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Can IVUS Define Plaque Features that Impact Patient Care?

Can IVUS Define Plaque Features that Impact Patient Care?. A Pichard L Satler, K Kent, R Waksman, W Suddath, N Bernardo, N Weissman, M Angelo, D Harrington, J Lindsay, J Panza. Washington Hospital Center Washington DC. Conflict of Interest. None related to this presentation.

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Can IVUS Define Plaque Features that Impact Patient Care?

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  1. Can IVUS Define Plaque Features that Impact Patient Care? A Pichard L Satler, K Kent, R Waksman, W Suddath, N Bernardo, N Weissman, M Angelo, D Harrington, J Lindsay, J Panza. Washington Hospital Center Washington DC

  2. Conflict of Interest • None related to this presentation

  3. IVUS at the WHC • Washington Hospital Center in last 12 months: • Diagnostic catheterizations: 10,000 • Coronary angioplasties: 5,000 • IVUS use: 70% (AP: 95%) • Organization • 10 Labs: 8 Labs have IVUS integrated into the Cath Table (Volcano and Boston). • IVUS setup is ready before physician arrives into the room. • 2 CV technicians supervise all IVUS cases. 15 CV technicians trained in IVUS. • Core Lab analyzes of all IVUS data.

  4. Vessel Size Remodeling.

  5. Positive Remodeling: • large plaque mass. • plaque is soft. • more likely to have thrombus. • associated with higher CRP. • More common in young people. • Very common in acute coronary syndrome. • More common no reflow during PCI. • Negative Remodeling: • less plaque mass • plaques are fibrotic. • less likely to have thrombus.

  6. Remodeling in Varying Coronary Lesion Morphologies Macrophage infiltration Posit Remodeling A. NC 5 Medial SMC loss 4 3 SMC loss 2 IEL-Expected IEL (/plaque area) 1 0 -1 -2 -3 Stable Erosion Acute rupture Healed rupture Total occlusion Thin cap atheroma Medial SMC apoptosis Plaque hemorrhage Virmani 2009

  7. Cardiac CT can be as good as IVUS to detect Positive Remodeling

  8. Positive Remodeling and Plaque Composition by OCT.Raffel et al. EHJ 2008;29:1721-8

  9. Positive Remodeling and ISRSOkura et al. JACC 2001, 37: 1031-35 n= 108 BMS Positive Remodeling Intermed. or Negative Remodeling

  10. Plaque Burden and In-Stent Intimal Hyperplasia WHC: Shiran et al, AJC 2000; 86:1318-21 Maximal IH at 6 months angio was at the zone of maximal pre intervention plaque. Pre-intervention plaque area was an independent predictor of IH at follow up.

  11. Remodeling and ISRS in DES.Mintz, Park et al. Circulation. 2003;108:1295-8 ASPECT (ASian Paclitaxel-Eluting Stent Clinical Trial) positive intermed negative Cypher RS 28.6% vs 16.7% for positive and non posit remodeling p=ns. AHA 2009

  12. Mild LMCA Disease and Remodeling.WHC:YJ Hong et al. JIC 2007;19:500-5 236 patients with mild (<50%) LMCA stenosis by angiography 1 year MACE

  13. Positive Remodeling and Outcome in ACS.Okura, Mintz et al. AJC 2009;103:791-5

  14. Prospect. MACE in Non Culprit Lesions

  15. Attenuated Plaque(Black Holes, Echo Signal Attenuation)WHC: SY Lee, Mintz et al. JACC Interv 2009;2:65-72 Shadowing in spite of no visible calcium Two attenuated plaques 6.4 mm apart were seen in this RCA.

  16. Attenuated Plaque in ACS.WHC: SY Lee, Mintz et al. JACC Interv 2009;2:65-72 293 ACS patients: 26% with attenuated plaque ( 40% STEMI, 18% NSTEMI) • Attenuated plaque in ACS patients was associated with: • positive remodeling and higher CRP, • more thrombus and complex lesion morphology, • more plaque burden and plaque rupture, • frequent no-reflow after PCI.

  17. Echo Signal Attenuation (EA).Kimura et al. Circ CV Interv. 2009;2:444-54. • 687 patients. • EA: 43.8% in ACS vs. 27.9% in Stable AP, p<0.001. • EA had Positive Remodeling: 55% vs 23 % for lesions without EA. • Histology after DCA: • higher prevalence of lipid-rich plaque, macrophage infiltration, cholesterol clefts, thrombus, and microcalcification.

