Hospital-Ullevål, KG Jebsen Cardiac Research Center and Center for Heart Failure Research, Institute for Clinical Medicine, University of Oslo, Department of Cardiology, Oslo University Hospital-Ullevål and Section of Rheumatology, Oslo University Hospital-Rikshospitalet, Oslo, Norway.
Rheumatology (Oxford). 2014 Dec;53(12):2214-22. doi: 10.1093/rheumatology/keu256. Epub 2014 Jul 4.
The aim of this study was to examine the influence of chemokines and lipids on cardiac function in patients with active and inactive JDM and matched controls.
Fifty-four JDM patients were clinically examined a median 16.8 years (range 2-38) after disease onset and compared with 54 sex- and age-matched controls. Inactive disease was defined by the PRINTO criteria. Serum levels of chemokines were analysed by Luminex technology. Echocardiography was performed and analysed blinded to patient information. Long-axis strain and e' were used as parameters of systolic and diastolic function, respectively.
In patients, but not in controls, eotaxin and monocyte chemoattractant protein 1 (MCP-1) correlated with systolic (r = -0.65 and r = -0.45) and diastolic (r = -0.59 and r = -0.65) function, particularly in those with active disease (systolic function, r = -0.74 and r = -0.60; diastolic function, r = -0.69 and r = -0.80). Total cholesterol level was lower in patients than controls [mean 4.19 mmol/l (s.d. 0.82) vs 4.60 (0.87), P ≤ 0.01]. However, total cholesterol levels in the upper normal range were associated with systolic (r = -0.56, P < 0.01) and diastolic (r = -0.64, P < 0.001) dysfunction and with high eotaxin and MCP-1 (r = 0.56 and r = 0.50, P < 0.01) in patients with active disease, but not in those with inactive disease or in controls (all r < ±0.2).
In the active disease state of JDM, eotaxin and MCP-1 were associated with cardiac dysfunction, possibly through sustained inflammation. In those with active disease and cholesterol levels in the upper normal range, eotaxin and MCP-1 might enhance susceptibility to cardiac dysfunction.
本研究旨在探讨趋化因子和脂质对活动期和非活动期皮肌炎(JDM)患者及匹配对照组心脏功能的影响。
54例JDM患者在疾病发作后中位时间16.8年(范围2 - 38年)接受临床检查,并与54例性别和年龄匹配的对照组进行比较。非活动期疾病根据PRINTO标准定义。采用Luminex技术分析趋化因子的血清水平。进行超声心动图检查并在对患者信息不知情的情况下进行分析。分别采用长轴应变和e'作为收缩和舒张功能的参数。
在患者中,而非对照组中,嗜酸性粒细胞趋化因子和单核细胞趋化蛋白1(MCP - 1)与收缩功能(r = -0.65和r = -0.45)及舒张功能(r = -0.59和r = -0.65)相关,尤其在活动期疾病患者中(收缩功能,r = -0.74和r = -0.60;舒张功能,r = -0.69和r = -0.80)。患者的总胆固醇水平低于对照组[平均4.19 mmol/l(标准差0.82)对4.60(0.87),P≤0.01]。然而,在正常范围上限的总胆固醇水平与活动期疾病患者的收缩功能(r = -0.56,P < 0.01)和舒张功能(r = -0.64,P < 0.001)以及高嗜酸性粒细胞趋化因子和MCP - 1(r = 0.56和r = 0.50,P < 0.01)相关,但在非活动期疾病患者或对照组中则不然(所有r < ±0.2)。
在JDM的活动期疾病状态下,嗜酸性粒细胞趋化因子和MCP - 1可能通过持续炎症与心脏功能障碍相关。在活动期疾病且胆固醇水平在正常范围上限的患者中,嗜酸性粒细胞趋化因子和MCP - 1可能会增加心脏功能障碍的易感性。