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Review
. 2025 Jul 8:12:1620313.
doi: 10.3389/fcvm.2025.1620313. eCollection 2025.

Atrial remodelling and dysfunction in hypertrophic cardiomyopathy: prognostic role and therapeutic target

Chiara Piazzai  1 , Alessio Petrone  1 , Andrea Stefanini  2 , Flavio D'Ascenzi  2 , Iacopo Olivotto  1   3 , Matteo Cameli  2
Affiliations
Review

Atrial remodelling and dysfunction in hypertrophic cardiomyopathy: prognostic role and therapeutic target

Chiara Piazzai et al. Front Cardiovasc Med. .

Abstract

Introduction: Hypertrophic cardiomyopathy (HCM) is a common genetic cardiac disease marked by abnormal ventricular hypertrophy. Recent studies have highlighted that left atrial (LA) remodelling-including dilation, fibrosis, and functional impairment-plays a key role in disease progression and prognosis, notably increasing the risk of atrial fibrillation (AF) and stroke.

Material and methods: This review article systematically examines published clinical, imaging, and interventional studies. The analysis focuses on identifying the determinants of atrial myopathy, its relationship with diastolic dysfunction and left ventricular outflow tract obstruction (LVOTO), and the effects of therapeutic interventions such as septal reduction therapy and cardiac myosin inhibitors.

Results: The findings reveal that LA remodelling in HCM is characterized by increased LA volume, reduced atrial strain, and prolonged conduction times-all of which are strongly linked to the onset and recurrence of AF. Moreover, interventions that reduce LVOTO (e.g., surgical myectomy) have been shown to induce LA reverse remodelling and improve diastolic parameters. Emerging therapies, like cardiac myosin inhibitors, also improve LV function but present complex effects on atrial performance, with some evidence suggesting a reduction in atrial strain that warrants further investigation.

Conclusion: Atrial remodelling is a significant marker of disease severity in HCM and an important independent predictor of adverse outcomes, including AF and cardioembolic events. Early detection through comprehensive multimodal imaging and timely therapeutic intervention can potentially mitigate these risks, making atrial myopathy both a critical prognostic factor and a promising therapeutic target.

Keywords: atrial fibrillation; atrial myopathy; cardiac myosin inhibitors; hypertrophic cardiomyopathy; multimodal imaging; septal reduction therapy.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

Figures

None
Graphical abstract
Figure 1
Figure 1
Causes of atrial myopathy. Prolonged exposure to mitral regurgitation, LVOTO, and myocardial disarray with resulting fibrosis, microvascular dysfunction, and diastolic dysfunction leads to adverse remodelling of the LA characterized by dilation and functional deterioration, a condition known as atrial myopathy. LVOTO, left ventricular outflow tract obstruction.
Figure 2
Figure 2
Evolution of atrial myopathy. The figure schematizes the main parameters that increase (in red) or decrease (in blue) as the severity of atrial myopathy progresses. ET-1, endothelin-1; AF, atrial fibrillation; LACi, left atrioventricular coupling index; PA-TDI, total atrial conduction time; LAVi, indexed left atrial volume. Dr. Chiara Piazzai, Four Hearts on Canvas, Oil and Turpentine, 2024.
Figure 3
Figure 3
Multimodal imaging of atrial myopathy. AF, atrial fibrillation; CMR, cardiac magnetic resonance; EDV, end-diastolic volume; HCM, hypertrophic cardiomyopathy; HFpEF, heart failure with preserved ejection fraction; LA, left atrium; LACi, left atrioventricular coupling index; LAVi, indexed left atrial volume; LV, left ventricle; PA-TDI, total atrial conduction time; PALS, peak atrial longitudinal strain; SCD, sudden cardiac death.
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