# Atrial Secondary Mitral Regurgitation: Pathophysiology, Diagnosis, and Surgical Implications

## TL;DR

Atrial secondary mitral regurgitation is a distinct heart condition linked to atrial enlargement and requires tailored diagnosis and treatment strategies.

## Contribution

This paper provides a comprehensive review of A-SMR's pathophysiology, diagnosis, and surgical implications.

## Key findings

- A-SMR is driven by atrial remodeling and annular dilatation, not ventricular distortion.
- Echocardiography and MRI are key for diagnosing and characterizing A-SMR subtypes.
- Surgical mitral valve repair with annuloplasty shows favorable outcomes in selected patients.

## Abstract

Background and Objectives: Atrial secondary mitral regurgitation (A-SMR), also referred to as atrial functional mitral regurgitation, has emerged as a distinct clinical phenotype characterized by left atrial enlargement, mitral annular dilatation, and preserved left ventricular geometry and systolic function. Frequently associated with long-standing atrial fibrillation (AF) and heart failure with preserved ejection fraction (HFpEF), A-SMR challenges the traditional ventricular-centered classification of functional mitral regurgitation (MR) and is increasingly recognized as a clinically relevant condition. Materials and Methods: This narrative review provides an updated and critical overview of current evidence on A-SMR. We summarize available data on pathophysiology, diagnostic imaging, natural history, and therapeutic strategies, with particular emphasis on implications for cardiac surgery and clinical decision-making. Evidence was derived from observational studies, registry analyses, interventional reports, and contemporary guideline documents. Results: A-SMR is primarily driven by atrial remodeling and annular dilatation, with minimal contribution from ventricular distortion or leaflet tethering. Echocardiography and Magnetic Resonance Imaging (MRI) play a central role in diagnosis and phenotypic characterization, allowing differentiation from ventricular functional MR and identification of distinct A-SMR subtypes with potential therapeutic implications. A-SMR is a progressive condition associated with worsening symptoms and adverse clinical outcomes. Rhythm control strategies may reduce MR severity in selected patients by promoting atrial reverse remodeling. Transcatheter edge-to-edge repair (TEER) represents a treatment option for selected high-risk patients, although concerns regarding long-term durability remain in this predominantly annular disease. From a pathophysiological standpoint, surgical mitral valve repair based on annuloplasty directly targets the dominant mechanism of A-SMR and has been associated with favorable outcomes in appropriately selected patients. Conclusions: A-SMR is a distinct and increasingly recognized form of functional MR requiring a mechanism-oriented diagnostic and therapeutic approach. The 2025 ESC/EACTS Guidelines for the management of valvular heart disease have acknowledged A-SMR as a specific clinical phenotype, although dedicated phenotype-specific management recommendations remain limited. Surgical mitral valve repair, particularly when combined with AF ablation, represents a rational treatment strategy in selected patients and may improve long-term outcomes.