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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.
Journal of Cardiovascular Translational Research
|February 20, 2016
Summary
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.
Keywords:
Aortic transvalvular pressure gradientAortic valve inflammation, fibrosis and calcific nodule buildupAortic valvular stenosis (AVS)Bicuspid aortic valve disease (BAVD)Compensatory myocardial hypertrophy in pressure overload (PO)Feedback control of myocardial hypertrophyFetal type genesGenomics of calcific aortic valve disease (CAVD)HemodynamicsImmediate early-response genes (IEGs)Intrinsic component of the total systolic ventricular loadMacromolecular crowding and cardiomyocyte diameters in PO hypertrophyPressure loss recoveryReplication of cardiomyocyte sarcomeres in-parallel and in-series
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