Tracy R E, Devaney K, Kissling G
Virchows Arch A Pathol Anat Histopathol. 1985;405(4):411-27. doi: 10.1007/BF00737168.
Young men dying suddenly and autopsied by the coroner sometimes have coronary thrombosis at a relatively early stage of arteriosclerosis. The plaques under such thrombi often have a complex of features, a) rupture, b) hemorrhage, c) medial destruction, d) nodular collections of foam cells, e) calcification, f) cellular infiltrates of the fibrous cap, fibrous base and adventitia, and g) a newly described kind of phagocytic activity at the boundary between the necrotic core and the fibrous base of the plaque. Commonplace innocuous plaques in most middle and old aged subjects without heart disease also often have some of these features. What structural characteristics might distinguish rare thrombogenic from commonplace innocuous plaques? Twenty-one thrombotic plaques from 18 cases of sudden coronary heart disease (CHD) death were histologically compared with 129 nonthrombotic plaques from these same 18 cases, 85 plaques from 23 cases of CHD death due to arteriosclerotic occlusion, and 94 plaques from 22 cases having no CHD. Plaques with thrombosis all had necrotic cores; plaques for comparison with these were therefore chosen all to have necrotic cores. Rupture and hemorrhage were found in 90% of thrombotic plaques, with mixing of plaque gruel and blood in the thrombus. Medial destruction, foam cells and calcification (features c, d, and e) were commonplace in all types of plaques. Small-cell infiltrates and atherophagocytosis (features f or g) were found in 72-94% of the 21 thrombotic plaques, but only in 18-24% of the 94 not CHD plaques. The necrotic core, characterized by crystalline cholesterol, appears to incite cellular responses in some plaques but not others; those responses distinguish thrombogenesis. The findings imply that thrombogenicity and its accompanying plaque cellularity are incited not by cholesterol, but by some trace or minor component of the plaque gruel of the necrotic core. The possibility of testing these hypotheses by practical methods has been shown to be feasible.
年轻男性突然死亡并经法医尸检，有时会在动脉粥样硬化相对早期阶段出现冠状动脉血栓形成。此类血栓下的斑块通常具有一系列特征：a) 破裂；b) 出血；c) 中膜破坏；d) 泡沫细胞结节状聚集；e) 钙化；f) 纤维帽、纤维基底部和外膜的细胞浸润；g) 在斑块坏死核心与纤维基底部之间的边界处新发现的一种吞噬活性。大多数无心脏病的中老年受试者中常见的无害斑块也常常具有其中一些特征。哪些结构特征可能将罕见的致血栓形成斑块与常见的无害斑块区分开来？对18例冠心病猝死病例中的21个血栓形成斑块进行了组织学检查，并与来自同一18例病例的129个非血栓形成斑块、23例因动脉粥样硬化闭塞导致冠心病死亡病例中的85个斑块以及22例无冠心病病例中的94个斑块进行了比较。有血栓形成的斑块均有坏死核心；因此选择与之比较的斑块均有坏死核心。90%的血栓形成斑块发现有破裂和出血，血栓中有斑块粥样物质和血液混合。中膜破坏、泡沫细胞和钙化（特征c、d和e）在所有类型斑块中都很常见。在21个血栓形成斑块中有72 - 94%发现有小细胞浸润和动脉粥样硬化吞噬作用（特征f或g），但在94个无冠心病斑块中仅18 - 24%有此现象。以结晶胆固醇为特征的坏死核心似乎在一些斑块中引发细胞反应，而在另一些斑块中则不然；这些反应区分了血栓形成。研究结果表明，致血栓形成性及其伴随的斑块细胞性不是由胆固醇引发的，而是由坏死核心斑块粥样物质中的某些微量或次要成分引发的。已证明通过实际方法检验这些假设是可行的。
