Frenzel H
Wien Med Wochenschr. 1984 Dec 31;134(23-24):517-24.
Exact pathological investigations revealed 90% of transmural infarctions to be caused by thrombotic occlusion of "Infarction branch". This is the reason for and not the consequence of the myocardial infarction. The myogenic theory could be disproved for the overwhelming majority of cases. The subendocardial infarction is caused by stenosed three-vessel-disease occasionally combined with severe anemia or attacks of tachycardia. In about 30% of cases fibrinous pericarditis could be found over the infarction area. Mural thromboses were detected in about one third of the transmural infarctions, a myocardial rupture was found in 10 to 15% of autopsies. A ventricular aneurysm developed in 5 to 10% of those cases, who survived more than 3 months. In cases of sudden death a severe stenosis or occlusion of one or more coronary vessels were found in more than 80%. A fresh thrombotic occlusion was also found due to rupture of arteriosclerotic plaques. An infarction is in this condition often not detectable, because the time between the onset of the attack and death was too short to develop a myocardial necrosis.
确切的病理检查显示,90%的透壁性梗死是由“梗死支”的血栓性闭塞所致。这是心肌梗死的原因而非结果。对于绝大多数病例,肌原学说可被证伪。心内膜下梗死是由三支血管病变狭窄偶尔合并严重贫血或心动过速发作引起的。在约30%的病例中,可在梗死区域发现纤维蛋白性心包炎。在约三分之一的透壁性梗死中检测到壁血栓形成,尸检中发现心肌破裂的占10%至15%。在存活超过3个月的病例中,5%至10%会形成室壁瘤。在猝死病例中,超过80%发现一根或多根冠状动脉严重狭窄或闭塞。还发现由于动脉粥样硬化斑块破裂导致新鲜的血栓性闭塞。在这种情况下,梗死往往无法检测到,因为发作开始到死亡之间的时间太短,不足以发展为心肌坏死。