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Plaque Collagen Synthesis and Calcification: Working Together to Protect Against Instability and Rupture

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Abstract

The Framingham score is known to underestimate cardiovascular risk but the search for additional risk factors has proved fruitless. This paper suggests that the problem lies with the failure to recognise that plaque development is in fact a healing response to endothelial injury. The initial wound healing response involves migration of vascular smooth muscle cells from the medial to the intimal layer, together with additional collagen synthesis. If this proves insufficient or more collagen is degraded by collagenases than is synthesised, then plaque calcification may develop. Both collagen and calcification act to stabilise the plaque and prevent rupture. Microcalcification develops in the gaps between collagen fibres; this has been considered pathogenic but more likely it is the lack of collagen that is pathogenic, while the microcalcification is merely substituting for the absent collagen. Once the calcification has further developed into a fibrocalcific plaque cap, many are agreed that it now serves a protective function. The fact that statins increase calcification progression has long puzzled researchers but since statins can also increase collagen synthesis, this may simply be a means by which statins reduce cardiovascular risk. Administration of collagen tripeptide can also reduce plaque area and lower some of the cardiovascular risk factors. A clinical trial of statins with and without collagen tripeptide in atherosclerosis patients is proposed.

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Nicoll, R. (2022). Plaque Collagen Synthesis and Calcification: Working Together to Protect Against Instability and Rupture. In: Henein, M. (eds) Cardiovascular Calcification. Springer, Cham. https://doi.org/10.1007/978-3-030-81515-8_1

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