Outcome of clinical and subclinical myocardial injury in systemic lupus erythematosus - A prospective cohort study
Outcome of clinical and subclinical myocardial injury in systemic lupus erythematosus - A prospective cohort study
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DOI：
10.1177/0961203320976960
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发表时间：
2021-02-01
期刊：
影响因子：
2.6
通讯作者：
Doubell, Anton F.
中科院分区：
文献类型：
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作者：
du Toit, Riette;Herbst, Phillip G.;Doubell, Anton F.
目的了解亚临床狼疮性心肌炎(LM)患者12个月内的病死率、临床LM发生率和影像参数(超声心动图和心脏磁共振(CMR))的变化。目的探讨免疫抑制对心肌组织损伤CMR证据的影响。方法根据2009年Lake Louise标准，对有和无CMR证据的系统性红斑狼疮患者进行研究。基线分析和随访包括：临床评估、实验室和影像分析(超声心动图和CMR)。临床肌萎缩侧索硬化症被定义为有超声心动图和/或生化证据支持的肌萎缩侧索硬化的临床特征。亚临床LM定义为无临床LM的CMR心肌损伤。结果纳入49例SLE患者，36例获得12个月的随访分析。25名患者(51%)在与系统性红斑狼疮相关的适应症随访期间接受了强化免疫抑制治疗。疾病活跃度(SLEDAI-2K)从13(中位数；智商：9-20)提高到7(3-11)(p<；0.001)。1例无心肌损伤初步CMR证据的患者发展为临床心肌梗死。有和无CMR心肌损伤的患者死亡率(n=10)和SLE临床特征相似。超声心动图左室射血分数(p=0.014)、右室功能(p=0.001)和室壁运动异常(p=0.056)显著改善，但应变分析和左室内径指数均无明显改善。心肌质量指数(p=0.011)和左心室射血分数(p<；0.001)随随访而改善，但识别心肌组织损伤(LLC)的参数未见改善。CMR标准的减少趋势被患者的持续性(n=7)/新标准的发展(n=11)所抵消。CMR质量指数的改变与T2加权信号的改变(心肌水肿)相关(r=386；p=0.024)。加强免疫抑制治疗对CMR参数无明显影响。结论尽管SLEDAI-2K、血清标志物、心功能和CMR质量指数有所改善，但亚临床LM的CMR证据仍然存在。亚临床LM没有进展到临床LM，并且在12个月内没有显著的预后意义。免疫抑制治疗对心肌组织损伤的CMR证据没有任何显著影响。CMR质量指数的改善与心肌水肿的减轻相关，可用于监测SLE心肌损伤。
ObjectivesTo determine the outcome of subclinical lupus myocarditis (LM) over twelve months with regards to: mortality; incidence of clinical LM and change in imaging parameters (echocardiography and cardiac magnetic resonance [CMR]). To evaluate the impact of immunosuppression on CMR evidence of myocardial tissue injury.MethodsSLE patients with and without CMR evidence of myocardial injury (as per 2009 Lake Louise criteria [LLC]) were included. Analysis at baseline and follow-up included: clinical evaluation, laboratory and imaging analyses (echocardiography and CMR). Clinical LM was defined as clinical features of LM supported by echocardiographic and/or biochemical evidence of myocardial dysfunction. Subclinical LM was defined as CMR myocardial injury without clinical LM.ResultsForty-nine SLE patients were included with follow-up analyses (after 12 months) available in 36 patients. Twenty-five patients (51%) received intensified immunosuppressive therapy during follow-up for indications related to SLE. Disease activity (SLEDAI-2K) improved (p < 0.001) from 13 (median;IQR:9-20) to 7 (3-11). One patient without initial CMR evidence of myocardial injury developed clinical LM. Mortality (n = 10) and SLE clinical features were similar between patients with and without initial CMR myocardial injury. Echocardiographic left ventricular ejection fraction (LVEF) (p = 0.014), right ventricular function (p = 0.001) and wall motion abnormalities (p = 0.056) improved significantly but not strain analyses nor the left LV internal diameter index. CMR mass index (p = 0.011) and LVEF (p < 0.001) improved with follow-up but not parameters identifying myocardial tissue injury (LLC). A trend towards a reduction in the presence of CMR criteria was counterbalanced by persistence (n = 7) /development of new criteria (n = 11) in patients. Change in CMR mass index correlated with change in T2-weighted signal (myocardial oedema) (r = 386;p = 0.024). Intensified immunosuppressive therapy had no significant effect on CMR parameters.ConclusionCMR evidence of subclinical LM persisted despite improved SLEDAI-2K, serological markers, cardiac function and CMR mass index. Subclinical LM did not progress to clinical LM and had no significant prognostic implications over 12 months. Immunosuppressive therapy did not have any significant effect on the presence of CMR evidence of myocardial tissue injury. Improvement in CMR mass index correlated with reduction in myocardial oedema and may be used to monitor SLE myocardial injury.