Key result
Advanced fibroatheromas show lower Nogo-B expression, suggesting an inverse link to plaque progression.
Observational (n=19)
p-value: p=0.013
Atherosclerotic plaque progression is inversely associated with Nogo-B expression, suggesting its local reduction may contribute to plaque instability.
Nogo-B reduction may mark plaque progression; hypothesis-generating and requires prospective validation before any clinical consideration.
The relation of Nogo-B to atherosclerotic plaque progression is not well understood. Thus, the purpose of this study was to assess the expression of Nogo-B in fibroatheromas (FA) of different stages, classified using virtual histology intravascular ultrasound (VH-IVUS) analysis in 19 autopsied cases of non-sudden cardiac death. VH-IVUS imaging analysis was performed 30 mm from the ostium of each coronary artery. VH-IVUS revealed 11 early FAs (34.5+/-8.3 yr), 12 late FAs (42.6+/-16.6 yr), 8 thick-cap FAs (TkCFAs) (46.4+/-11.1 yr), and 6 thin-cap FAs (TCFAs) (51.8+/-6.8 yr). TkCFAs and TCFAs were defined as advanced FA. FA progression advanced with age (P=0.04). VH-IVUS analysis of small, early FAs showed smaller necrotic cores and relatively less calcium compared to more advanced FAs with large necrotic cores (P<0.001). Histopathology and immunohistochemical stains demonstrated that early or late FAs had smaller necrotic cores, less empty space of decalcification, and greater Nogo-B expression compared to advanced FAs (vs. early FA, P=0.013; vs. late FA, P=0.008, respectively). These findings suggest that FA progression is inversely associated with Nogo-B expression. Local reduction of Nogo-B may contribute to plaque formation and/or instability.
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Lee et al. (2009) conducted an observational in Atherosclerosis (n=19). Advanced fibroatheromas (thick-cap and thin-cap) vs. Early or late fibroatheromas was evaluated on Nogo-B expression (p=0.013). Advanced fibroatheromas had significantly lower Nogo-B expression compared to early (P=0.013) and late (P=0.008) fibroatheromas, suggesting an inverse association with plaque progression.
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