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Inflammation is not specific to culprit lesion

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Inflammation is not specific to culprit lesion

  1. 1. Inflammation is NOT specific to culprit lesions. PRO Gerard Pasterkamp, UMC Utrecht
  2. 2. First: What is the definition of the vulnerable plaque? First: What is the definition of the culprit lesion? Lesion that is pathological substrate of clinical syndrome? Lesion that is pathological substrate of plaque rupture? Lesion that hides inflammatory cells?
  3. 3. 74 coronary arteries 3 random (non ruptured) sections per artery Nr cross-sections revealing plaque inflammation 50 femoral arteries 6 sites per artery Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:54-58
  4. 4. Vink et al. J Anatomy 2001
  5. 5. Radial artery
  6. 6. Specificity: Proportion of negatives that are correctly identified by the test Sensitivity: proportion of positives that are correctly identified by the test For diagnosis we do not need “spec” and “sens”, but we need the probability of the test giving the correct diagnosis.
  7. 7. Values for diagnostic testing: Positive predictive value:: proportion of patients with positive test results who are correctly diagnosed Negative predictive value:: proportion of patients with negative test results who are correctly diagnosed
  8. 8. Inflammation Culprit lesion + - + 5 0 5 - 195 400 595 200 400 Specificity: 5/5 = 1.0 PPV: 5/200 = 0.025 Sensitivity: 400/595= 0.67 NPV: 400/400 = 1.0
  9. 9. Inflammation culprit lesion MI?
  10. 10. Inflammation specific for culprit lesion (MI)? Inflammation specific for culprit lesion (plaque rupture)? NO We do not know Not in cross-sectional post mortem studies, but maybe over time?
  11. 11. Inflammation: local arterial system The number of inflammatory lesions observed during catheterization: a predictive marker for adverse outcomes?
  12. 12. METHODS: • Post mortem • 30 pairs of left and right femoral arteries equally present left and right systemically influenced unilateral prevalence locally determined
  13. 13. Plaque vulnerability: • 60 arteries (30 pairs), 6 cross sections per artery • (Immuno)histochemistry – smooth muscle cells (SMC) – collagen – macrophages – T lymphocyes • Plaque “vulnerable” if: 1. Heavy staining macrophages or T lymphocytes 2. Absent/minor staining of SMC and collagen
  14. 14. y = 1.2x - 2.7 r2 = 0,71 0 10 20 30 40 50 0 10 20 30 40 50 plaque area left (mm2 ) plaquearearight(mm2 )
  15. 15. Right No Vulnerable Plaque Right ≥1 Vulnerable Plaque Left No Vulnerable Plaque 9 (30%) 5 (17%) Left ≥1 Vulnerable Plaque 5 (17%) 11 (37%) Agreement 67%, kappa = 0.35 (p=0.05) Vulnerable plaque: atheroma ≥40% and a thin cap with inflammation Plaque vulnerability
  16. 16. 1. Large lipid pool 2. Inflammatory cells in cap Vulnerable Plaque
  17. 17. Right No Atheroma ≥40% Right ≥1 Atheroma ≥40% Left No Atheroma ≥40% 5 (17%) 4 (13%) Left ≥1 Atheroma ≥40% 3 (10%) 18 (60%) Agreement 77%, kappa = 0.43 (p=0.02) Atheroma ≥40%: atheroma occupying ≥40% of total plaque area Large atheroma
  18. 18. Right No Vulnerable Cap Right ≥1 Vulnerable Cap Left No Vulnerable Cap 1 (3%) 5 (17%) Left ≥1 Vulnerable Cap 11 (37%) 13 (43%) Agreement 47%, kappa = −0.21 (p=0.19) Vulnerable cap: a thin cap with at least moderate inflammation irrespective of atheroma size Thin cap with inflammation
  19. 19. Conclusion • Association plaque size left and right arteries • 32/42 (76%) similarity in presence or absence significant correlation PA and VA • plaque vulnerability: – large lipid pool: moderate agreement left and right – thin cap with inflammation: left independent of right Vink et al. J Am Coll Cardiol 2001;38:718-723
  20. 20. Conclusion: • Inflammation (cells) as a diagnostic marker probably probably has a very low positive predictive value for the culprit lesion (lesion that may lead to clinical syndrome). • Thus far, local segmental sampling for the presence of inflammation does not seem strongly representative for inflammatory responses throughout the arterial system (cave: cross- sectional studies in 2D).

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