石川 寛

OBJECTIVES The purpose of this study was to evaluate the effect of statin treatment on coronary plaque composition and morphology by optical coherence tomography (OCT), grayscale and integrated backscatter (IB) intravascular ultrasound (IVUS) imaging. BACKGROUND Although previous studies have demonstrated that statins substantially improve cardiac mortality, their precise effect on the lipid content and fibrous cap thickness of atherosclerotic coronary lesions is less clear. While IVUS lacks the spatial resolution to accurately assess fibrous cap thickness, OCT lacks the penetration of IVUS. We used a combination of OCT, grayscale and IB-IVUS to comprehensively assess the impact of pitavastatin on plaque characteristics. METHODS Prospective serial OCT, grayscale and IB-IVUS of nontarget lesions was performed in 42 stable angina patients undergoing elective coronary intervention. Of these, 26 received 4 mg pitavastatin after the baseline study; 16 subjects who refused statin treatment were followed with dietary modification alone. Follow-up imaging was performed after a median interval of 9 months. RESULTS Grayscale IVUS revealed that in the statin-treated patients, percent plaque volume index was significantly reduced over time (48.5 +/- 10.4%, 42.0 +/- 11.1%; p = 0.033), whereas no change was observed in the diet-only patients (48.7 +/- 10.4%, 50.4 +/- 11.8%; p = NS). IB-IVUS identified significant reductions in the percentage lipid volume index over time (34.9 +/- 12.2%, 28.2 +/- 7.5%; p = 0.020); no change was observed in the diet-treated group (31.0 +/- 10.7%, 33.8 +/- 12.4%; p = NS). While OCT demonstrated a significant increase in fibrous cap thickness (140 +/- 42 mu m, 189 +/- 46 mu m; p = 0.001), such changes were not observed in the diet-only group (140 +/- 35 mu m, 142 +/- 36 mu m; p = NS). Differences in the changes in the percentage lipid volume index (-6.8 +/- 8.0% vs. 2.8 +/- 9.9%, p = 0.031) and fibrous cap thickness (52 +/- 32 mu m vs. 2 +/- 22 mu m, p < 0.001) over time between the pitavastatin and diet groups were highly significant. CONCLUSIONS Statin treatment induces favorable plaque morphologic changes with an increase in fibrous cap thickness, and decreases in both percentage plaque and lipid volume indexes. (J Am Coll Cardiol Img 2012;5:169-77) (C) 2012 by the American College of Cardiology Foundation

To assess the fate of incomplete stent apposition (ISA) after deployment of sirolimus-eluting stents (SESs). Thirty-two patients having intravascular ultrasound (IVUS)-guided PCI with SESs underwent assessment of stent deployment with quantitative coronary angiography, IVUS, and optical coherence tomography (OCT) pre-procedure, post-procedure, and at 10 months follow-up. Incomplete stent apposition was defined as separation of a stent strut from the inner vessel wall by > 160 mu m. At follow-up, 4.67% of struts with ISA at deployment failed to heal and 7.59% which were well apposed did not develop neointimal hyperplasia even after 10 months. Lesion remodelling was responsible for the development of late ISA in only 0.37% of struts. Failure of adequate neointimal hyperplasia was quantitatively the most important mechanism responsible for persistent acute ISA, classified in previous studies, which relied only on follow-up OCT, as late ISA. Thrombus was visualized in 20.6% of struts with ISA at follow-up and in 2.0% of struts with a good apposition (P < 0.001). In patients with SESs, ISA can fail to heal and even complete apposition can be associated with no neointimal hyperplasia. Incomplete stent apposition without neointimal hyperplasia was significantly associated with the presence of OCT-detected thrombus at follow-up, and may constitute a potent substrate for late stent thrombosis.