Mechanisms of restenosis and redilation within coronary stents--quantitative angiographic assessment

This study was designed to assess the relative contributions of intimal hyperplasia and stent compression to the lumen narrowing seen after intracoronary stenting and to determine whether the lumen enlargement produced by angioplasty of in-stent restenosis results primarily from compression or extrusion of intimal hyperplasia through the stent or from additional stent expansion.

Palmaz-Schatz stent placement outwardly displaces plaque and eliminates elastic vessel recoil to provide a large and smooth lumen. Some degree of late lumen narrowing occurs within each stent and causes significant restenosis (> or = 50% stenosis) in 25% to 30% of treated lesions. It has not been clear, however, whether this narrowing results from stent compression (crush) or from in-stent intimal hyperplasia. Because the Palmaz-Schatz stent has a distinct radiographic shadow, it is possible to determine the late diameter of both the stent and the enclosed vessel lumen to assess the relative contributions of these two processes.

From cineangiograms, initial (after stenting) and late (follow-up) lumen and stent diameters were examined in 55 patients (59 stents, group I) who had both immediate and 6-month (192 +/- 117 days) angiography. Lumen and stent diameter were also examined before and after dilation in 30 patients (30 stents, group II) who underwent angioplasty of severe in-stent restenosis.

Late loss in minimal lumen diameter was 0.99 +/- 0.87 mm for group I despite only a slight (0.03 +/- 0.23-mm) reduction in the corresponding stent diameter. After redilation for in-stent restenosis, the acute gain in minimal lumen diameter was 1.51 +/- 0.82 mm for group II, again without appreciable increase (0.06 +/- 0.20 mm) in stent diameter.

Restenosis after intracoronary Palmaz-Schatz stenting appears to be due predominantly to lumen encroachment by intimal hyperplasia within the stent, with minimal contribution of stent compression. Lumen enlargement after coronary angioplasty of in-stent restenosis appears to be due primarily to compression or extrusion of intimal hyperplasia through the stent, or both, rather than to further stent expansion.