Carotid plaque vasa vasorum angiogenesis from adventitia may be influenced by inflammation, could promote intraplaque hemorrhage and decrease the thickness of fibrous cap, finally, the cap is prone to rupture. Drug therapy and assessment to the vulnerable plaque, in vivo, would be of major clinical interest. To investigate whether lipid therapy leads to changes in vasa vasorum characteristics of carotid unstable plaque in chinese patients, as measured by using dynamic contrast-enhanced (DCE) MRI. Focus on inflammation to monitor the early beneficial therapy using vasa vasorum MR imaging, biomarker in vivo.
Among the 32 subjects, there were 2 cases shows IPH. After 12 and 24 months of treatment, there was a obvious reduction was found in mean adventitial Vp (0.134 ± 0.090[standard deviation] to 0.061 ± 0.036, 0.046±0.024. Fig. 1), but no statistically significant trend between baseline and 3 months(0.126 ± 0.073. Fig. 1). The HRMRI indicated that there was no significant improvement in composition of IPH during 24-month treatment (Fig. 2). HRMRI example of irreversible IPH and time points.
In total, 6 cases had thin fibrous caps without intraplaque hemorrhage. After 12 and 24 months of treatment, there was a obvious reduction was found in mean plaque Ktrans (0.0486 ± 0.0289[standard deviation] to 0.0422 ± 0.0166, 0.0370 ± 0.0179. Fig. 3), no statistically significant trend between baseline and 3 months(0.0486 ± 0.0149). The thinning of fibrous caps might be gradually thickening within the first one year after treatment(Fig. 4).
In conclusion, evaluation of effects of lipid-lowering therapy on atherosclerotic plaques with IPH should be focused on inflammatory activity rather than composition and plaque burden. IPH may be irreversible content within the first one year after treatment.
Evaluation of effects of lipid-lowering therapy on atherosclerotic plaque with thinning fibrous caps should be focused on inflammatory activity rather than plaque burden.
Lipid-lowering therapy might reduce vasa vasorum perfusion, suppress plaque inflammation, as well as stabilize vulnerable plaque with IPH or thin caps of this study. Imaging markers of inflammation by the DCE-MRI may monitor the early response of the beneficial therapy to carotid unstable plaque. Kinetic parameters of DCE-MRI has the most possibility to become the biomarker in vivo, noninvasively.
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