Wednesday, April 28 - Friday, April 30, 2010 (E-Poster Abstract Zone)
VULNERABLE PLAQUE (Abstract nos. AS-273–AS-274)
AS-273 Intravascular Ultrasound Predictors of No-Reflow after Percutaneous Saphenous Vein Graft Intervention. Young Joon Hong1, Gary S. Mintz2, Sang Wook Kim3, Sung Yun Lee4, Seok Yeon Kim5, Youngkeun Ahn1, Myung Ho Jeong1, Jung Chaee Kang1, Augusto D. Pichard6, Ron Waksman6, Neil J. Weissman6. 1Chonnam National University Hospital, Gwangju, Republic of Korea; 2Cardiovascular Research Foundation, New York, New York, USA; 3Chung-Ang University Hospital, Seoul, Republic of Korea; 4Inje University Ilsan Paik Hospital, Ilsan, Republic of Korea; 5Seoul Medical Center, Seoul, Republic of Korea; 6Washington Hospital Center, Washington, DC, USA.
EP O S T E R A B S T R A C T S
Background: Intravascular ultrasound (IVUS) predictors of no-reflow after percutaneous coronary intervention (PCI) for saphenous vein graft (SVG) were not well known. The aim of this study was to investigate the relationship between IVUS findings and the no-reflow phenomenon after PCI of SVG lesions. Methods: Of 311 patients who underwent pre- and poststenting IVUS, no-reflow was observed in 39 patients overall and in 19 of 125 patients treated using distal protection devices. Results: Degenerated SVGs (62% vs 36%, p ⫽ 0.002) and angiographic thrombus (41% vs 21%, p ⫽ 0.006) were more significantly observed in the no-reflow group. IVUS-detected intraluminal mass (82% vs 43%, p ⬍0.001), culprit lesion multiple plaque ruptures (23% vs 6%, p ⬍0.001), and plaque prolapse (51% vs 35%, p ⫽ 0.043) were significantly more common in patients with no-reflow. In the multivariate logistic regression analysis, an intraluminal mass (hazard ratio [HR] ⫽ 4.84; 95% confidence interval [CI] 1.98 –10.49, p ⫽ 0.001), culprit lesion multiple plaque ruptures (HR ⫽ 3.46; 95% CI 1.46 – 8.41, p ⫽ 0.014), and degenerated SVGs (HR ⫽ 3.17; 95% CI 1.17– 6.56, p ⫽ 0.024) were independent predictors of post-PCI no-reflow. In the subgroup of 125 patients treated using distal protection devices, culprit lesion multiple plaque ruptures (HR ⫽ 7.99; 95% CI 1.95–32.98, p ⫽ 0.003), plaque prolapse (HR ⫽ 4.13; 95% CI 1.48 –13.45, p ⫽ 0.018), and degenerated SVGs (HR ⫽ 3.13; 95% CI 1.19 – 6.41, p ⫽ 0.027) were independent predictors of post-PCI no-reflow. Conclusion: IVUS-detected intraluminal mass, multiple plaque ruptures, plaque prolapse, and degenerated SVGs are associated with post-PCI no-reflow in SVG lesions.
AS-274 Relationship between Coronary Calcium Score by Cardiac Computed Tomography Angiography and Plaque Components by Virtual Histology-Intravascular Ultrasound. Yun Ha Choi, Young Joon Hong, Myung Ho Jeong, Eun Hye Ma, Keun Ho Park, Jum Suk Ko, Min Goo Lee, Doo Sun Sim, Ju Han Kim, Youngkeun Ahn, Jeong Gwan Cho, Jong Chun Park, Jung Chaee Kang. Chonnam National University Hospital, Gwangju, Republic of Korea. Background: Coronary calcium is a specific marker of atherosclerosis. Previous studies have shown that coronary calcium score is associated with plaque burden and morphology. However, few data are available about the relationship between coronary calcium score and plaque components. We evaluated this relationship between coronary calcium score using cardiac computed tomography angiography (CCTA) and plaque components by virtual histology–intravascular ultrasound (VHIVUS) in patients with coronary artery disease (CAD). Methods: The study included 106 CAD patients with 170 coronary lesions who underwent CCTA and were enrolled retrospectively; plaque components were analyzed using VH-IVUS. Coronary calcium score was assessed according to Agatston scoring method by CCTA: group I (calcium score ⫽ 0, n ⫽ 34); group II (calcium score ⫽ 1–100, n ⫽ 56); group III (calcium score ⫽ 101– 400, n ⫽ 69); group IV (calcium score ⬎400, n⫽11). VH-IVUS classified the color-coded tissue into 4 major components: fibrotic, fibrofatty, dense calcium (DC), and necrotic core (NC). Results: At the minimum lumen site, the percent DC area was greatest, and the percent fibrotic area was smallest in Group IV (5.6% ⫾ 6.8% vs. 12.0% ⫾ 10.4% vs. 15.4 ⫾ 11.5% vs. 19.4% ⫾ 13.5%, p ⬍0.001, and 63.1% ⫾ 14.7% vs. 56.6% ⫾ 13.9% vs. 49.6 ⫾ 13.3% vs. 50.1% ⫾ 15.4%, p ⬍0.001, respectively). At the largest NC site, the percent DC area was greatest, and the percent fibrotic area was smallest in Group IV (7.9% ⫾ 6.9% vs. 15.6% ⫾ 9.8% vs. 16.7% ⫾ 9% vs. 23.8% ⫾ 9.4%, p ⬍0.001, and 58.2% ⫾ 10.7% vs. 49.1% ⫾ 12.5% vs. 45.7% ⫾ 11.7% vs. 41.6% ⫾ 13.7%, p ⬍0.001, respectively). The absolute DC and NC volumes were greatest, and percent DC volumes were greatest in Group IV (5.2 ⫾ 6.6 mm3 vs. 10.9 ⫾ 9.2 mm3 vs. 15.9 ⫾ 14.6 mm3 vs. 35 ⫾ 20 mm3, p ⬍0.001, and 13.4 ⫾ 16.8 mm3 vs. 19.1 ⫾ 19.4 mm3 vs. 22.8 ⫾ 20.4 mm3 vs. 36.4 ⫾ 26.4 mm3, p ⫽ 0.007, and 6.2% ⫾ 4.7% vs. 12.0% ⫾ 6.5% vs. 13.8% ⫾ 6.8% vs. 21.3% ⫾ 7.1%, p ⬍0.001, respectively). The absolute plaque and DC and NC volumes and the percent DC volumes positively correlated with calcium score (r ⫽ 0.233, p ⫽ 0.002, r ⫽ 0.539, p ⬍0.001, r ⫽ 0.301, p ⬍0.001, and r ⫽ 0.450, p ⬍0.001, respectively). Conclusion: CAD patients with a high calcium score had more vulnerable plaque components (greater DC- and NC-containing plaques) compared with those with a low calcium score.
116BThe American Journal of Cardiology姞 APRIL 28 –30 2010 ANGIOPLASTY SUMMIT ABSTRACTS/E-Poster