Guidelines now recommend high-intensity
statin therapy in all patients with proven atherosclerotic disease. Yet the impact of baseline
lipoprotein and
C-reactive protein (CRP) levels on measures of disease regression to this
therapy are unknown. The aim of this study was to test the hypothesis that high-intensity
statin therapy causes equivalent degrees of coronary
atheroma regression irrespective of baseline
lipoprotein and CRP levels. In 8 prospective randomized trials using serial coronary intravascular ultrasound, 1,881 patients who maintained or switched to 18- to 24 months of high-intensity
statin therapy (
rosuvastatin 40 mg or
atorvastatin 80 mg) were stratified according to baseline
lipoprotein and CRP levels. Changes in coronary percentage
atheroma volume (PAV) and total
atheroma volume (TAV) were evaluated. High-intensity
statin therapy produced significant reductions from baseline in
low-density lipoprotein cholesterol by 38.4%, non-
high-density lipoprotein (
HDL) cholesterol by 33.6%,
triglycerides by 13.1%, and CRP by 33.3%, while increasing
HDL cholesterol by 11.7% (p <0.001 for all). This was associated with regression of PAV by 0.7% and of TAV by 8.2 mm(3) (p <0.001 for both). No significant differences of changes in PAV and TAV were observed across baseline quintiles of
low-density lipoprotein cholesterol,
HDL cholesterol, non-
HDL cholesterol,
triglycerides, or CRP. Moreover, across all measured
lipoproteins and CRP, most patients demonstrated plaque regression (defined as any change from baseline in PAV or TAV <0). In conclusion, high-intensity
statin therapy attenuated the natural progression of
coronary atherosclerosis in all strata of patients with
coronary artery disease irrespective of baseline
lipoprotein or CRP levels. These findings provide support for the latest United States guideline recommendations for the broad use of high-intensity
statin therapy in all patients with
atherosclerosis, regardless of baseline
lipid status.