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Background Despite standard statin therapy, a majority of patients retain a high “residual risk” of cardiovascular events. Objectives The aim of this study was to evaluate the effects of ezetimibe plus atorvastatin versus atorvastatin monotherapy on the lipid profile and coronary atherosclerosis in Japanese patients who underwent percutaneous coronary intervention (PCI). Methods This trial was a prospective, randomized, controlled, multicenter study. Eligible patients who underwent PCI were randomly assigned to atorvastatin alone or atorvastatin plus ezetimibe (10 mg) daily. Atorvastatin was uptitrated with a treatment goal of low-density lipoprotein cholesterol (LDL-C) Results The combination of atorvastatin/ezetimibe resulted in lower levels of LDL-C than atorvastatin monotherapy (63.2 ± 16.3 mg/dl vs. 73.3 ± 20.3 mg/dl; p Conclusions Compared with standard statin monotherapy, the combination of statin plus ezetimibe showed greater coronary plaque regression, which might be attributed to cholesterol absorption inhibition–induced aggressive lipid lowering. (Plaque Regression With Cholesterol Absorption Inhibitor or Synthesis Inhibitor Evaluated by Intravascular Ultrasound [PRECISE-IVUS]; NCT01043380 )

Previous studies have showed that the intensive lipid lowering therapy (ILLT) with statins could decrease coronary atheroma plaque, but the effect is weak in acute coronary syndrome (ACS) patients with diabetes mellitus (DM). We conducted to evaluate whether ILLT by ezetimibe combined with statin

To examine the constrictor response of the infarct-related stenotic coronary artery in comparison with that of noninfarct-related stenotic arteries, acetylcholine in maximal doses of 100 μg for the left and 50 μg for the right coronary artery was injected into the 16 infarct-related coronary arteries of 16 patients with previous myocardial infarction (group 1) and into 19 stenotic coronary arteries of 16 patients with stable angina without myocardial infarction (group 2). Acetylcholine's effects on lumen diameter and area were quantitatively analyzed at the stenotic segment and its proximal segment without significant stenosis.Acetylcholine decreased lumen diameter and area at the stenotic segments from 0.72 ± 0.18 to 0.18 ± 0.33 mm and from 0.45 ± 0.22 to 0.10 ± 0.22 mm2, respectively, in group 1 (both p < 0.01) and from 0.75 ± 0.22 to 0.49 ± 0.30 mm and 0.48 ± 0.29 to 0.26 ± 0.23 mm2, respectively, in group 2 (both p < 0.01). Acetylcholine decreased the diameter and area at the proximal segment from 2.71 ± 0.75 to 2.38 ± 0.6 mm and from 6.18 ± 3.4 to 4.71 ± 2.23 mm2, respectively, in group 1 (both p < 0.01) and from 2.31 ± 0.67 to 1.95 ± 0.59 mm and from 4.5 ± 2.97 to 3.22 ± 1.96 mm2, respectively, in group 2 (both p < 0.01). The changes in diameter and area at the stenotic segment in group 1 were significantly greater than those in group 2 (both p < 0.01); there were no significant differences between groups in the changes at the proximal segment. Total or subtotal occlusion of the stenotic artery was induced in 11 (69%) patients in group 1 compared with 4 (21%) patients in group 2 (p < 0.01 group 1 vs. group 2).It is concluded that the constrictor response to acetylcholine of the stenotic segment of the infarct-related coronary artery is enhanced as compared with that of noninfarct-related arteries.