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PATHOGENESIS OF CARDIAC RUPTURE FOLLOWING ACUTE MYOCARDIAL INFARCTION

机译:急性心肌梗死后心脏破裂的发病机制

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Myocardial rupture is a known complication of acute infarction (Datta, 1975 and Becker, 1975). The morphological variation associated with this phenomenon can be explained by the formation of an endocardial tear followed by a dissecting hemorrhage. The model explains the correlation between rupture, hypertension, and the age of an infarct. However, it is incomplete as it fails to predict what causes the endocardial tear. Infarcted myocardium remains irreversibly more compliant than non-infarcted muscle and passive (Baroldi, 1991). Rupture usually occurs early post infarction, at the margin of the infarct, and is most often associated with transmural infarcts (Whittaker, 1991 and Lewis, 1969). This suggests that stress concentration effects, due to a material mismatch at the border of the infarcted and non-infarcted muscle, are the cause of an endocardial tear. Some degree of aneurysm formation is almost always present with acute infarction. Thus, a common mechanism exists between myocardial rupture post infarction and the formation of a left ventricular (LV) aneurysm. Because of the common mechanism in rupture and aneurysm formation, prior LV aneurysm models are reviewed. Radhakrishnan (1986) described an ellipsoidal shell model (Fig. 1) of the LV with isotropic layered walls. Myocardial rupture was not predicted with infarctions of less than 70% of the wall thickness. For a fixed LV geometry, increases in the angle-of-damage of the infarct were associated with a smaller thickness of infarction to avoid rupture. Similarly, for a fixed thickness of the infarct, increases in the angle-of-damage of the infarct were associated with larger ratios of b{sub}0/a{sub}0 to avoid rupture. Myocardial rupture was more dependent upon the percentage of infarcted wall thickness and LV shape than the angle-of-damage of the infarct. These generalizations were based upon average wall stress and deformations. Although insightful in general terms, insufficient detail in the stress distributions is available for correlation to the morphologic data for rupture.
机译:心肌破裂是一种已知的急性梗塞并发症(Datta,1975和Becker,1975)。可以通过形成细胞内膜撕裂,然后进行解剖出血,解释与这种现象相关的形态学变异。该模型解释了破裂,高血压和梗塞的年龄之间的相关性。然而,它不完整,因为它未能预测导致心内膜撕裂的原因是什么。梗死的心肌仍然比非梗塞肌肉和被动(Baroldi,1991)仍然符合不可逆转的更符合要求的。破裂通常发生早期梗死,在梗塞的边缘处,通常与透际梗塞(Whittaker,1991和Lewis,1969)相关。这表明,由于梗死的边界和非梗死肌的边界处的材料不匹配,压力集中效应是心内膜撕裂的原因。一定程度的动脉瘤形成几乎总是存在急性梗死。因此,心肌破裂后梗死与左心室(LV)动脉瘤的形成之间存在常见机制。由于破裂和动脉瘤形成的常见机制,综述了先前的LV动脉瘤模型。 Radhakrishnan(1986)描述了LV的椭圆形壳模型(图1),其具有各向同性层状壁。没有用墙壁厚度的梗塞不到70%的梗塞的心肌破裂。对于固定的LV几何形状,梗死角度的损伤的增加与较小的梗塞厚度相关,以避免破裂。类似地,对于梗塞的固定厚度,梗死角度的损伤角度的增加与B {Sub} 0 / A {Sub} 0的较大比例相关联,以避免破裂。心肌破裂更依赖于梗塞壁厚和LV形状的百分比而不是梗塞的损伤。这些概括基于平均墙体应力和变形。虽然一般而言,但是,应力分布中的细节不足的细节可用于与破裂的形态数据相关。

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