  18. No Reflow in SVG’s with ACS.WHC: YJ Hong et al. TCT 06

  19. Plaque Regression by IVUSTardif et al. AJC 2006;98:2327 Intense Lipid Therapy x 2 years in 432 lesions <50%. Baseline IVUS IVUS at 24 months IVUS images of the same cross section of coronary artery at baseline (left) and follow-up (right). The presence of a large branch at 10 o’clock and a smaller branch at 7 o’clock confirms that the same matched cross section has been studied at the 2 time points.

  20. Progression of Disease in SVGWHC: YJ Hong JACC 2009;53:1257-64 Change in area (mm2) Change in area (mm2) Change in area (mm2)

  21. Statin Therapy and Fibrous Cap ThicknessTakarada et al. Atherosclerosis 2009;202:491-7 Statin Group Statin Group Control Group

  22. Statin Therapy and Plaque RuptureChia et al. Cor Art Dis 2008;19:237-42 • OCT study in 48 patients. • Statin therapy patients had: • - less plaque rupture (8 vs 36%) • - increased fibrous cap thickness (78 vs 49 microns)

  23. Summary • Positive remodeling with large plaque burden is an important observation that determines clinical and PCI outcomes.

  24. CALCIFIED LESIONS

  25. Patient with Angina and LAD Perfusion Defect Simple PCI ?

  26. IVUS of LAD In view of IVUS findings Roto-DES or LIMA need to be chosen

  27. Different Strategies based on IVUS findings Direct Stenting A 5 mm Roto-Stent B

  28. Concealed Vessel Perforation

  29. Most Perforations are Not Seen by Angio. Maehara et al. WHC 2001 • 15,000 IVUS reviewed • 76 perforations found on IVUS. • Angio: • 21% totally normal • 33% dissections • 22% mild stenosis • 24% perforation suspected • 12 months Follow up • 30% MACE

  30. Virtual Histology • Pathological intimal thickening. • (B) Thin-capped fibroatheroma. • (C) Thick-capped fibroatheroma. • (D) Fibrotic plaque. • (E) Fibrocalcific plaque.

  31. The PROSPECT Trial QCA of entire coronary tree IVUS with Virtual histology Palpography (n=~350) Meds rec Aspirin Plavix 1yr Statin Repeat biomarkers @ 30 days, 6 months MSCT Substudy N=50-100 Repeat imaging in pts with events IVUS of culprit lesion + 2 non culprit vessels 700 pts with ACS F/U: 1 mo, 6 mo, 1 yr, 2 yr, ±3-5 yrs

  32. PROSPECT: MACE 25 20.4% 20 All 15 12.9% MACE (%) Culprit Lesion 10 11.6% Non Culprit Les. 5 2.7% Indeterminate 0 0 1 2 3 Time in Years Number at risk

  33. Plaque Burden, VH and Outcomes • A ≥ 70% plaque burden lesion by gray scale IVUS has a risk of 9.2% at three years • A ≥ 70% plaque burden lesion defined as VH TCFA has an elevated risk of 15.3% at three years • A ≥ 70% plaque burden lesion defined as PIT has a reduced risk of only 2.6% at three years • VH Definitions in PROSPECT can swing the risk profile MACE in non Culprit lesions The same lesions by grayscale IVUS (Plaque Burden ≥ 70%)have dramatically different risk profiles when looking at VH

  34. Progressive ACTIVE Dynamic Nature of Plaque by VH.Kubo, Maehara et al. JACC 2010;55:1590-7 Stable

  35. Stenting and Plaque by VH.Koenig, Margolis, Virmani, Klaus. Nature Clinical Practice 2008 5;4 Koenig, Margolis, Virmani, Klaus. Nature Clinical Practice 2008 5;4

  36. 40% 50% 10% Stent in AMIDarius Dudek. TCT 2009 NC covered NC uncovered Proximal segment Distal segment

  37. Plaque Healing after StentingKubo et al. Am Heart J. 2010;159:271-7. Necrotic Core in contact with stent before and after Stenting DES DES BMS BMS

  38. Conclusions • Plaque characterization by IVUS allows for: • Better PCI planning and execution. • Better PCI outcome. • Better prediction of near and long term outcome. • Better delineation of need for optimal medical therapy for that lesion. • Better understanding of Coronary Atherosclerosis.

  39. The end

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