Essed C E, Van den Brand M, Becker A E
Br Heart J. 1983 Apr;49(4):393-6. doi: 10.1136/hrt.49.4.393.
Transluminal coronary angioplasty was performed in a 51 year old man with a localised narrowing of the proximal segment of the left anterior descending coronary artery. Initial inflations with a small size balloon catheter were unsuccessful. A second attempt, during the same procedure, using a larger calibre catheter relieved the obstruction but produced a dissection. Angina pectoris reappeared approximately three months later. Another attempt to relieve the obstruction by angioplasty, five months after the initial procedure, induced ST segment elevation before angioplasty, followed by ventricular fibrillation and death. The necropsy showed a split in the pre-existent sclerotic plaque and a dissecting aneurysm of the media. A proliferation of fibrocellular tissue filled the false channel and almost totally occluded the pre-existent arterial lumen. The observation suggests that wall laceration with exposure of smooth muscle cells to blood may have initiated the excessive fibrocellular tissue response. This event may be the underlying pathogenetic mechanism for the occurrence of early restenosis after transluminal coronary angioplasty.
对一名51岁男性进行了经皮冠状动脉腔内血管成形术，该患者左前降支冠状动脉近端节段存在局限性狭窄。最初使用小尺寸球囊导管进行扩张未成功。在同一手术过程中，第二次尝试使用更大口径的导管解除了梗阻，但导致了夹层形成。大约三个月后心绞痛再次出现。在初次手术后五个月，再次尝试通过血管成形术解除梗阻，在血管成形术前出现ST段抬高，随后发生心室颤动并导致死亡。尸检显示，原有硬化斑块出现裂开，中膜形成夹层动脉瘤。纤维细胞组织增生填充了假腔并几乎完全闭塞了原有的动脉管腔。该观察结果表明，血管壁撕裂使平滑肌细胞暴露于血液中可能引发了过度的纤维细胞组织反应。这一事件可能是经皮冠状动脉腔内血管成形术后早期再狭窄发生的潜在发病机制。
