These findings suggest that stenosis of the right coronary ostium is a high-risk lesion for stent restenosis. In addition to excessive intimal growth, chronic stent recoil might be an important etiologic factor at this particular location.

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A 29-year-old woman who worked as a KAATSU (a type of body exercise that involves blood flow restriction) instructor visited our emergency room with a chief complaint of swelling and left upper limb pain. Chest computed tomography (CT) showed non-uniform contrast images corresponding to the site from the left axillary vein to the left subclavian vein; vascular ultrasonography of the upper limb revealed a thrombotic obstruction at the same site, leading to a diagnosis of Paget-Schroetter syndrome (PSS). We herein report our experience with a case of PSS derived from thoracic outlet syndrome (TOS), in a patient who was a KAATSU instructor.

Abstract:Background: While preprocedural statin treatment for acute coronary syndrome (ACS) is widely regarded as beneficial, there has been no prospective randomized multicenter trial of patients with non-ST elevation ACS in the Japanese population to examine the efficacy of preprocedural aggressive statin use. The aim of this study was to confirm this effect by prospective randomized multicenter design. Methods: Fifty patients who presented with non-ST elevation ACS were enrolled, and randomly assigned to aggressive statin administration before percutaneous coronary intervention (PCI). Troponin-T (TnT), creatine phosphokinase (CK), CK-myocardial band (CK-MB), high-sense Creactive protein (hs-CRP), and brain natriuretic peptide (BNP) were measured at baseline and/ or after procedure. Results: Three days after PCI, the statin group had significantly less CK elevation compared with the nonstatin group (84±17 IU/l versus 180±68 IU/l, respectively, p ¼ 0.02). CK-MB elevation also tended to be lower in the statin group than in the nonstatin group (3.2±1.9 versus. 7.0±3.0, respectively, p ¼ 0.07), as was BNP level (3.2±1.9 versus 7.0±3.0 pg/ml, respectively, p ¼ 0.07). The change of serum LDL cholesterol was significantly correlated with CK (p ¼ 0.01) and TnT (p ¼ 0.02) at 1 day after PCI. Conclusions: Aggressive statin usage before PCI to Japanese patients with non-ST elevation ACS appears to reduce myocardial damage after procedure. The degree of serum lipid level reduction may reflect the vulnerability of atheromatous plaques that could cause cardiac damage after PCI.

When performing intravascular ultrasound studies, the backward echo image can show marked attenuation, although there are no calcified deposits and it may be impossible to detect the intraplaque architecture. The pathology underlying this phenomenon was investigated in autopsy specimens. We hypothesize that the mechanism responsible for the attenuation involves micro-calcification and lipid in unstable plaques causing ultrasonic wave reflection and dispersion.

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The restenosis rate was significant in this cohort of patients with DES-ISR. Angiographic pattern of DES-ISR and diabetes mellitus are the most important predictors of TLR, whereas re-stenting with DES is protective.

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