Proarrhythmic risk and determinants of cardiac autonomic dysfunction in collagen-induced arthritis rats

Ting Tse Lin, Yen Ling Sung, Chih En Wu, Hong Zhang, Yen Bin Liu, Shien-Fong Lin

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Backgrounds: 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. Methods: 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. Results: 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. Conclusions: 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.

Original languageEnglish (US)
Pages (from-to)1-8
Number of pages8
JournalBMC Musculoskeletal Disorders
Volume17
Issue number1
DOIs
StatePublished - Nov 29 2016
Externally publishedYes

Fingerprint

Experimental Arthritis
Arthritis
Deceleration
Reflex
Sudden Cardiac Death
Rheumatoid Arthritis
Heart Rate
Inflammation
Intradermal Injections
Collagen Type II
Emulsions
Cardiac Arrhythmias
Electrocardiography
Population

Keywords

  • Autonomic function
  • Collagen-induced arthritis
  • Deceleration capacity
  • Heart rate variability
  • Rheumatoid arthritis

ASJC Scopus subject areas

  • Rheumatology
  • Orthopedics and Sports Medicine

Cite this

Proarrhythmic risk and determinants of cardiac autonomic dysfunction in collagen-induced arthritis rats. / Lin, Ting Tse; Sung, Yen Ling; Wu, Chih En; Zhang, Hong; Liu, Yen Bin; Lin, Shien-Fong.

In: BMC Musculoskeletal Disorders, Vol. 17, No. 1, 29.11.2016, p. 1-8.

Research output: Contribution to journalArticle

Lin, Ting Tse ; Sung, Yen Ling ; Wu, Chih En ; Zhang, Hong ; Liu, Yen Bin ; Lin, Shien-Fong. / Proarrhythmic risk and determinants of cardiac autonomic dysfunction in collagen-induced arthritis rats. In: BMC Musculoskeletal Disorders. 2016 ; Vol. 17, No. 1. pp. 1-8.
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AB - Backgrounds: 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. Methods: 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. Results: 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. Conclusions: 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.

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