Has our understanding of calcification in human coronary atherosclerosis progressed?
Has our understanding of calcification in human coronary atherosclerosis progressed?
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我们对人冠状动脉粥样硬化中钙化的理解是否有所发展？
DOI：
10.1161/atvbaha.113.302642
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发表时间：
2014-04
期刊：
影响因子：
--
通讯作者：
Virmani R
中科院分区：
文献类型：
--
作者：
Otsuka F;Sakakura K;Yahagi K;Joner M;Virmani R
冠状动脉钙化是未来心脏事件的公认预测因子。然而，它并不是不稳定斑块的预测因子。动脉粥样硬化斑块的内膜钙化可能始于平滑肌细胞凋亡和/或基质囊泡释放，并且几乎总是在显微镜下看到病理性内膜增厚（PIT），表现为微钙化（≥0.5μm，通常直径<15μm）。在早期纤维粥样瘤中，随着巨噬细胞浸润到脂质池中，钙化增加，巨噬细胞在脂质池中经历细胞凋亡和/或释放基质囊泡。钙化区汇合处涉及细胞外基质和坏死核心，通过X线检查可识别为斑点状（≤2mm）或碎片状（>2、<5mm）钙化。薄帽纤维粥样斑块和斑块破裂中的钙化通常少于稳定斑块中观察到的钙化，并且通常呈斑点状或碎片状。碎片钙化扩散到周围富含胶原蛋白的基质中，形成钙化片，这是纤维钙化斑的标志。钙化片可破裂成结节并伴有纤维蛋白沉积，若伴有管腔突出，则与血栓形成有关。纤维钙化斑块中钙化程度最高，其次是愈合斑块破裂，糜烂和 PIT 中钙化程度最低。男性的钙化程度比女性更大，尤其是在绝经前，白人的钙化程度也比黑人更大。人类内膜钙化的机制仍然知之甚少。钙化通常发生在平滑肌细胞和巨噬细胞凋亡、基质囊泡伴随血管壁内成骨标志物表达的情况下。
Coronary artery calcification is a well-established predictor of future cardiac events; however, it is not a predictor of unstable plaque. The intimal calcification of the atherosclerotic plaques may begin with smooth muscle cell apoptosis and/or release of matrix vesicles, and is almost always seen microscopically in pathologic intimal thickening (PIT), which appears as microcalcification (≥0.5 μm, typically <15 μm in diameter). Calcification increases with macrophage infiltration into the lipid pool in early fibroatheroma where they undergo apoptosis and/or release matrix vesicles. The confluence of calcified areas involves extracellular matrix and the necrotic core, which can be identified by radiography as speckled (≤2 mm) or fragmented (>2, <5 mm) calcification. The calcification in thin-cap fibroatheromas and plaque rupture is generally less than what is observed in stable plaques and is usually speckled or fragmented. Fragmented calcification spreads into the surrounding collagen-rich matrix forming calcified sheets, the hallmarks of fibrocalcific plaques. The calcified sheets may break into nodules with fibrin deposition, and when accompanied by luminal protrusion, it is associated with thrombosis. Calcification is highest in fibrocalcific plaques followed by healed plaque rupture and is the least in erosion and PIT. The extent of calcification is greater in men than women especially in the premenopausal period and is also greater in whites compared with blacks. The mechanisms of intimal calcification remain poorly understood in man. Calcification often occurs in the presence of apoptosis of smooth muscle cells and macrophages with matrix vesicles accompanied by expression of osteogenic markers within the vessel wall.