Key result
This review highlights the intimate interplay between the hemodynamic environment and biological responses in aortic valve remodeling, inflammation, and calcification.
This review highlights the critical role of mechanical stimuli and hemodynamics in driving aortic valve pathology, including inflammation and calcification.
Provides mechanistic insights into aortic valve disease; leaves open whether modulating hemodynamics improves outcomes.
Cardiac valves function in a mechanically complex environment, opening and closing close to a billion times during the average human lifetime, experiencing transvalvular pressures and pulsatile and oscillatory shear stresses, as well as bending and axial stress. Although valves were originally thought to be passive pieces of tissue, recent evidence points to an intimate interplay between the hemodynamic environment and biological response of the valve. Several decades of study have been devoted to understanding these varied mechanical stimuli and how they might induce valve pathology. Here, we review efforts taken in understanding the valvular response to its mechanical milieu and key insights gained from in vitro and ex vivo whole-tissue studies in the mechanobiology of aortic valve remodeling, inflammation, and calcification.
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Balachandran et al. (2011) conducted a review in Aortic valve inflammation and calcification. This review highlights the intimate interplay between the hemodynamic environment and biological responses in aortic valve remodeling, inflammation, and calcification.
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