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Background: Arterial repair delays after intracoronary implantation of Cypher sirolimus-eluting stents (SES), a representative first-generation drug-eluting stent. It remains unclear whether this delay would catch up with bare metal stents (BMS) during extremely long observation. The aim of this study was angioscopic observation of extremely late arterial repair after Cypher SES implantation., Methods: Thirty-seven SES and 17 BMS were implanted into 22 and 9 patients with angina pectoris, respectively. Duration after implantation (DAI) ranged from 3 to 10.5years in both stents. Coronary angioscopy revealed neointimal stent coverage (NSC), presence of in-stent yellow plaque (YP), and mural thrombi (MT). NSC was semi-quantified into 4 grades (grade 0, no coverage; grade 1, thin coverage; grade 2, thick coverage; grade 3, fully embedded into neointima)., Results: In the BMS-implanted lesions (BMSL), NSC was either grade 1 (24%) or grade 3 (74%), with rare YP and no MT. In the SES-implanted lesions (SESL), NSC was various, i.e. grade 0 (5%), grade 1 (59%), grade 2 (22%), and grade 3 (14%). YP and MT were observed in 27 and 24% of in SESL, respectively. In SESL with DAI>8years (n=5), NSC was either grade 1 (40%) or grade 3 (60%), although YP and MT were more frequently observed (60 and 40%, respectively)., Conclusions: Arterial repair after SES implantation caught up with BMS at around 8years with regards to NSC, although prevalence of YP and MT remained still greater in SESL than BMSL at extremely late phase., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Background: Arterial repair after intracoronary stenting depends on stent types and plaque vulnerability. The aim of this study was angioscopic comparison of arterial repair after implantation of the second-generation drug-eluting stents (G2-DES) between the stable and vulnerable plaques., Methods: Four types of G2-DES were successfully implanted into stable plaques (n=41) and vulnerable plaques (n=34): 13 and 9 Xience-everolimus-, 7 and 6 Endeavor-zotarolimus-, 15 and 9 Resolute-zotarolimus-, and 6 and 10 Nobori-biolimus-eluting stents (EES, E-ZES, R-ZES, and BES), respectively. Coronary angioscopy at 1-year follow-up revealed in-stent appearance, such as neointimal stent coverage (NSC), presence of yellow plaques (YP), and in-stent mural thrombus (MT). NSC was graded into poor and good coverage., Results: Yellow plaques and mural thrombi were found more frequently in the vulnerable plaques than in the stable plaques (29% vs. 12%, P=0.06; 12 vs. 0%, P=0.02; respectively). In EES, poor NSC was observed more frequently in the vulnerable plaques than in the stable plaques (54% vs. 11%, P=0.04). In BES, YP was observed more frequently in the vulnerable plaques than in the stable plaques (80% vs. 17%, P=0.01). In E-ZES and R-ZES, there were no significant differences with regards to angioscopic parameters between the stable and vulnerable plaques., Conclusions: Arterial repair after EES and BES implantation into the vulnerable plaques remained vulnerable even at 1-year follow-up., (Copyright © 2016. Published by Elsevier Ireland Ltd.)

Background: Pre-hospitalization medication such as aspirin and nitrates has been shown to affect the mode of presentation in acute coronary syndrome (ACS). However, it is not formally assessed whether other cardiovascular medications may be contributed to the differences in the mode of presentation, especially in relation to coronary risk factors., Methods and Results: We conducted a registration study of patients (M/F 850/323) with either ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI) or unstable angina (UA), and examined the differences in the mode of presentation, pre-hospitalization medication, and coronary risk factors. The ratio of the incidence of STEMI and NSTEMI/UA was significantly reduced in patients having pre-hospitalization medication with aspirin, nitrates or statins, but not with other medications such as beta-blockers in multivariate analysis. Pre-hospitalization medication with aspirin and nitrates was significantly associated with the same reduction of the ratio in patients with male gender, hypertension, diabetes mellitus and a history of coronary artery disease. However, in patients who smoked, were obese and hypercholesterolemic, pre-hospitalization medication with nitrates was significantly associated with the reduced ratio. The ratio was significantly low in patients with males and hypercholesterolemia treated with statins before admission., Conclusion: Depending on their coronary risk factors, pre-hospitalization medication with aspirin, nitrates or statins was associated with a different presentation and evolution of ACS., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Lipocalin-type prostaglandin D synthase (L-PGDS), which is responsible for the biosynthesis of prostaglandin (PG) D(2), has been found to be present in the atherosclerotic plaque of the human coronary artery and also to be detectable in human serum. This multicenter cooperative study was designed to establish the diagnostic value of measuring serum L-PGDS for coronary artery disease. The study included 1013 consecutive patients suspected of having stable coronary artery disease who underwent diagnostic coronary angiography. Peripheral blood was collected prior to angiography. The serum level of L-PGDS, as determined by a sandwich ELISA, was 58.1 +/- 2.2, 62.0 +/- 1.8 and 80.6 +/- 2.6 microg/dl for patients with no stenotic lesion (N, n=241), single-vessel coronary artery disease (S, n=351), and multi-vessel coronary artery disease (M, n=421), respectively (N vs. S; P<0.001, S vs. M; P<0.01, N vs. M; P<0.001). Multiple regression analysis indicated that the most powerful independent predictor of the coronary severity score (Gensini Score) was the L-PGDS level (R=0.55, P<0.0001). The serum L-PGDS level is suitable to evaluate the severity of coronary artery disease. The measurement of serum L-PGDS can be a strategy for screening of stable coronary artery disease prior to coronary angiography.

So-called "ampulla" cardiomyopathy is characterized by transient abnormal left ventricular wall motion showing hypokinesia around the apical area and hyperkinesia at the basal area, without any detectable coronary lesion. We recently treated a patient with "ampulla" cardiomyopathy (Case 1) and a patient with acute myocardial infarction showing similar abnormal left ventricular wall motion (Case 2). A 75-year-old female (Case 1) presented with "ampulla" cardiomyopathy without coronary lesion. Vasospasm was induced at segment 8 on the left anterior descending (LAD) coronary artery by intracoronary administration of acetylcholine. A 58-year-old male (Case 2) presented with acute myocardial infarction due to occlusion at segment 8 and underwent successful coronary reperfusion therapy by direct percutaneous transluminal coronary angioplasty. Both Case 1 and Case 2 revelaed similar abnormal left ventricular wall motion, with hypokinesia around the apical area and hyperkinesia at the basal area by echocardiography, in the acute phase. Furthermore, these two patients showed elevated ST segment at both anterior and inferior leads by electrocardiography, and markedly reduced uptake of beta-methyl-p-iodophenyl-pentadecanoic acid around the apical area in the acute phase by scintigraphy. Interestingly, the LAD perfused a relatively wide area including the anterior, apical and part of the inferior area of the left ventricle in both patients by coronary angiography. The abnormal wall motion of Case 1 disappeared 4 weeks after onset, but that of Case 2 did not disappear. Although the diagnoses of Case 1 and Case 2 were different, abnormal wall motion of these cases might be due to myocardial ischemia due to distal LAD lesion. "Ampulla" cardiomyopathy might develop from transient myocardial ischemia induced by coronary vasospasm at the distal LAD which perfuses a relatively wide area.