Angiotensin-converting enzyme inhibitors, angiotensin II type 1 receptor blockers, and statins may constitute upstream therapy for atrial fibrillation by preventing structural remodeling.
Do upstream therapies (ACEI, ARB, statins) prevent structural remodeling and reduce the promotion or recurrence of atrial fibrillation?
Upstream therapies targeting the renin-angiotensin system and inflammation (ACEI, ARB, statins) may prevent structural remodeling and reduce the incidence and recurrence of atrial fibrillation.
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 AT(1)R 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.
Koichiro Kumagai (Mon,) conducted a review in Atrial Fibrillation. Upstream therapy (ACE inhibitors, ARBs, statins) was evaluated. Angiotensin-converting enzyme inhibitors, angiotensin II type 1 receptor blockers, and statins may constitute upstream therapy for atrial fibrillation by preventing structural remodeling.
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