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Updated: Aug 17, 2026

Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro
Published on: May 10, 2021
Pathological mineralization of cardiac valves: causes and mechanism
Elena I Suvorova1, Philippe A Buffat
1Institute of Crystallography of Russian Academy of Sciences, Moscow, Russia. Suvorova@ns.crys.ras.ru
Objective:
Mechanism of calcification of cardiac valves was investigated through a comparative characterization of structure, morphology, and size of hydroxyapatite (HAP) crystals formed in mineral deposit on cardiac valves, bone tissue, and crystals synthesized from aqueous solutions under definite conditions.
Methods:
All deposits on cardiac valves and bone samples were characterized by scanning electron microscopy (SEM) and energy dispersive X-ray microanalysis (EDS) in a Philips XL30 FEG microscope to evaluate their overall view and structure, to estimate the sizes of particles, and to carry out the chemical analysis. High resolution transmission electron microscopy (HRTEM) and electron micro diffraction was done for precise phase identification of individual crystals and measurements of their sizes.
Results:
Mineral deposit on cardiac valves contained hydroxyapatite crystals (HAP) crystals with lengths from a few nanometers to a few hundred nanometers. Similar to the HAP precipitation in aqueous solutions, crystals in deposit were randomly oriented relative to each other and without the substrate effect on their orientation. Octacalcium phosphate (OCP) phase was also detected in the form of large (up to a few microns) crystals. The quantity of the OCP crystals was quite low in comparison with the amount of the HAP crystals. HAP crystals in bone samples were no more than 20 nm in length and textured in the HAP [0001] direction along collagen fibers. The HAP crystals from cardiac valves and bones were of uniform thickness comparable with the crystallographic unit cell.
Conclusions:
Mass crystallization model and hemodynamics in heart and arteries determine the mechanism of pathological calcification through the mediation of hydroxyapatite nanocrystals perpetually circulating with the bloodstream.
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