arge-scale clinical studies have recently shown an inhibitory effect on cardiovascular events of lipidlowering therapy with HMG-CoA reductase inhibitors (statins), indicating the usefulness of this therapy. [1][2][3][4][5][6][7][8] The benefit is particularly marked in patients with coronary heart disease (CHD), and the guidelines of the American National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III positively state the utility of lipid-lowering therapy in reducing low-density lipoprotein (LDL)-cholesterol (C) to below 70 mg/dl in patients with coronary artery disease. 9 In Japan, the guidelines for prevention of arteriosclerotic diseases specify a target value of LDL-C of less than 100 mg/dl for control of CHD patients in category C. 10 Evaluation of coronary arterial plaques by imaging diagnosis has progressed markedly in recent years. In the REVERSAL study, intravascular ultrasonography (IVUS) was used to compare the effect of lipid-lowering therapy between CHD patients treated with standard and active regimens, with the latter found to inhibit expansion of coronary plaques. 11 Size reduction of coronary plaques on IVUS by statin treatment in patients with acute coronary syndrome (ACS) has also been reported in Japan (the ESTABLISH study). 12 Subsequent multicenter studies such as the JAPAN-ACS study have verified the ESTABLISH results through investigation of strong statin-induced volume reduction of coronary plaques. [13][14][15] However, these studies have all evaluated quantitative changes of the plaques, and there have been fewer qualitative evaluations. 16 Spectral analysis of IVUS radiofrequency (RF) data can provide detailed quantitative and qualitative information on coronary plaque composition in vivo. [17][18][19][20][21] Nasu et al found that in vivo characterization of coronary plaques by 'virtual histology (VH)' correlated favorably with the results of in vitro histopathological examination of tissue samples obtained by directional coronary atherectomy. 22 In this study, we used VH-IVUS to evaluate short-term quantitative and qualitative changes in non-culprit lesions in a comparison of pitavastatin, a new strong statin, with atorvastatin after administration in the early stage (2-3 weeks) after onset of ACS. The follow-up period of 2-3 weeks was chosen to evaluate the inhibition of short-term events within 1 month by early statin administration after ACS onset, and to examine if the statin effect starts to appear in this period. Methods Study Design and Patient PopulationThe study was performed as a prospective, randomized, single-center trial to assess the effect of 2-to 3-weeks of (Received November 5, 2008 Patients with acute coronary syndrome who underwent emergency percutaneous coronary intervention (PCI) were randomly assigned to receive pitavastatin (n=80; 2 mg/day) or atorvastatin (n=80; 10 mg/day) immediately after PCI. All patients underwent a blood lipid test and VH-IVUS evaluation of non-PCI lesions at admission and after 2-3 weeks of statin administration. A...

In our experience, the clinical features of SCAD appear to be similar to those reported previously. SCAD appears to be rare, but it should be considered in ACS patients, especially in younger females.

Pathological features of restenotic tissues after DES implantation showed a stronger inflammatory response compared with those after BMS implantation. Thus, the mechanism of restenosis after DES implantation may be different from that observed after BMS implantation.

It has been suggested that n-3 polyunsaturated fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), protect against cardiovascular diseases, and EPA/arachidonic acid (AA) and DHA/AA ratios in serum are potential risk markers for coronary artery disease (CAD). The purpose of this study was to clarify the clinical significance of the difference in the EPA/AA ratio and the DHA/AA ratio in patients with CAD. In 369 patients with confirmed or suspected CAD who underwent diagnostic coronary angiography, we measured serum levels of EPA, DHA and AA and calculated the EPA/AA and DHA/AA ratios. The EPA/AA ratio was significantly lower in patients with acute coronary syndrome (ACS) than in patients with chronic CAD or chest pain syndrome (0.27±0.19 vs. 0.44±0.20, respectively; P<0.01), whereas the DHA/AA ratio was similar in the two groups (0.78±0.27 vs. 0.79±0.37). Multiple logistic regression analyses using various biomarkers related to coronary risk discriminated ACS from other disease entities and demonstrated that the EPA/AA ratio (odds ratio: 0.0012, 95% confidence interval: 0.00-0.16, P<0.01) but not the DHA/AA ratio (odds ratio: 1.05, 95% confidence interval: 0.98-1.12) was a significant independent predictive factor. Our findings suggest that the EPA/AA ratio might be more closely associated with the pathophysiology of CAD, especially with that of ACS, than the DHA/AA ratio. Our findings suggest that interventions with EPA agents or supplemental EPA intake, compared with DHA agents or supplemental DHA, may confer greater benefit for plaque stabilization to prevent the onset of ACS in patients with CAD.

Recent advances in drug-eluting stent (DES) technology have succeeded in preventing restenosis. In addition to inhibiting smooth muscle cell proliferation, DES greatly inhibits the local inflammatory response in the acute phase after implantation, leading to prevention of restenosis. However, a unique issue in DES implantation is an impairment of reendothelialization, which may result in abnormal wound healing. Consequently, a late-phase inflammatory relapse could appear in the long term after DES implantation. In this study, we measured serum levels of inflammatory markers, including interleukin (IL)-6, IL-8, tumor necrosis factor-α, monocyte chemoattractant protein-1, matrix metalloproteinase-9, and myeloperoxidase, as well as high-sensitivity C-reactive protein at follow-up coronary angiography (mean 9 months) in 54 patients who received DES stenting who did not experience restenosis, and compared them with 51 patients receiving bare-metal stents (BMS) without restenosis. The level of IL-6 was over the measurement threshold (≥2.22 pg/ml) in 12 patients (21 %) in the DES group, but in only 2 patients (4 %) in the BMS group (P = 0.003). IL-8 was significantly higher in the DES group than in the BMS group (4.51 ± 2.40 vs 3.84 ± 1.34 pg/ml, P = 0.015). The levels of other biomarkers were similar between the two groups. DES showed an increase in inflammatory cytokines in the late phase after implantation in comparison with patients who received BMS, suggesting late-stage inflammation. Therefore, the wound-healing response after DES implantation might be different from that after BMS.