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Updated: Jul 14, 2026
28:13
Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation
Published on: February 26, 2013
Upstream therapy for atrial fibrillation.
1Department of Cardiology, School of Medicine, Fukuoka University, Jonan-ku, Fukuoka 814-0180, Japan. kxk@fukuoka-u.ac.jp
Summary
Atrial fibrillation (AF) involves factors like stretch and inflammation, increasing angiotensin II and calcium overload. Upstream therapies targeting angiotensin II may prevent structural changes that promote AF.
Area of Science:
- Cardiology
- Molecular Biology
- Pharmacology
Background:
- Atrial fibrillation (AF) is a complex arrhythmia with multiple contributing factors.
- Stretch and inflammation elevate angiotensin II, leading to calcium overload and AF initiation.
- Angiotensin II promotes atrial interstitial fibrosis, impairing conduction and facilitating AF maintenance.
Purpose of the Study:
- To elucidate the role of angiotensin II in AF pathogenesis.
- To explore the potential of upstream therapies in preventing AF-related structural remodeling.
Main Methods:
- Review of existing literature on AF etiology and pathophysiology.
- Analysis of the molecular pathways involving angiotensin II and the Erk cascade.
- Evaluation of the impact of angiotensin II on atrial structure and electrophysiology.
Main Results:
- Stretch and inflammation increase angiotensin II, causing calcium overload and ectopic beats that trigger AF.
- Angiotensin II activates the Erk cascade via AT(1)R, inducing interstitial fibrosis and conduction abnormalities.
- Current anti-arrhythmic drugs manage symptoms but do not prevent AF substrate development.
Conclusions:
- Upstream therapies, including ACE inhibitors, angiotensin II type 1 receptor blockers, and statins, show promise.
- These therapies may prevent structural remodeling, offering a novel approach to AF management.
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