Author + information
- Chee Yuan Ng, MD⁎ ()
- ↵⁎Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Room 5512, Los Angeles, California 90048
Koyama et al. (1) conducted an excellent study on the prevention of atrial fibrillation recurrence with corticosteroids after radiofrequency catheter ablation. However, the mechanism by which a short course of corticosteroids for 3 days right after catheter ablation could prevent long-term recurrence of atrial fibrillation remains unclear and puzzling. Inflammation and atrial remodeling during the early phase seem to play a role.
In reference to that, I would like to point out that corticosteroids could decrease atrial fibrillation recurrence by stimulating the release of heat shock proteins (HSPs). Corticosteroids induce a heat stress response with the release of HSPs (2). In an in vitro model, artificially up-regulating HSP27 protects against atrial remodeling, which was measured as calcium transient and cell shortening (3). In a canine model, HSP induction attenuates tachypacing-induced decreases in the effective refractory period (ERP) (3). This study also demonstrated that remodeling changes occur in as little as 4 h of tachypacing (3). In another study, overexpressing HSP27 significantly reduced tachypacing-induced myolysis (4).
So far, studies have shown that HSPs have cardioprotective effects at an in vitro level in an animal model. Altering HSP expression at a clinical level has not yet been studied, and it is unclear whether it has any disease modification properties in patients with atrial fibrillation. Future studies should focus on the interactions between corticosteroids, HSPs, and the recurrence of atrial fibrillation after cardioversion and catheter ablation. HSPs could be a novel target for intervention in atrial fibrillation.
- American College of Cardiology Foundation
- Koyama T.,
- Tada H.,
- Sekiguchi Y.,
- et al.
- Brundel B.J.,
- Shiroshita-Takeshita A.,
- Qi X.,
- et al.