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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.

Background Elevation of C‐reactive protein ( CRP ) as a marker of vascular inflammation at a late phase of drug‐eluting stent ( DES ) implantation may predict subsequent major adverse cardiac events ( MACE ). Methods and Results In 1234 consecutive patients undergoing DES implantation, CRP was measured both before (baseline) and 8 to 12 months after (late phase) stenting, and the relationship between elevation of CRP (>2.0 mg/L) and subsequent MACE (all cause death, nonfatal myocardial infarction, target lesion revascularization, and other additional revascularization) was assessed. As results, CRP was elevated in 38.0% of patients at baseline and in 23.6% during late phase ( P HR ) for MACE was 1.52 (95% confidence interval [95% CI ] 1.21–1.93, P =0.0004) at baseline versus 4.00 (95% CI 3.16–5.05, P CRP elevation ( HR 3.60, 95% CI : 2.78–4.68, P CKD ) ( HR 1.41, 95% CI : 1.10–1.84, P =0.01), and number of diseased segments ( HR 1.19, 95% CI : 1.08–1.30, P =0.0002) were positive predictors of MACE , whereas statin use ( HR 0.66, 95% CI 0.50–0.87, P =0.003) was a negative predictor. Propensity score–matched analysis also confirmed the effect of late‐phase CRP on MACE ( HR 3.39, 95% CI 2.52–4.56, P CRP elevation, CKD (odds ratio [ OR ] 1.71, 95% CI 1.24–2.36, P =0.001) and baseline CRP elevation ( OR 3.48, 95% CI 2.55–4.74, P DES ( OR 0.59, 95% CI 0.41–0.84, P =0.003) and statin therapy ( OR 0.68, 95% CI 0.47–0.97, P =0.03) were negative predictors. Conclusions Monitoring the late‐phase CRP may be helpful to identify a high‐risk subset for MACE among patients undergoing DES implantation.

Summary Background The best way to treat in-stent restenosis (ISR) after drug-eluting stent (DES) implantation remains unclear. The aim of this study was to evaluate angiographic restenosis and target lesion revascularization (TLR) at 8 months after intervention in patients with DES-ISR, and to identify predictive factors of subsequent TLR after treatment of DES-ISR. Methods and results A total of 100 patients with 105 lesions underwent subsequent intervention for DES-ISR between April 2004 and January 2009. At baseline, focal and diffuse ISR were observed in 76.2% and 23.8%. DES-ISR was treated by five modalities: sirolimus-eluting stent (n = 42); paclitaxel-eluting stent (n = 24); balloon angioplasty (n = 23); cutting balloon angioplasty (n = 14); and bare-metal stent (n = 2). Angiographic follow-up data were available for 95 lesions (91%). The rates of angiographic restenosis and TLR were 37.9% and 33.3%. Late loss of sirolimus-eluting stent, paclitaxel-eluting stent, cutting balloon, and balloon angioplasty were 0.50 mm, 0.49 mm, 0.93 mm, and 1.10 mm. By multivariate analysis, totally occluded ISR (OR 15.43, p = 0.0005), diabetes mellitus (OR 3.45, p = 0.02), and re-stenting with DES (OR 0.14, p = 0.0002) were identified as independent predictors of TLR. Conclusions 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.

Both the presence of peripheral arterial disease and chronic kidney disease has been reported to be independent risk factors associating with poor prognosis. However, the impact of combination of peripheral arterial disease and chronic kidney disease remains unknown.The long-term outcome in 715 consecutive patients who had undergone coronary angiogram for the evaluation of chest pain was analyzed. Patients on haemodialysis were excluded from this analysis. Cohort patients were divided into four groups according to the Ankle Brachial Index (ABI0.9) and glomerular filtration rate (GFR60 mL/min per m(2)): group A (n= 498; ABI0.9, GFR60); B (n = 65, ABI0.9, GFR60); C (n = 99; ABI0.9, GFR60); and D (n = 53; ABI0.9, GFR60). The mean follow-up period was 620 +/- 270 days and evaluated the major cardiac adverse events included survival, stroke, acute coronary syndrome and heart failure.The mean follow-up period was 620 +/- 270 days. Total long-term event was present in 89 patients (groups A-D were 9.4%, 18.5%, 15.2% and 28.3%, respectively). Long-term event rate was 28.3% for patients with the presence of peripheral arterial disease and chronic kidney disease, compared to 9.4% for those without peripheral arterial disease and chronic kidney disease (P0.0001). Kaplan-Meier event-free survival curves also showed that the combination of peripheral arterial disease and chronic kidney disease predicted long-term event rate.The combination of chronic kidney disease and ABI of less than 0.9 undergoing coronary angiogram is strongly associated with long-term event rate.

