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BackgroundsPatients 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.MethodsTo 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.ResultsCompared 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.ConclusionsWe 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.Electronic supplementary materialThe online version of this article (doi:10.1186/s12891-016-1347-6) contains supplementary material, which is available to authorized users.

Atrial fibrillation mechanisms and arrhythmia mechanisms / Atrial fibrillation mechanismsful ablation (RVOT n=29, LVOT n=28) were included. Mean age was 48.7 yrs SD 21.9. A mean of 1.1 pre-procedural Holter monitors per patient were analyzed. There were no significant gender differences in VE CoV (male and female LVOT CoV 81% SD 10 vs 79% SD 23, p=0.08; male and female RVOT CoV 83% SD 20 vs 94% SD 17%, p=0.45). The overall VE burden was similar in the RVOT and LVOT groups (RVOT 16.6% SD 12.8 vs LVOT 17.3% SD 11.5). A greater proportion of the LVOT group had mildly reduced LVEF, attributed to VE burden (42.9% vs 17.2%). The LVOT VE group had lower overall hourly CoV compared to RVOT VE (84.5 SD 11.6 vs 95.3 SD 13.5, p=0.005). During daytime hours (0700-2000), the LVOT group had lower hourly CoV (77% SD 7% vs RVOT CoV 90% SD 10%, p=0.001). Consistent daytime VE burden (CoV <0.9) was independently associated with an LVOT origin (OR 35.5, p=0.01). Conclusions: There is significantly less hourly variability of LVOT VE compared to RVOT VE, regardless of gender. Daytime VE CoV may be a useful marker of outflow tract origin in ambiguous cases. Background: Inflammation in form of rheumatoid arthritis (RA) causes not only joint pain but also excessive sudden cardiac death. While systemic inflammation related atherosclerosis was established, the arrhythmogenic substrate in RA was hardly discussed. The aim of this study was to investigate the effect of systemic inflammatory activation on cardiac electrophysiology. Methods: Arthritis was induced in Lewis rats by intradermal injection of emulsion of type II collagen at days 0 and 7. Single lead electrocardiogram (ECG) recordings were made weekly in CIA rats and controls. We assessed the autonomic activity and conduction system of heart by heart rate variability (HRV), the intrinsic heart rate (IHR), direct sympathetic nerve measurement, and optical mapping in a rat collagen-induce arthritis (CIA) model. Results: Rats were divided into 3 groups, normal rats (Con; n=8), collageninduced arthritis (CIA; n=8) and collagen-induced arthritis treated with propranolol (CIA-PRO; n=8). The HRV disclosed significant higher LF/HF of CIA group while no difference was noted between Con and CIA-PRO groups. The sympathetic tone measured by difference between IHR and maximal HR after atropine injection was higher in CIA than CON. The action potential durations (APDs) and the conduction velocity (CV) were no significant differences in this three groups, but the maximal slope of CIA (slope=1.01±0.3) was higher than CON (slope=0.43±0.1). Unexpectedly, after treated with propranolol, the maximal slope of CIA-PRO (slope=0.46±0.1) was much lower than CIA. P1710 | BENCHHRV between control and CIA rats Linear HRV parameters 1st week 2nd week 3rd week 4th week 5th week 6th week Conclusion:In conclusion, the sympathetic overactivation caused by systemic inflammation plays an important role causing arrhythmogenesis in RA. P1711 | BENCHThe influence of the new pharmaceutical composition containing botuli...