Abstract
There are multiple factors for the etiology of atrial fibrillation (AF), including stretch, autonomic imbalance, hyperthyroidism, and inflammation. Of these factors for AF, stretch and inflammation increase the angiotensin II level, thereby inducing calcium over load, and inducing ectopic focal activities that initiate AF. Angiotensin II activates the Erk cascade through the AT1R and induces interstitial fibrosis of the atria, which compromises intra-atrial conduction. Short atrial refractoriness and slow conduction form multiple re-entry, before maintaining AF. Anti-arrhythmic drugs used for downstream therapy can suppress the focal activities and re-entry, but cannot prevent the development of a structural substrate. In contrast, angiotensin-converting enzyme, angiotensin II type 1 receptor blocker and statins might constitute upstream therapy through the prevention of structural remodeling that promotes AF. (Circ J 2007; Suppl A: A-75 - A-81)
