[Role of smooth muscle cell proliferation after balloon angioplasty]

The long-term success of percutaneous transluminal coronary angioplasty (PTCA) is severely limited by the high incidence of restenosis, which occurs in up to 30 to 40% of primary successfully treated patients. Several postmortem and experimental studies have demonstrated that restenosis after balloon angioplasty is caused by intimal proliferation of smooth muscle cells (SMCs). As a result of the vessel wall injury due to the mechanical intervention, endothelial injury and platelet aggregation at the site of dilatation can be observed. SMCs are activated for migration and proliferation in the early phase after angioplasty by subsequent expression of several growth factors, activation of macrophages, and expression of a variety of mitogens (Figure 1). Since several other alternative interventional devices like atherectomy, excimer laser angioplasty and stenting are also limited by the occurrence of SMC proliferation following treatment, there is an obvious need for a pharmacological approach to inhibit SMC proliferation after PTCA. It has been shown in experimental studies that the proliferative response of the vessel wall in the intima occurs within the first seven days after dilatation. A significant increased mitosis rate of SMCs in the media, however, can be observed within three weeks after intervention (Figure 2). As suggested by several authors, macrophages are thought to play an important role in the restenosis process after balloon angioplasty. However, our experimental results demonstrate that no significant accumulation of macrophages occurred prior to seven days following balloon angioplasty (Figure 3).(ABSTRACT TRUNCATED AT 250 WORDS)