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April 25, 2026Journal of the American College of Cardiology695 citations

Calcific Aortic Stenosis

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MDMarc R. DweckNBNicholas A. BoonDNDavid E. Newby

Key Result

Aortic stenosis progression is driven by valve narrowing and secondary left ventricular hypertrophy, highlighting the need for novel therapies targeting inflammation, fibrosis, and calcification.

Key Points

  • The review aims to understand the pathophysiology of aortic stenosis and explore potential therapeutic strategies.
  • Examined the mechanisms of aortic stenosis focusing on valve and myocardial interactions.
  • Highlighted the roles of inflammation, fibrosis, and calcification in disease progression.
  • Discussed comparisons with other pathological conditions to identify novel therapies.
  • Identified inflammation and fibrosis as key factors in valve narrowing and left ventricular hypertrophy.
  • Addressed the transition from hypertrophy to heart failure as a critical outcome of disease progression.
  • Proposed potential therapeutic strategies based on shared mechanisms with other cardiovascular diseases.

Structured PICO

P
Population
Patients with calcific aortic stenosis

This review highlights the pathophysiology of calcific aortic stenosis and left ventricular hypertrophy, emphasizing the need for novel medical interventions to halt disease progression.

Abstract

Although aortic stenosis is a common condition associated with major morbidity, mortality, and health economic costs, there are currently no medical interventions capable of delaying or halting its progression. Re-evaluation of the underlying pathophysiology is therefore required so that novel therapeutic strategies can be developed. Aortic stenosis is characterized by progressive aortic valve narrowing and secondary left ventricular hypertrophy. Both processes are important because in combination they drive the development of symptoms and adverse events that characterize the latter stages of the disease. In this review, the authors examine the pathophysiology of aortic stenosis with respect to both the valve and the myocardium. In particular, the authors focus on the role of inflammation, fibrosis, and calcification in progressive valve narrowing and then examine the development of left ventricular hypertrophy, its subsequent decompensation, and the transition to heart failure. Finally the authors discuss potential therapeutic strategies on the basis of similarities aortic stenosis shares with other pathological conditions.

Expert Takes3 quotes

1/3

“We are starting to appreciate that CAVS is not simply a passive degenerative process associated with aging but that it involves active mechanisms that may be amenable to intervention. We believe we can improve on the current commonly employed strategy of watchful waiting until patients become eligible for aortic valve replacement.”

Milind Desai, Vice-Chair, Heart Vascular & Thoracic Institute, Cleveland ClinicCleveland Clinicauto_pipelineSupportiveView source
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Cite This Study

Dweck et al. (2012) conducted a review in Calcific Aortic Stenosis. Aortic stenosis progression is driven by valve narrowing and secondary left ventricular hypertrophy, highlighting the need for novel therapies targeting inflammation, fibrosis, and calcification.

synapsesocial.com/papers/69ec8702b203de571d6f13c3https://doi.org/10.1016/j.jacc.2012.02.093
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Twelve-Year Comparison of a Bjork–Shiley Mechanical Heart Valve with Porcine Bioprostheses1991 · 433 citations
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  3. 3Untitled2011 · 535 citations
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  5. 5Inflammatory regulation of extracellular matrix remodeling in calcific aortic valve stenosis2005 · 240 citations