Abstract

The intimal calcification of atherosclerotic plaque develops simultaneously with the progression of atherosclerosis. Pathologically, atherosclerotic calcification initially occurs as microcalcifications (0.5–15μm) and may progress into larger dense calcifications, eventually becoming sheet-like calcifications (>3mm). Stratified by plaque type, the degree of calcification is highest in fibrocalcific plaques followed by healed plaque rupture and is the least in plaque erosions and pathologic intimal thickening lesions. Recent pathologic and imaging-based studies suggest that massive dense calcifications are usually associated with stable plaques while punctate or fragmented calcifications in thin fibrous cap or plaque ruptures, which may be detected by invasive or noninvasive imaging, are related to unstable plaques. Although the mechanisms of calcification are still to be elucidated, apoptotic smooth muscle cells and macrophages accompanied with bone-related proteins expression likely play a crucial role in initiation and progression of calcification.

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