Abstract 5827: The Occurrence of Carotid Intraplaque Hemorrhage is Driven by Local Rather Than Systemic Factors
Background: The systemic nature of atherosclerotic disease may cause a substantial association in the severity of disease between left and right carotid arteries. However, the etiology of intraplaque hemorrhage (IPH) has been attributed to local inflammatory factors and/or the surrounding vasa vasorum and neovasculature. In this study, we sought to explore the symmetry in plaque morphology and composition across a broad range of atherosclerotic disease severity.
Methods: Multi-contrast, carotid magnetic resonance images from 191 patients with carotid atherosclerosis were evaluated. Only subjects with consecutive images covering 10mm proximal and distal to the carotid bifurcation on both sides were analyzed. Trained reviewers using image analysis software identified the lumen and outer wall boundaries. Percent wall volume (PWV=100%×wall volume/total vessel volume) was subsequently calculated for each artery. In addition, the presence (and volume) or absence of calcification, lipid-rich necrotic core (LRNC), and IPH was documented. Associations in volume measurements were evaluated with Pearson’s correlation. Cohen’s kappa, κ, was used to assess agreement between dichotomous variables.
Results: 124 (64.9%) subjects with sufficient bilateral coverage showed a strong correlation between carotids in PWV (r=0.74, P<0.001). There was good agreement between carotids for calcification (κ= 0.54), but only mild for LRNC (κ= 0.44) and weak for IPH (κ= 0.23). When the feature was present bilaterally, there was a moderate correlation in size of calcification (r=0.60, P<0.001) and LRNC(r= 0.50, P<0.001), but not for IPH(r=0.30, P=0.10).
Conclusion: Our findings suggest that PWV, calcification and LRNC may develop symmetrically, albeit the LRNC may exhibit different temporal developments given the weaker correlation. In contrast, marked differences in the prevalence and size of IPH between right and left carotids suggests that the development of IPH may be regulated by local factors. In addition, systemic factors may have limited influence on progression of IPH. These findings suggest that development of carotid atherosclerotic disease may be systemic, but progression towards high-risk lesions may be partly governed by local factors as well.