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 C-reactive 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 = 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 = 0.07), as was BNP level (3.2±1.9 versus 7.0±3.0 pg/ml, respectively, p = 0.07). The change of serum LDL cholesterol was significantly correlated with CK ( p = 0.01) and TnT ( p = 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.

Background: While some therapies implemented for newly diagnosed Diabetes Mellitus (DM) or impaired Glucose Tolerance (IGT) are effective in preventing cardiovascular events, investigations of coronary plaque in patients with newly diagnosed DM or IGT are lacking. Methods: We evaluated 96 patients with acute coronary syndrome. The External Elastic Membrane (EEM), Lumen Cross-Sectional Area (CSA), plaque CSA, and plaque burden in the Left Anterior Descending (LAD) artery proximal to the lesion, diagnosed as normal by Coronary Angiography (CAG), were measured using Intravascular Ultrasound (IVUS). Patients were divided according to DM status (DM=35, non-DM=61). Non-DM patients underwent a 75g Oral Glucose Tolerance Test (OGTT) and were further divided into abnormal glucose tolerance (AGT; n=29) and Normal Glucose Tolerance (NGT) groups (n=32). Results: Quantitative Coronary Angiography (QCA) showed no significant differences in EEM or vessel diameter between groups. However, the lumen CSA was significantly smaller in the DM group than in the NGT group. The plaque CSA and plaque burden were significantly greater in the DM and AGT groups than in the NGT group. Total insulin and glucose values and insulin and glucose values at 120 min after the OGTT correlated with plaque CSA; insulin values at 120 min after the OGTT showed the strongest correlation (R=0.505, P

The aim of this study is to demonstrate initial results and long-term outcomes of patients after receiving cutting balloon angioplasty (CBA), balloon angioplasty (BA), or stenting for small vessel diseases. We studied a total of 327 lesions of small coronary disease treated either by CBA (n=87), BA (n=130), or stenting (n=110) in two affiliated institutes. A small coronary artery was defined as a reference vessel

OBJECTIVE The efficacy of coronary stenting of aorto-ostial atherosclerotic lesions is still unclear. We investigated the frequency and mechanism of stent restenosis at this particular lesion. METHODS Fifty-five consecutive patients with 64 native aorto-ostial lesions in the right coronary artery (RCA, n = 38) and the left main trunk (LM, n = 26) were treated by conventional stenting. Determinants of angiographic restenosis were established. The mechanism of stent restenosis was evaluated using post-stenting and follow-up intravascular ultrasound (IVUS) findings. RESULTS Restenosis was more frequent in the RCA than in the LM (50% compared with 19%, P < 0.03) and determinants included diabetes mellitus (63% compared with 21%, P < 0.03), calcium deposition (58% compared with 5%, P < 0.003), smaller stent cross-sectional area (SA) (as demonstrated by post-stenting IVUS studies, 8.1 +/- 1.4 mm compared with 10.2 +/- 2.2 mm, P < 0.01), larger plaque burden (64 +/- 6% compared with 57 +/- 8%, P < 0.03) and less circular expansion at the aorto-coronary junction. Serial IVUS examination was performed in 11 patients with restenosis of the right coronary ostium. The mean reduction in the SA was 21% at the aorto-coronary junction (6.4 +/- 1.9 mm, P < 0.003), whereas the SA at the distal edge was unchanged. Thirty-three per cent of late luminal loss was due to chronic stent recoil. CONCLUSION 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.

Coronary lesion stenting with aspiration and distal balloon occlusion is more often associated with embolic occlusion of interposed side branches when the branch arises at an angle of/=45 degrees and the artery containing the lesion is large. However, this event is infrequent, often resolving during the procedure and uniformly resolving by 6 months.

Thrombotic occlusion in the culprit lesion of acute myocardial infarction was successfully recanalized using a 4.5 Fr thrombectomy catheter (RESCUE), which was also used to normalize the coronary blood flow. The retrieved specimens were white thrombi containing red thrombi and cholesterol crystals, indicating plaque rupture.