Intraplaque hemorrhage and progression of coronary atheroma

Intraplaque hemorrhage and progression of coronary atheroma
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DOI:
10.1056/nejmoa035655
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发表时间:
2003-12-11
影响因子:
158.5
通讯作者:
Virmani, R
Virmani, R
中科院分区:
医学1区
文献类型:
--
作者:
Kolodgie, FD;Gold, HK;Virmani, R

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背景:斑块内出血在晚期冠状动脉粥样硬化病变中很常见。出血和斑块破裂的脆弱性之间的关系可能涉及从红细胞membranes.METHODS的游离胆固醇的积累:我们染色的多个冠状动脉病变从24例随机选择的患者谁突然死于冠状动脉的原因与抗血型糖蛋白A(一种蛋白质特异性红细胞,促进阴离子交换)和马洛里的染色铁(含铁血黄素),标记物以前的斑块内出血。冠状动脉病变分为病理性内膜增厚病变、坏死早期或晚期核心纤维帽状动脉粥样硬化或薄帽状纤维粥样硬化(易损斑块)。动脉反应斑块出血进一步定义在兔模型atherosclerosis.RESULTS:只有微量血型糖蛋白A和铁被发现在病变与病理性内膜增厚或纤维帽粥样硬化与核心在早期阶段的坏死。与此相反,纤维动脉粥样硬化的核心在晚期坏死或薄帽有显着增加血型糖蛋白A的胆固醇裂隙周围的铁沉积。大量的血型糖蛋白A和铁与更大的坏死核心和更大的巨噬细胞浸润相关。诱导壁内出血的家兔病变始终显示胆固醇晶体伴红细胞碎片、泡沫细胞和铁沉积。相比之下,从同一动物的对照病变有显着减少巨噬细胞和脂质contents.CONCLUSIONS:通过促进沉积的游离胆固醇,巨噬细胞浸润,扩大的坏死核心,积累的红细胞膜内的动脉粥样硬化斑块可能代表一个强有力的动脉粥样硬化刺激。这些因素可能会增加斑块不稳定的风险。
BACKGROUND:Intraplaque hemorrhage is common in advanced coronary atherosclerotic lesions. The relation between hemorrhage and the vulnerability of plaque to disruption may involve the accumulation of free cholesterol from erythrocyte membranes.METHODS:We stained multiple coronary lesions from 24 randomly selected patients who had died suddenly of coronary causes with an antibody against glycophorin A (a protein specific to erythrocytes that facilitates anion exchange) and Mallory's stain for iron (hemosiderin), markers of previous intraplaque hemorrhage. Coronary lesions were classified as lesions with pathologic intimal thickening, fibrous-cap atheromas with cores in an early or late stage of necrosis, or thin-cap fibrous atheromas (vulnerable plaques). The arterial response to plaque hemorrhage was further defined in a rabbit model of atherosclerosis.RESULTS:Only traces of glycophorin A and iron were found in lesions with pathologic intimal thickening or fibrous-cap atheromas with cores in an early stage of necrosis. In contrast, fibroatheromas with cores in a late stage of necrosis or thin caps had a marked increase in glycophorin A in regions of cholesterol clefts surrounded by iron deposits. Larger amounts of both glycophorin A and iron were associated with larger necrotic cores and greater macrophage infiltration. Rabbit lesions with induced intramural hemorrhage consistently showed cholesterol crystals with erythrocyte fragments, foam cells, and iron deposits. In contrast, control lesions from the same animals had a marked reduction in macrophages and lipid content.CONCLUSIONS:By contributing to the deposition of free cholesterol, macrophage infiltration, and enlargement of the necrotic core, the accumulation of erythrocyte membranes within an atherosclerotic plaque may represent a potent atherogenic stimulus. These factors may increase the risk of plaque destabilization.