o "N o k~ E Q (,J 36A ABSTRACTS - ACCIS2002 (Angiography & Interventional Cardiology) oped that predicted the true distance and area with high statistical precision. (R2=0.99) Conclusion: Area measurements vary between different catheter systems indicating inconsistenciesof their internal calibration scales, External calibration equations can cor- rect for these differences and allow the comparison of measurementsin multicenter intra- vascular ultrasound studies analyzing atheroscleroticdisease progression. %CSA-Diffcrences of Different Catheter-Systems Before After Calibration Calibration ;10% ~0 -10% 20% Section 1 2 3 4 5 Section 1 2 3 4 5 1104-16 Calcification In Saphenous Vein Graft: Clinical Correlates and Intrevascular Ultrasound Findings Marco T. Castaona. Gary S. Mintz, Nell J. Weissman, Akiko Maehara, Jun-ichi Kotani, Javed M. Ahmed, Marfine Gilard, Daniel Canos, William O. Suddath, Lowell F. Satier, Ron Waksman, Kenneth M. Kent, Augusto D. Pichard, Washington Hospital Center, Washington, Dist of Columbia, Cardiovascular Research Foundation, New York, New York. Background: The ability of angiography to detect calcium is limited. Intravascular ultra- sound (IVUS) has been used to study calcification in native coronary arteries, but not in saphenous vein grafts (SVG's). Native artery calcium is more often located within lesions (vs reference segments) and in the plaque (vs the wall). Methods: We analyzed clinical and pre-intervention IVUS findings in 334 consecutive SVG's in 274 pts. IVUS measure- ments included arc and length of calcium at the lesion, 10mm proximal and distal refer- ence segments, as well as the whole SVG from distal anastomosis to aorto-ostial junction. Results: Calcium was found in 40% of SVGs. It was evenly distributed at lesion site (14%), proximal (13%) and distal (13%) reference segments, and elsewhere in the SVG (10%). Calcium was located primarily in the SVG wall, not in the plaque. In pts with calcium, the maximum arc at the proximal reference, lesion site, and distal reference averaged 175 ° , 151 ° and 177 ° , respectively, with maximum arc over the entire length of the SVG averaging 174 °. The table shows the clinical correlates of SVG calcification. SVG calcium occurred more commonly in older grafts, in insulin-treateddiabetics (IDDM) and in smokers, Conclusion: Calcium occurs commonly in SVG's; however, patterns and clinical correlates are distinctly different from native arteries. This suggests that SVG calcium is a result of SVG wall degeneration is not part of SVG lesion formation and mat- uration. No Calcium Calcium p SVG age, years 7.5 10.5 <0.0001 IDDM, % 40 60 0.02 Tobacco use, % 44 55 0.060 Hypertension, % 60 40 0.9 Dilipidemia, % 60 40 0.6 Renal Insufficiency,% 55 45 0.5 1104-17 Negative Remodeling Is a Predominant Mechanism for Lumen Compromise in Intermal Mammary Artery Stenosie Formation: An Intrevaeculer Ultrasound Study Javed M. Ahmed. Gary S. Mintz, Marco T. Castagna, Marco Zamirino, Augusto D. Pichard, Lowell F. Salter, Kenneth M. Kent, Neil J. Weissman. To better understand the mechanism of stenosis formation in intemal mammary arlery (IMA), we used pre-intervention intravascular ultrasound (IVUS) imaging to study 41 patients (41 IMA lesions: 15 ostial, 23 anastomosis,3 distal shaft) undergoing percuta- neous intervention (PCI). IVUS measurements included reference and lesion site vessel area (EEM CSA), lumen area, plaque (vessel-lumen area) and plaque burden (plaque/ vessel area), and arc of calcium in degrees. The lesion EEM CSA was compared to the reference; positive remodelling was defined as lesion > reference EEM CSA (remodelling index _> 1.0) and negative remodelling was defined as lesion < reference EEM CSA (remodelling index < 1.0). Conclusion. IMA stenosis is distinctly different from coronary artery disease. In IMA stenosis, pre-intervention IVUS demonstrated that (1) reference plaque burden is mod- est, (2) negative remodelling contributes importantly to lumen compromise at both ostial and anastomotic sites, and (3) there is no significant calcium at either site. JACC March 6, 2002 Ostial Anastomosis P Refrenco EEM CSA, mm 2 10.8+1.18 10.6tO.85 0.58 Reference Lumen CSA, mm 2 7.9tO.92 7.9-+1.27 0.67 Reference P&M CSA, mm 2 2.9-J:0.66 2.6-+o.76 0.31 Reference plaque burden 25_+6 25+6 0.51 Lesion EEM CSA, mm 2 7.05:1.17 6.7±0.85 0.38 Lesion lumen CSA, mm 2 2.4-+0.82 2.7±0.58 0.16 Lesion P&M CSA, mm 2 4.6_+0.62 4.0i~.61 0.004 Lesion plaque burden 66±7 59-+6 0.005 Lesion Ca (°) 16.8±26.9 2.0t-9.5 0.04 Remodeling index 0.63±0.07 0.64±0.06 0.58 1104-18 Different Mechanism of Lumen Enlargement in Lesions With Stent Underexpansion After Balloon Angiopleety for In-Stent Restenosis Compared to Those With Optimal Stent Expansion: An Intrsvasculsr Ultrasound Study Farzana Adf. Yoshio Kobayashi, Makoto Hirose, Octavia Balan, Arlene Reyes, Ioannis lakovou, Milena Adamian, Roxana Mehran, George Dangas, AlexandraJ. Lansky, Issam Mousse, Gregg W. Stone, Martin B. Leon, Jeffrey W. Moses, Gary S. Mintz, Cardiovascular Research Foundation, New York, New York. Background: The mechanism of lumen enlargement after angioplasty (PCI) for in-stent restenosis (ISR) is a combination of further stant expansion and redistribution of intimal hyperplasia. However, the effect of stent underexpansion on lumen enlargement after PCI for ISR is not fully evaluated. Methods: Intravascular ultrasound (IVUS) was performed in 166 lesions with ISR. Those were divided in two groups: (1) stant underexpansion defined as stent area <7.0 mm 2 and <80% of reference lumen area (n=55) and (2) optimal expansion (n=111), Calcified plaque behind slant struts was defined as calcium arc >180 °. Conclusions: Stent underexpansionis observed in 33% of ISR lesions and is frequently associated with calcified plaque morphology. Further stant expansion is the main mecha- nism of lumen enlargement in these lesions. However, even using higher balloon pres- sures, post-PTCA stent and lumen CSA are smaller than lesions in which the stent was optimally expanded initially. Results Optimal Underexpansion p Value Calcium behind stent (%) 4 33 <0.01 Reference CSA (mm2) 6.8-+2.4 5.7±1.8 0.01 Pre-lumen CSA (mm2) 1.9±1.0 2.3±1.0 0.07 Pre-stent CSA (mm2) 6.7±1.9 3.9±0.9 <0.01 Pre-intima CSA (mm2) 4.9~1.7 1.7±1.3 <0.01 B/V ratio 1.17:L-0.13 1.15+0.15 NS Max. inflation pressure (atm) 13.8+4.0 15.8+4.2 <0.01 Post lumen CSA (mm2) 6.0:t:1.6 4.8+1.4 <0.01 Post stent CSA (mm2) 8.2+9.2 5.6+1.8 <0.01 Post intima CSA (mm2) 2.2+1.4 0.8~0.8 <0.01 A lumen CSA (mm2) 4.2±1.4 2.7+1.8 <0.01 ,', stent CSA (mm 2) 1.7±1.0 1.7±1.6 NS ~, intima CSA (mm2) 2.5+1.2 1.2~0.9 <0.01 ,1 stent CSA / ,1 lumen CSA 39+~?.0 53_+32 0.04 1104-19 Severity of the Worst Lesion Correlates With Total Plaque Burden in a Coronary Artery: In Vivo Analysis in Patients With Mild, Moderate, and Severe Atheroeclerosis Samir R. Kaoadia. FernandoA. Cura, Paul Schoenhagen,Jennifer Popovich, Robert E. Hobbs, Staven E. Nissen, E. M. Tuzcu, University of Washington, Seattle, Washington, Cleveland Clinic Foundation, Cleveland, Ohio. Background: Active coronary atherosclerosis has been associated with signs of sys- temic inflammation. If atherosclerosiswere a diffuse, generalized process, plaque area at the site with worst tesion would correlate with the total plaque volume in that vessel To test this hypothesis, we compared the worst plaque area to total plaque burden in patients with mild, moderate and severe atherosclerosis. Methods: Mild atherosclerosis group consisted of 171 donor hearts, studied within 60 days of transplantation. Moderate atherosclerosis group included 279 patients with <50% stenosis and severe atherescle- rosis group consisted of 79 patients undergoing percutaneous intervention for severe (>70%) stenosis. Automated pullback sequences were obtained in all patients. Plaque volumes were calculated by measuring all sites separated by 1 ram. Total plaque volume was correlated with the worst plaque area. Results: We ana;yzed 6207 sites from 171 patients with mild, 12031 sites from 279 patients with moderate and 2001 sites from 79 patients with severe atheroscleresis. Irrespective of the sevedty of atherosclerosis,there Downloaded From: http://173.193.11.214/ on 03/04/2013