Answers are grounded in this paper and cite their sources.
This editorial synthesizes recent findings on the molecular mechanisms (such as RUNX2 and mitochondrial oxidative stress), prognostic biomarkers (t-PA, EPO), and clinical management strategies for calcific aortic valve disease and aortic stenosis, highlighting the need for non-invasive therapies and early diagnostic tools.
Aortic valve stenosis (AS) caused by calcific aortic valve disease (CAVD) is the most prevalent heart valve disease of the elderly population in the Western world, and the disease burden is estimated to increase from 2.5 million in 2000 to 4.5 million in 2030 (1). Fibro-calcific remodeling is a hallmark of disease progression and a strong independent prognostic marker for adverse events in patients with asymptomatic AS. Currently, no medication exists to halt or even slow AS and CAVD progression. The only therapeutic options available are invasive—either surgical or catheterbased aortic valve replacement—thus, the CAVD research field focuses on discovering novel CAVD biomarkers and targets for developing non-invasive therapies [reviewed in (2)].
No takes yet. Share an insight, caveat, or question.
Hilaire et al. (2022) conducted an editorial in Aortic valve stenosis (AS) caused by calcific aortic valve disease (CAVD).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: