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Investigating Aortic Valve Calcification via Isolation and Culture of T Lymphocytes using Feeder Cells from Irradiated Buffy Coat
Published on: February 4, 2021
Calcific Aortic Valve Disease: Part 1--Molecular Pathogenetic Aspects, Hemodynamics, and Adaptive Feedbacks
Ares Pasipoularides1,2,3
1Duke University School of Medicine, Durham, NC, USA. apasipou@duke.edu.
Insights
Calcific aortic valve disease (CAVD) causing aortic valvular stenosis (AVS) involves active mechanisms beyond degeneration. Future research may lead to personalized treatments for CAVD and AVS.
Area of Science:
- Cardiovascular Medicine
- Pathobiology
- Genomics
Background:
- Aortic valvular stenosis (AVS) results from calcific aortic valve disease (CAVD), primarily affecting older adults and often necessitating valve replacement.
- Historically viewed as degenerative, CAVD is now understood to involve active, atherogenesis-like processes.
Purpose of the Study:
- To highlight the evolving understanding of CAVD pathogenesis.
- To emphasize the need for comprehensive management strategies for CAVD/AVS.
- To underscore the potential for novel therapeutic interventions.
Main Methods:
- Review of recent investigations into CAVD mechanisms.
- Analysis of genetic predisposition, signaling pathways, inflammation, and calcification in CAVD.
- Consideration of left ventricular and arterial system interactions.
Main Results:
- CAVD pathogenesis involves genetic factors, lipoprotein deposition, inflammation, and calcification/osteogenesis.
- Management requires a holistic approach, addressing the valve, left ventricle, and arterial system.
- Advanced understanding of genomic and cytomolecular mechanisms is emerging.
Conclusions:
- CAVD/AVS may be amenable to lifestyle and pharmacogenomic interventions.
- Future pluridisciplinary research will elucidate CAVD pathobiology and dynamics.
- Personalized medicine treatments for CAVD/AVS are anticipated.
Abstract:
Aortic valvular stenosis (AVS), produced by calcific aortic valve disease (CAVD) causing reduced cusp opening, afflicts mostly older persons eventually requiring valve replacement. CAVD had been considered "degenerative," but newer investigations implicate active mechanisms similar to atherogenesis--genetic predisposition and signaling pathways, lipoprotein deposits, chronic inflammation, and calcification/osteogenesis. Consequently, CAVD may eventually be controlled/reversed by lifestyle and pharmacogenomics remedies. Its management should be comprehensive, embracing not only the valve but also the left ventricle and the arterial system with their interdependent morphomechanics/hemodynamics, which underlie the ensuing diastolic and systolic LV dysfunction. Compared to even a couple of decades ago, we now have an increased appreciation of genomic and cytomolecular pathogenetic mechanisms underlying CAVD. Future pluridisciplinary studies will characterize better and more completely its pathobiology, evolution, and overall dynamics, encompassing intricate feedback processes involving specific signaling molecules and gene network cascades. They will herald more effective, personalized medicine treatments of CAVD/AVS.
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Aortic Regurgitation II: Clinical Features and Diagnostic Tests
Aortic Regurgitation III: Medical Management

