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.
Essed et al. (1983) studied this question.