Lin Ting-Tse, Sung Yen-Ling, Wu Chih-En, Zhang Hong, Liu Yen-Bin, Lin Shien-Fong
Department of Internal Medicine, National Taiwan University Hospital Hsin-Chu Branch, Hsinchu, Taiwan.
Institute of Biomedical Engineering, National Chiao-Tung University, 1001 Ta-Hsueh Road, Hsinchu, 300, Taiwan.
BMC Musculoskelet Disord. 2016 Nov 29;17(1):491. doi: 10.1186/s12891-016-1347-6.
Patients with rheumatoid arthritis (RA) have increased risk of sudden cardiac death (SCD), which is two-fold higher than general population. The driving cause of SCD was considered due to lift-threatening arrhythmia where systemic inflammation acts as the pathophysiological basis linking RA to autonomicdysfunction.
To assess the sympathetic over-activity of "inflammatory reflex", we measured heart rate variability (HRV) in a rat collagen-induced arthritis (CIA) model, whose arthritis is induced in Lewis rats by intradermal injection of emulsion of type II collagen. Single-lead electrocardiogram (ECG) was recorded for 30 min every two days. Time and frequency-domain parameters, detrended fluctuation analysis (DFA), deceleration (DC) and acceleration capacity (AC) were analyzed.
Compared with 9 control rats, many of HRV parameters of 9 CIA rats revealed significant different. At the beginning of arthritis, LF/HF was significant higher than controls (1st week: 2.41 ± 0.7 vs. 1.76 ± 0.6, p < 0.05; 2nd week: 2.24 ± 0.5 vs. 1.58 ± 0.5, p < 0.05) indicating intensive inflammatory reflex at the initial phase of inflammation but no significant difference was observed in the following recover phase. The similar trend of DFA parameters was noted. However, the DC appeared progressive lower despite of no significant increase of the LF/HF compared with controls since 4th week.
We observed sympathetic over-activation of inflammatory reflex during early stage of arthritis in CIA rats. The ongoing decline of DC indicated advanced cardiac autonomic dysfunction regardless of remission of acute arthritis.
类风湿关节炎（RA）患者心脏性猝死（SCD）风险增加，比普通人群高出两倍。SCD的驱动原因被认为是由于危及生命的心律失常，其中全身炎症是将RA与自主神经功能障碍联系起来的病理生理基础。
为了评估“炎症反射”的交感神经过度活动，我们在大鼠胶原诱导性关节炎（CIA）模型中测量了心率变异性（HRV），该模型通过在Lewis大鼠皮内注射II型胶原乳剂诱导关节炎。每两天记录30分钟的单导联心电图（ECG）。分析了时域和频域参数、去趋势波动分析（DFA）、减速（DC）和加速能力（AC）。
与9只对照大鼠相比，9只CIA大鼠的许多HRV参数显示出显著差异。在关节炎开始时，低频/高频显著高于对照组（第1周：2.41±0.7对1.76±0.6，p<0.05；第2周：2.24±0.5对1.58±0.5，p<0.05），表明在炎症初始阶段存在强烈的炎症反射，但在随后的恢复阶段未观察到显著差异。DFA参数也有类似趋势。然而，尽管自第4周起低频/高频与对照组相比没有显著增加，但DC却逐渐降低。
我们在CIA大鼠关节炎早期观察到炎症反射的交感神经过度激活。DC的持续下降表明存在晚期心脏自主神经功能障碍，尽管急性关节炎已缓解。
