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J Am Coll Cardiol, 1998; 32:329-337 © 1998 by the American College of Cardiology Foundation |
a Intravascular Ultrasound Imaging and Angiographic Core Laboratories, The Washington Hospital Center, Washington, DC, USA
Manuscript received December 9, 1996; revised manuscript received February 26, 1998, accepted April 23, 1998.
Address for correspondence: Dr. Martin B. Leon, Director of Research, Cardiology Research Foundation, 110 Irving Street NW (4B-1), Washington, DC 20010
Objectives. The intravascular ultrasound (IVUS) substudy of OARS (Optimal Atherectomy Restenosis Study) was designed to assess the mechanisms of restenosis after directional coronary atherectomy (DCA).
Background. Recent serial IVUS studies have indicated that late lumen loss after interventional procedures was determined primarily by the direction and magnitude of arterial remodeling, not by cellular proliferation.
Methods. Complete quantitative coronary angiography (QCA) and IVUS were obtained in 104 patients before and after intervention and during follow-up. All studies were performed after administration of 200 µg of intracoronary nitroglycerin. Angiographic measurements included minimum lumen diameter (MLD), interpolated reference diameter and diameter stenosis (DS). Intravascular ultrasound measurements included lesion and reference external elastic membrane (EEM), lumen and plaque+media cross-sectional area (CSA). The axial location of the lesion site was at the smallest follow-up lumen CSA; the reference segment was the most normal-looking cross section within 10 mm proximal to the lesion but distal to any major side branch. Results are reported as mean ± one standard deviation.
Results. The QCA reference decreased from 3.51 ± 0.46 mm to 3.22 ± 0.44 mm; the MLD decreased from 3.22 ± 0.47 mm to 2.03 ± 0.72 mm; and the DS increased from 8 ± 10% to 38 ± 20%. On IVUS, the decrease in lumen CSA (from 8.8 ± 2.5 mm2 to 5.5 ± 4.0 mm2) was associated with a significant decrease in EEM (from 19.7 ± 5.6 mm2 to 16.9 ± 6.2 mm2); there was no significant increase in P+M (from 10.9 ± 4.2 mm2 to 11.3 ± 3.9 mm2). A change in lumen correlated with a change in EEM (r = 0.790, p < 0.0001), not with a change in P+M (r = 0.133, p = 0.2258). A decrease in reference EEM (from 19.1 ± 7.7 mm2 to 17.6 ± 8.0 mm2) also correlated with a decrease in lesion EEM (r = 0.665, p < 0.0001). Results in restenotic lesions were similar.
Conclusion. Restenosis after optimal DCA is caused primarily by a decrease in EEM CSA that extends into contiguous reference segments.
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