论文部分内容阅读
46～70岁的6(男5、女1)例急性透壁心肌梗塞患者虽经链激酶溶栓治疗仍有高度狭窄,随即(5例)或34天后(1例)接受经皮冠状动脉腔内成形术(PTCA)治疗.PTCA后第8、9、12、13和14天(早期)或第54天各死亡1例.死亡原因有:心源性休克4例,顽固性心律失常1例,左室破裂和二尖瓣反流经手术治疗后多器官功能衰竭1例.各例梗塞区供血动脉均为左前降支.尸检见PTCA后动脉壁内侧部分损伤(内膜层裂隙、内膜下层夹层分离、中膜层撕裂和中膜下层夹层分离)和中膜层平滑肌细胞坏死(似系各细胞破裂或外膜层营养血管损伤造成动脉壁缺血所致).早期死亡者均有新生内膜层(neointima)形成,而晚期死亡者新生内膜层增生再次阻塞管腔.本组观察支持:外观完整的动脉壁外侧部分的不可逆性扩张(动脉瘤形成)导致动脉壁内侧部分的断裂和夹层分离并导致中膜层坏死,均是PTCA的最重要的机制.对PTCA后动脉壁损伤的反应为成纤维肌细胞(fibromyoblast)形
Patients with acute transmyocardial infarction of 6 (male 5, female 1) 46 to 70 years of age were still highly stenosed by streptokinase thrombolysis and subsequently received percutaneous coronary artery lumen (5 patients) or 34 days (1 patient) One patient died on the 8th, 9th, 12th, 13th, 14th (early) or 54th day after PTCA.The causes of death were: cardiogenic shock in 4 cases, refractory arrhythmia in 1 case , Left ventricular rupture and mitral regurgitation after surgery in 1 case of multiple organ failure.The blood supply artery in each case were left anterior descending branch.After autopsy see the part of the medial wall of the arterial wall after PTCA (endometrial fissure, intima Lower interlayer dissection, middle layer tear and dissection of the middle layer under the dissection) and the middle layer of smooth muscle cell necrosis (like the Department of cell rupture or damage caused by nutrient vessels in the outer wall caused by arterial wall ischemia.) Early deaths were Neointima formation, whereas advanced neointimal hyperplasia in late-stage patients again occludes the lumen This group of observations supports the view that irreversible dilatation (aneurysm formation) of the lateral portions of the intact arterial wall results in Fracture and dissection and lead to necrosis of the media, are the most important mechanism of PTCA. PTC The response of arterial wall injury after A is fibromyoblast-shaped