Abstract
To clarify whether inflammation is a cause or consequence of atrial fibrillation (AF), we measured high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α) before and after pharmacological cardioversion in 15 patients with paroxysmal AF. Levels of hs-CRP, IL-6, and TNF-α after cardioversion were significantly higher than those in controls (P < 0.05). Furthermore, the levels of these indices did not differ significantly even at 24 hours and 2 weeks after cardioversion. These results suggest that inflammation is a causative agent of paroxymal AF. Copyright © 2004 by the Japanese Heart Journal.
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Sata, N., Hamada, N., Horinouchi, T., Amitani, S., Yamashita, T., Moriyama, Y., & Miyahara, K. (2004). C-reactive protein and atrial fibrillation: Is inflammation a consequence or a cause of atrial fibrillation? Japanese Heart Journal, 45(3), 441–445. https://doi.org/10.1536/jhj.45.441
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