Calcification in a coronary artery is accepted as definite evidence of coronary atherosclerosis. The extent and density of calcification, as combined in the Agatston score, is associated with the risk of a patient experiencing a major acute coronary event. Atherosclerosis occurs because damaged endothelial cells allow low-density lipoprotein cholesterol (LDLc) to leak into subintimal tissue. Proteoglycans in subendothelial collagen have a high affinity for LDLc, retaining the lipoprotein cholesterol complex. As the endothelial damage is repaired, the subintimal LDLc is trapped. Retained LDLc induces an inflammatory response in the overlying endothelium, causing the endothelium to express chemotactic peptides. Chemotactic peptides attract circulating monocytes, which follow the concentration gradient, enter the tissue, and become tissue macrophages to phagocytize and digest the irritating LDLc in the atheroma. In the process of digesting LDLc, enzymes in the macrophages oxidize the LDLc complex. Oxidized LDL is toxic to macrophages; when present in sufficient quantity, it may cause death of macrophages, contributing to inflammation in the atheroma. In a necrotic inflammatory lesion, the regulatory mechanisms that control tissue concentrations of calcium and phosphorus are lost, allowing the solubility product of calcium phosphate to be exceeded, resulting in the formation of microscopic calcium-phosphate crystals. With ongoing inflammation, additional calcium-phosphate crystals are formed, which may aggregate. When these aggregated calcium phosphate crystals exceed 1 mm, the lesions become visible on clinical CT as coronary calcifications. Serial gated CT scans of the heart have demonstrated that once formed, CT-visible calcifications do not decrease significantly in size but may increase.
Keywords: calcification; cardiology (clinical); coronary artery; coronary atherosclerosis; vascular.
© 2019 by the Society of Nuclear Medicine and Molecular Imaging.