IVUS Study Investigates Mechanisms of DES Restenosis

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While intimal hyperplasia remains the predominant mechanism for in-stent restenosis with drug-eluting stents (DES), another key factor, stent underexpansion, remains both important and preventable, according to results of an intravascular ultrasound (IVUS) analysis published online January 25, 2011, ahead of print in Circulation: Cardiovascular Interventions.

Researchers led by Seung-Jung Park, MD, PhD, of Asan Medical Center (Seoul, South Korea), used IVUS to characterize the lesions of 366 patients who received DES at their institution, 82 of whom developed angiographic restenosis. Sirolimus-eluting stents (SES), paclitaxel-eluting stents (PES), and zotarolimus-eluting stents (ZES) were the devices used. Seventy-six (93%) of the 82 restenotic lesions fit the IVUS definition of in-stent restenosis (minimum lumen area [MLA] < 4 mm²). In the 312 lesions without angiographic restenosis, 83 (27%) fit the IVUS definition.

In the 76 IVUS restenotic lesions, 32 (42%) had stent underexpansion (minimal stent area [MSA] < 5 mm²). This was true of 75 (24%) of the 312 lesions without angiographic restenosis. Despite the relatively frequent occurrence of underexpansion, intimal hyperplasia (> 50% of the stent area) was found to be the general mechanism of in-stent restenosis, showing incidences of 93% at any location within the stented segments and 88% at the minimum lumen site in the 76 IVUS restenotic lesions.

Stent Length Makes a Difference

There was a significant negative association between total stent length and both MSA (P < 0.001) and stent area at the minimum lumen site (P < 0.001) but not MLA (P = 0.472).

Total stent length of 28 mm was the cutoff value that best separated MSA above or below 5 mm² (70% sensitivity, 61% specificity). For instance, underexpansion was present at the minimum lumen site in 15 of 43 lesions (35%) with stent length greater than 28 mm, despite the presence of significant intimal hyperplasia in 34 lesions (79%). Conversely, in 32 of 33 lesions (97%) with stent length of 28 mm or less, the minimum lumen site was not associated with stent underexpansion but only with significant hyperplasia.

Focal in-stent restenosis was the most common pattern (47%), followed by diffuse and multifocal. This was true for each of the DES types used (with the exception of ZES), with no significant differences between the 3 types (table 1).

Table 1. Patterns of In-Stent Restenosis

Overall, significant intimal hyperplasia greater than 10 mm in length was less common with SES (9%), than with PES (32%) or ZES (33%; P = 0.038).

“In most DES restenosis, [intimal hyperplasia] was the dominant mechanism of [in-stent restenosis],” the researchers conclude. “Nevertheless, underexpansion associated with longer stent length remained an important preventable mechanism of [in-stent restenosis].”

Dr. Park and colleagues add that IVUS guidance may be especially helpful in avoiding underexpansion in long lesions, small vessels, and other complex stenoses. Also, a potential explanation for the role of longer stent length in restenosis could be a greater possibility for “occult” focal stent underexpansion somewhere in the longer stent segments.

Note: Gary S. Mintz, MD, a coauthor of the paper, serves as Medical Director and Editor-in-Chief of TCTMD.

Source:

Kang S-J, Mintz GS, Park D-W, et al. Mechanisms of in-stent restenosis after drug-eluting stent implantation. Intravascular ultrasound analysis. Circ Cardiovasc Interv. 2011;4:9-14.

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