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Updated: Jan 15, 2026

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
Monocytes at the crossroads of aortic stenosis and myocardial damage
Nervana Issa1, Alexandre Candellier1,2, Cédric Boudot1
1UR UPJV 7517 MP3CV, CURS, Université de Picardie Jules Verne, Avenue René Laennec, Amiens 80054, France.
Insights
Aortic stenosis (AS) involves inflammation, particularly from monocytes, contributing to valve damage and heart remodeling. Targeting monocytes may offer new treatments for AS and prevent complications after aortic valve replacement (AVR).
Area of Science:
- Cardiology
- Immunology
- Pathophysiology
Background:
- Aortic stenosis (AS) is a prevalent heart valve disease causing significant morbidity and mortality.
- Current treatment for symptomatic AS is aortic valve replacement (AVR), but understanding of its pathophysiology is limited.
- Inflammation, especially involving monocytes, is increasingly recognized as central to AS progression and outcomes.
Purpose of the Study:
- To provide an updated overview of monocyte involvement in AS pathophysiology.
- To explore the role of monocytes in valvular and myocardial remodeling in AS.
- To discuss the potential of monocytes as biomarkers and therapeutic targets in AS and post-AVR.
Main Methods:
- Review of current literature on monocyte function in AS.
- Analysis of monocyte subsets in relation to AS progression.
- Examination of monocyte roles in structural valve deterioration (SVD) post-AVR.
Main Results:
- Monocytes contribute to fibrocalcific remodeling of the aortic valve leaflets.
- Monocytes are implicated in myocardial injury during AS progression.
- Monocytes play a role in SVD after AVR, affecting long-term outcomes.
Conclusions:
- Monocytes are key players in AS pathogenesis, influencing both valve and myocardial remodeling.
- Monocyte subsets show promise as biomarkers for AS progression and post-AVR prognosis.
- Targeting monocytes presents a potential therapeutic strategy for AS and related complications.
Abstract:
Aortic stenosis (AS) is the most common heart valve disease in high-income countries, causing significant morbidity and mortality. It results from progressive thickening and calcification of the aortic valve (AV) leaflets, leading to AV narrowing and myocardial remodeling-both key contributors to disease progression and symptoms. With no pharmacological treatment to slow AS, aortic valve replacement (AVR) remains the only therapeutic option for symptomatic patients. However, limited understanding of AS pathophysiology and the absence of reliable prognostic markers hinder improved patient outcomes. A comprehensive reassessment of AS pathophysiology, integrating both valvular and myocardial remodeling is essential for advancing prognostic tools and therapeutic strategies. Inflammation plays a central role in these processes, drawing increasing attention to monocytes. This review provides an updated overview of monocytes' multifaceted involvement in AS, including: (i) fibrocalcific remodeling of the valve, (ii) myocardial injury during disease progression, and (iii) structural valve deterioration (SVD) after surgical or transcatheter AVR. We will also discuss the potential of monocyte subsets as biomarkers for AS progression and post-AVR prognosis, as well as the therapeutic targeting of monocytes to prevent AS, SVD, and subsequent myocardial dysfunction.
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