Inflammation is NOT specific to culprit lesions.
PRO
Gerard Pasterkamp,
UMC Utrecht
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?
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
Vink et al. J Anatomy 2001
Radial artery
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.
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
InflammationCulprit 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
Inflammation culprit lesion MI?
Inflammation specific for culprit lesion (MI)?
Inflammation specific for culprit lesion (plaque rupture)?
NO
We do not knowNot in cross-sectional post mortem studies, but maybe over time?
Inflammation: local arterial system
The number of inflammatory lesions observed during catheterization: a predictive marker
for adverse outcomes?
METHODS:
• Post mortem• 30 pairs of left and right femoral arteries
equally present left and right systemically influenced
unilateral prevalence locally determined
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 lymphocytes2. Absent/minor staining of SMC and collagen
y = 1.2x - 2.7r2 = 0,71
0
10
20
30
40
50
0 10 20 30 40 50plaque area left (mm2)
plaq
ue a
rea
righ
t (m
m2 )
Right NoVulnerable
Plaque
Right 1Vulnerable
PlaqueLeft No VulnerablePlaque 9 (30%) 5 (17%)
Left 1 VulnerablePlaque 5 (17%) 11 (37%)
Agreement 67%, kappa = 0.35 (p=0.05)
Vulnerable plaque: atheroma 40% anda thin cap with inflammation
Plaque vulnerability
1. Large lipid pool
2. Inflammatory cells in cap
Vulnerable Plaque
Right NoAtheroma 40%
Right 1Atheroma 40%
Left NoAtheroma 40% 5 (17%) 4 (13%)
Left1 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
Right NoVulnerable Cap
Right 1Vulnerable 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 moderateinflammation irrespective of atheroma size
Thin cap with inflammation
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
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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