Quantitative assessment of in-stent dimensions: a comparison of 64 and 16 detector multislice computed tomography to intravascular ultrasound.

OBJECTIVES: To determine the utility of multislice computed tomography (MSCT) technology to evaluate coronary stent luminal diameter. BACKGROUND: Stent metal induced "blooming" artifact makes quantitative coronary angiography by MSCT difficult. There is a paucity of data on the efficacy of using 64 and 16 detector MSCT in evaluating coronary stents. METHODS: We evaluated four commercially available bare metal and polymer coated drug eluting stents using 64 and 16 detector MSCT for the following: (1) Strut density in Hounsfield's Units (Hu) using a 2 mm MIP; (2) In-stent luminal diameter (ISLD) measured by MSCT compared to intravascular ultrasound (IVUS). RESULTS: Increased strut thickness did not correlate with greater strut density as measured in Hu (R(2) = 0.05, P = 0.29). The ISLD by 16 MSCT vs. IVUS is: Vision 1.63 +/- 0.58 mm vs. 2.8 +/- 0.0; Cypher 1.80 +/- 0.00 vs. 2.9 +/- 0.0; Taxus 1.87 +/- 0.58 vs. 2.9 +/- 0.0; Liberté 1.80 +/- 0.10 vs. 3.0 +/- 0.1 (P < 0.01). ISLD determined by 64 MSCT vs. IVUS is: Vision 1.73 +/- 0.06 mm vs. 2.8 +/- 0.0; Cypher 1.87 +/- 0.12 vs. 2.9 +/- 0.0; Taxus 1.77 +/- 0.06 vs. 2.9 +/- 0.0; Liberté 1.80 +/- 0.10 vs. 3.0 +/- 0.1 (P < 0.01). CONCLUSIONS: When compared to IVUS measurements, MSCT results in a significant, underestimation of ISLD. This consistent underestimation (even with 64 MSCT) limits the applicability of CT angiography to quantify in-stent restenosis.

Antirestenotic effects of a locally delivered caspase inhibitor in a balloon injury model.

BACKGROUND: The precise role of arterial barotrauma-mediated apoptosis in causing restenosis is unclear. The purpose of this study was to determine if a link exists between angioplasty-mediated medial smooth muscle cell apoptosis and subsequent neointimal hyperplasia. METHODS AND RESULTS: Bilateral iliac artery angioplasty was performed in 25 male New Zealand White rabbits. Simultaneous with balloon injury, each artery was treated locally with either the caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp(Ome)-fluoromethylketone (ZVAD-fmk) or control. In the acute cohort that was survived to 4 hours (n=10, 7 high dose and 3 low dose), an apoptotic index was calculated using the terminal deoxynucleotidyl TUNEL method. In the intermediate cohort that was survived to 2 weeks (n=5), luminal reendothelialization was measured via CD-31 staining. In the chronic cohort that was survived to 4 weeks (n=10), neointimal area was measured. In the acute cohort, there was a 40% reduction in the apoptotic index with high-dose ZVAD-fmk (P=0.008) and a 33% reduction with low-dose ZVAD-fmk (P=0.08). At 2 weeks, there was no significant difference in the degree of luminal reendothelialization. However, at 4 weeks, there was a 33% (0.33+/-0.23 versus 0.22+/-0.20 mm2) (P<0.005) reduction in neointimal area in ZVAD-fmk-treated arteries. CONCLUSIONS: The local delivery of ZVAD-fmk during balloon injury inhibits smooth muscle cell apoptosis. This corresponds to a significant reduction in neointimal proliferation seen at 4 weeks without a significant change in the degree of reendothelialization at 2 weeks.