Abstract

Cardiovascular calcification occurs in a variety of location and structure in the heart and the vasculature. Many hypotheses exist in describing local phenomena, however, there is no known global and unifying mechanism to explain all types of cardiovascular soft tissue calcification. The observed calcific changes in the cardiovascular system, however, does have a general pattern of occurring at structurally altered sites either due to disease processes or surgical manipulations. Areas of structural alterations, in conjunction with the pulsatile environment of the cardiovascular system, have been shown to disrupt normal pulsewave transmission throughout the arterial tree and induce local junctional or interfacial stress gradients. As such, these induced stress gradients can potentially aggregate and deposit cellular products and ionic particles at local sites to initiate calcification. A fundamental mechanism influencing all cardiovascular calcification is proposed based on pathophysiologic pulsewave propagations and reflections at these sites of structural changes. Initial supporting results of the theoretical model and experimentations are discussed leading to a call for future research in this direction.

Full Text
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