Abstract 3730: Rosuvastatin Treatment in Carotid Atherosclerosis: Effect of Framingham Risk Factors and Baseline Intima-Media Thickness in the METEOR Trial
Background and methods: The METEOR trial (Measuring Effects on intima media Thickness: an Evaluation Of Rosuvastatin) was a randomized, double-blind, placebo-controlled study in 984 subjects with low Framingham risk scores and signs of subclinical atherosclerosis evidenced by a maximum baseline carotid intima-media thickness (CIMT) ≥ 1.2 and <3.5 mm. Subjects were randomized in a 5:2 ratio to rosuvastatin (40 mg/day) or placebo and followed for 2 years. Primary results of METEOR have been reported previously and demonstrated that rosuvastatin significantly slowed progression of CIMT in this patient group. Here, we examine the consistency of this effect in 876 evaluable subjects across subgroups defined by Framingham risk factors [RF] (less than 2 RF vs 2 or more RF) and maximum baseline CIMT (< median [1.749 mm] vs ≥ median).
Results: Results from a multilevel, repeated-measures, mixed-effects model are presented below as the annualized change (slope in micrometers per year) for the maximum CIMT from each of 12 arterial sites representing the near and far walls of the left and right common carotid artery, bifurcation and internal carotid artery segments. Rosuvastatin significantly slowed the progression of CIMT in all 4 strata (all p<0.02). In the placebo group, higher rates of progression occurred in those with 2 or more RFs, with little effect of baseline thickness. In the rosuvastatin-treated group, a greater trend toward regression (greater negative slope) occurred in those with more RFs and in those with greater baseline thickness. This resulted in an overall treatment effect in those with both these attributes that was almost twice that of those without them.
Conclusions: These results highlight the ability of rosuvastatin to slow progression of carotid atherosclerosis in subjects at relatively low risk of cardiovascular disease, and suggest that regression of disease may be possible in individuals with higher levels of baseline risk and baseline wall thickness.