Abstract

Cardiovascular calcification has traditionally been considered a passive process that correlates with plaque burden, but without a major role on plaque vulnerability. However, more recent data suggest that cardiovascular calcification may encompass both passive (e.g., biochemical factors, circulating nucleating complexes) and active processes (e.g., cell-mediated processes involving cell death of macrophages and smooth muscle cells (SMCs), and/or the release of matrix vesicles by SMCs). The longstanding cap rupture paradigm is that the culprit plaque of an acute coronary event is not calcified, or has a low amount of calcification. However, this paradigm has been changing since the existence of numerous microcalcifications (μCalcs) was first demonstrated in human atheroma caps. High-resolution 3D finite element analysis has demonstrated that μCalcs in atheroma caps can increase the local tissue stresses by a factor of two to five, and transform a stable lesion into a vulnerable plaque.

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