SMALL STENT SIZE AND INTIMAL HYPERPLASIA CONTRIBUTE TO RESTENOSIS - A VOLUMETRIC INTRAVASCULAR ULTRASOUND ANALYSIS

Objectives. The purpose of this study was to use volumetric intravascular ultrasound analysis of Palmaz-Schatz stents to assess the in-stent restenotic process. Background. By reducing lesion elastic recoil and chronic arterial remodeling, stents improve the long term results of coronary angioplasty. However, stents are prone to the development of neointimal hyperplasia. Angiographic studies of stent restenosis have suggested that these hyperplastic responses are the cause of in stent restenosis; however, it is difficult to visualize the radiolucent Palmaz-Schatz stent by angiography. Intravascular ultrasound provides detailed cross-sectional imaging of the coronary arteries, especially the intense metallic reflection of endovascular stents. Methods. Forty-four patients with 60 Palmaz-Schatz stents underwent intravascular ultrasound imaging at follow up ([mean +/- SD] 8.8 +/- 7.2 months after implantation). Thirty-four stents were placed in saphenous vein grafts and 26 in native coronary arteries; 30 were placed in restenotic lesions. Intravascular ultrasound with automatic transducer pullback at 0.5 mm/s allowed measurement of stent, lumen and intimal hyperplasia cross-sectional areas at 1-mm axial increments within the stents. Using Simpson's rule, stent, lumen and intimal hyperplasia volumes were calculated. Patterns of in stent restenosis were then identified. Results. Restenotic stents had smaller stent volumes (120 +/- 41 vs, 147 +/- 43 mm(3), p = 0.016) and lumen volumes (62 +/- 28 vs. 118 +/- 42 mm(3), p < 0.0001) but larger intimal hyperplasia volumes (58 +/- 36 vs. 29 +/- 18 mm(3), p < 0.001) than nonrestenotic stents. A focal restenosis pattern was more common (20 [77%] of 26) than a diffuse restenosis pattern (6 [23%] of 26), Stents with focal restenosis and stents with diffuse restenosis had equally small stent volumes (120 +/- 44 vs. 120 +/- 31 mm(3), respectively, p = NS); however, stents with diffuse restenosis had larger intimal hyperplasia volumes (84 +/- 30 vs. 50 +/- 34 mm(3), p < 0.05), Focal restenosis was most commonly located at the central articulation (45%); the location of focal restenosis was related to the focal accumulation of neointimal tissue. Conclusions. Stent volume and magnitude and distribution of intimal hyperplasia are important in the development of in-stent restenosis. Stent volume was smaller and intimal hyperplasia volume greater in restenotic stents. Stent restenosis is more commonly focal in nature and located at the central articulation.