Key result
Adding ezetimibe is linked to carotid plaque regression of ~3 mm² compared to pre-treatment progression.
Why the study?
There has been controversy over ezetimibe's failure to reduce carotid intima-media thickness, partly due to differences among ultrasound phenotypes of atherosclerosis.
Does the addition of ezetimibe reduce carotid plaque burden in patients followed in vascular prevention clinics?
Cohort (n=231)
Does the addition of ezetimibe reduce carotid plaque burden in patients followed in vascular prevention clinics?
Adding ezetimibe to standard therapy is associated with regression of carotid plaque burden, highlighting the utility of measuring total plaque area rather than just intima-media thickness to assess antiatherosclerotic therapies.
Answers are grounded in this paper and cite their sources.
Ezetimibe addition was associated with carotid plaque regression in this cohort; leaves open whether plaque area measurement should guide therapy pending randomized trials.
BACKGROUND AND PURPOSE: There has been recent controversy over failure of ezetimibe to reduce carotid intima-media thickness. Much of this is based on failure to understand important differences among ultrasound phenotypes of atherosclerosis. METHODS: We analyzed the effect of adding ezetimibe to the regimen of patients being followed in vascular prevention clinics where measurement of carotid plaque burden (total plaque area) is used to guide therapy. RESULTS: There were complete data in 231 patients with total plaque area for 2 years before and 2 years after initiation of ezetimibe. In the 2 years before and after initiation of ezetimibe, total cholesterol decreased significantly before (P<0.0001) and after initiation of ezetimibe (P<0.0001); low-density lipoprotein cholesterol declined significantly before (P<0.0001) and after (P=0.003) initiation of ezetimibe. Triglycerides declined significantly before ezetimibe (P<0.0001) but did not change after addition of ezetimibe (P=0.48). High-density lipoprotein cholesterol did not change significantly before (P=0.87) but declined significantly after ezetimibe (P=0.03). Despite the decline in low-density lipoprotein cholesterol before addition of ezetimibe, there was a significant mean increase in within-individual total plaque area in the 2 years before addition of ezetimibe by 6.89±39.57 mm(2) (SD); after addition of ezetimibe, despite the decline in high-density lipoprotein, plaque area decreased by -3.05±SD 38.18 mm(2) SD (P<0.01). CONCLUSIONS: Ezetimibe appears to regress carotid plaque burden. To assess effects of antiatherosclerotic therapies, it is important to measure plaque burden. These findings should be tested in a clinical trial.
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Bogiatzi et al. (2012) conducted a cohort in Carotid atherosclerosis (n=231). Ezetimibe vs. 2 years prior to ezetimibe initiation (within-individual) was evaluated on Change in within-individual total plaque area (p=<0.01). Addition of ezetimibe was associated with a decrease in total carotid plaque area (-3.05 mm2) compared to an increase (6.89 mm2) in the 2 years prior to initiation (P<0.01).
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