# The Left Atrial Appendage in Sinus Rhythm and Atrial Fibrillation: From Functional Structure to Potential Thromboembolic Reservoir, Rationale for Medical or Radical Exclusion

## TL;DR

This review explores how the left atrial appendage changes from a normal heart function to a source of blood clots in atrial fibrillation and discusses strategies to prevent stroke.

## Contribution

The paper provides a comprehensive review of the evolving rationale for radical anatomical exclusion of the left atrial appendage in atrial fibrillation.

## Key findings

- The left atrial appendage transforms from a functional structure to a thromboembolic reservoir in atrial fibrillation.
- Multiple strategies for exclusion exist, each with specific indications and limitations.
- Emerging directions aim to minimize foreign material and thrombogenicity for better stroke prevention.

## Abstract

The left atrial appendage (LAA) is a highly dynamic anatomical structure that plays a key role in left atrial reservoir function, pressure and volume modulation, and endocrine hormone secretion during sinus rhythm. However, its physiological contribution is profoundly altered in atrial fibrillation (AF). Electrical and structural remodeling, impaired contractility, and blood stasis within the LAA collectively transform this functional component into the principal cardiac source of thrombus formation and embolic events in patients with AF. This review focuses on the conceptual continuum from physiological LAA function in sinus rhythm to its pathological transformation in AF and the evolving rationale for progressively more complete (“radical”) anatomical exclusion A variety of strategies, including systemic anticoagulation therapy, percutaneous device-based exclusion, and surgical closure, are currently employed, each with specific indications, limitations, and procedure-related risks. Beyond summarizing available techniques, this review critically synthesizes mechanistic, anatomical, and clinical data to address unresolved controversies regarding patient selection, residual leaks, device-related thrombosis, and post-procedural antithrombotic management. Finally, emerging directions toward minimizing residual foreign material, reducing thrombogenicity, and achieving durable exclusion are discussed, supporting a more personalized and radical approach to stroke prevention in AF.