Galankina I E
Arkh Patol. 1985;47(2):36-44.
The main features of hemorrhagic myocardial infarction (HMI) are presented basing on the light and electron microscopic study of 32 cases. HMI is distinguished macroscopically from the ischemic infarction by its dark-red colour due to a diffuse hemorrhagic imbibition and by the clear borders already seen within, the first hours of the disease. Histologically HMI is distinct due to the fibrinoid necrosis of the walls of small arteries, capillaries and, first of all, veins with their thrombosis. This results in the increasing vessel permeability, large hemorrhages into the interstitium with the fibrin deposits and the penetration of erythrocytes and fibrin into cardiomyocytes. Pathogenetic peculiarity of HMI is the blockade of the microcirculatory and venous bed in the background of normal coronary circulation. These events develop probably primarily in natural course of HMI and secondarily when fibrinolytic therapy is used. The thrombi of big arteries found in 9 out of 32 cases seem to arise secondarily in the background of the altered venous circulation. Possible causes of the microcirculatory-venous blockade in HMI may be persistent angiospasm, alteration of the blood coagulation, complications of the fibrinolytic therapy as well as toxicoallergic reactions and microembolism.
基于对32例病例的光镜和电镜研究,阐述了出血性心肌梗死(HMI)的主要特征。HMI在宏观上与缺血性梗死的区别在于,由于弥漫性出血性浸润,其颜色呈暗红色,且在疾病最初几小时内就可见清晰的边界。组织学上,HMI的特征是小动脉、毛细血管尤其是静脉壁的纤维蛋白样坏死并伴有血栓形成。这导致血管通透性增加,间质内大量出血并伴有纤维蛋白沉积,红细胞和纤维蛋白渗入心肌细胞。HMI的发病机制特点是在冠状动脉循环正常的情况下,微循环和静脉床受阻。这些情况可能主要在HMI的自然病程中发生,其次在使用纤溶治疗时出现。在32例病例中有9例发现大动脉血栓,似乎是在静脉循环改变的背景下继发形成的。HMI中微循环 - 静脉受阻的可能原因包括持续性血管痉挛、凝血改变、纤溶治疗的并发症以及毒过敏反应和微栓塞。