Upstream therapy for 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.
Kumagai
Koichiro
K
Department of Cardiology, School of Medicine, Fukuoka University, Jonan-ku, Fukuoka 814-0180, Japan. kxk@fukuoka-u.ac.jp
D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D016275:Atrial Function / Q000187:drug effects; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D012084:Renin-Angiotensin System / Q000187:drug effects; D013997:Time Factors; D016896:Treatment Outcome
D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents; D000893:Anti-Inflammatory Agents; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors