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While primary percutaneous coronary intervention (PCI) has significantly contributed to improve the mortality in patients with ST segment elevation myocardial infarction even in cardiogenic shock, primary PCI is a standard of care in most of Japanese institutions. Whereas there are high numbers of available facilities providing primary PCI in Japan, there are no clear guidelines focusing on procedural aspect of the standardized care. Whilst updated guidelines for the management of acute myocardial infarction were recently published by European Society of Cardiology, the following major changes are indicated; (1) radial access and drug-eluting stent over bare metal stent were recommended as Class I indication, and (2) complete revascularization before hospital discharge (either immediate or staged) is now considered as Class IIa recommendation. Although the primary PCI is consistently recommended in recent and previous guidelines, the device lag from Europe, the frequent usage of coronary imaging modalities in Japan, and the difference in available medical therapy or mechanical support may prevent direct application of European guidelines to Japanese population. The Task Force on Primary Percutaneous Coronary Intervention of the Japanese Association of Cardiovascular Intervention and Therapeutics (CVIT) has now proposed the expert consensus document for the management of acute myocardial infarction focusing on procedural aspect of primary PCI.

<b>Background:</b> Cellular senescence is one of the hallmarks of COPD. The miR-34a and mir-570 are involved in the induction of cellular senescence by inhibiting anti-ageing sirtuins. Extracellular vesicles (EVs) play a key role in intercellular communication. Senescent cells produce high amounts of EVs and contain miRNA that can regulate cellular senescence. The role of EVs in spreading cell senescence remains unclear. <b>Aim:</b> To characterize extracellular vesicles released by epithelial cells in response to oxidative stress and to assess their effect on epithelial cells senescence. <b>Methods:</b> BEAS-2B bronchial epithelial cells were stimulated with H2O2 for 24 or 48h. Microvesicles and exosomes were isolated by differential ultracentrifugation of cell supernatant and characterised by Western blot and labelling membrane with the dye PKH67. The RNA content of EVs was determined by fluorescence and by qRT-PCR. <b>Results:</b> After 48h treatment, EVs are released by cells stimulated with medium or H2O2. The fluorescence intensity of pkh67 increased in response to H2O2 (n=2, from 2.6 fold for microvesicles, and 1.4 fold for exosomes) suggesting that epithelial cells release more EVs in response to oxidative stress. In response to H2O2, miR-34a and miR-570 expression is augmented only in exosomes. <b>Conclusion:</b> These data suggest that in response to oxidative stress, epithelial cells produced exosomes enriched in miRNA involved in cellular senescence. This may contribute to COPD pathophysiology by spreading senescence in adjacent epithelial and other cells.

An imbalance between proteases and antiproteases may play a role in emphysema, which is characterized by increased degradation of extracellular matrix, and in airway remodeling in chronic bronchitis and asthma, in which there is increased collagen deposition. We assessed the effect of smoking on release of matrix metalloprotease-9 (MMP-9) and of its inhibitor, tissue inhibitor of metalloprotease-1 (TIMP-1), from alveolar macrophages, and determined the effects of proinflammatory (interleukin [IL]-1 β and lipopolysaccharide [LPS]) and antiinflammatory (IL-10) stimuli on the release of MMP-9 and TIMP-1. We performed bronchoalveolar lavage in 11 smokers and 11 nonsmokers, and cultured airway macrophages in the presence of control medium, IL-1 β , and LPS. Airway macrophages from smokers released greater amounts of MMP-9 and TIMP-1 at baseline and in response to IL-1 β and LPS than did those of nonsmokers. Airway macrophages from smokers produced more TNF- α and IL-10. IL-10 increased TIMP-1 release without modifying that of MMP-9, leading to a decrease in the MMP-9 to TIMP-1 ratio. Anti-IL-10 antibody had no effect on MMP-9 production induced by LPS. We conclude that the release of proteases and antiproteases by airway macrophages is increased in cigarette smokers, and can be regulated by exogenous IL-10.

The main objective of the present randomized pilot study was to explore the effects of upstream prasugrel or ticagrelor or clopidogrel for patients with ST-segment-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI).Administration of clopidogrel "as soon as possible" has been advocated for STEMI. Pretreatment with prasugrel and ticagrelor may improve reperfusion. Currently, the angiographic effects of upstream administration of these agents are poorly understood.A total of 132 patients with STEMI within the first 12 hr of chest pain referred to primary angioplasty were randomized to upstream clopidogrel (600 mg), prasugrel (60 mg), or ticagrelor (180 mg) while still in the emergency room. All patients underwent protocol-mandated thrombus aspiration.Macroscopic thrombus material was retrieved in 79.5% of the clopidogrel group, 65.9% of the prasugrel group, and 54.3% of the ticagrelor group (P = 0.041). At baseline angiography, large thrombus burden was 97.7% vs. 87.8% vs. 80.4% in the clopidogrel, prasugrel, and ticagrelor groups, respectively (P = 0.036). Also, at baseline, 97.7% presented with an occluded target vessel in the clopidogrel group, 87.8% in the prasugrel group and 78.3% in the ticagrelor group (P = 0.019). At the end of the procedure, the percentages of patients with combined TIMI grade III flow and myocardial blush grade III were 52.3% for clopidogrel, 80.5% for prasugrel, and 67.4% for ticagrelor (P = 0.022).In patients with STEMI undergoing primary PCI within 12 hr, upstream clopidogrel, prasugrel or ticagrelor have varying angiographic findings, with a trend toward better results for the latter two agents. © 2015 Wiley Periodicals, Inc.

No abstract is provided for this article.

No abstract is provided for this article.

Because of the unavoidable occurrence of vessel disruption after successful coronary balloon angioplasty, the reliability of quantitative angiographic analysis in that setting has been questioned. For this reason and the suggested occurrence of delayed elastic recoil, repeat angiography at 24 hours has been advocated in clinical interventional trials. In this study, these issues are confronted by performing comprehensive quantitative analysis (Cardiovascular Angiographic Analysis System) of coronary angiograms, acquired in multiple identical projections immediately after and 24 hours after angioplasty, in 102 patients with 110 successfully dilated lesions. Vasomotion was controlled by intracoronary nitrate before angiography and all patients were fully anticoagulated (activated partial thromboplastin time 85 to 120 seconds) for >24 hours. Paired Student's (tests applied to angiographic measurements revealed that there was no significant deterioration in minimal luminal diameter or cross-sectional area from immediately after angioplasty to 24 hours later. It can thus be inferred that there is no phenomenon of delayed elastic recoil, at least during this time period. Measurement accuracy and precision of the Cardiovascular Angiographic Analysis System from the postangioplasty angiogram are highly acceptable, at < 0.01 and ± 0.20 mm, respectively. Therefore, it is concluded that routine repeat 24-hour angiography is not indicated after successful angioplasty. A highly significant increase (p < 0.001) in reference diameter (+0.11 ± 0.18 mm) was responsible for the apparent increase in percent diameter stenosis (2.4 ± 7%), a finding that demonstrates the potential for error by selective application of percent diameter stenosis measurements atone. Preferential use of absolute luminal measurements is thus strongly recommended for clinical trials with angiographic monitoring.

Corrected QT dispersion (cQTD) has been correlated with non-uniform ventricular repolarisation and increased mortality. In patients with aortic stenosis, cQTD has been shown improved after surgical valve replacement, but the effects of transcatheter aortic valve implantation (TAVI) are unknown. Therefore, we sought to explore the frequency, predictors and prognostic effects of defective cQTD recovery at 6 months after TAVI.A total of 222 patients underwent TAVI with the Medtronic-CoreValve System between November 2005 and January 2012. Patients who were on class I or III antiarrhythmics or on chronic haemodialysis or who developed atrial fibrillation, a new bundle branch block or became pacemaker dependent after TAVI were excluded. As a result, pre-, post- and follow-up ECG (median: 6 months) analysis was available in 45 eligible patients. Defective cQTD recovery was defined as any progression beyond the baseline cQTD at 6 months.In the 45 patients, the mean cQTD was 47 ± 23 ms at baseline, 45 ± 17 ms immediately after TAVI and 40 ± 16 ms at 6 months (15% reduction, P = 0.049). Compared to baseline, cQTD at 6 months was improved in 60% of the patients whereas defective cQTD recovery was present in 40%. cQTD increase immediately after TAVI was an independent predictor of defective cQTD recovery at 6 months (per 10 ms increase; OR: 1.89, 95% CI: 1.15-3.12). By univariable analysis, defective cQTD recovery was associated with late mortality (HR: 1.52, 95% CI: 1.05-2.17).Despite a gradual reduction of cQTD after TAVI, 40% of the patients had defective recovery at 6 months which was associated with late mortality. More detailed ECG analysis after TAVI may help to avoid late death.