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The introduction of metallic drug-eluting stents has reduced the risk of restenosis and widened the indications of percutaneous coronary intervention in treatment of coronary artery disease. However, this medical device can induce hypersensitive reaction that interferes with the endothelialization and healing process resulting in late persistent or acquired malapposition of the permanent metallic implant. Delayed endotheliaization and malapposition may lead to late and very late stent thrombosis. Bioresorbable scaffolds (BRS) have been introduced to potentially overcome these limitations, as they provide temporary scaffolding and then disappear, liberating the treated vessel from its cage. Magnesium is an essential mineral needed for a variety of physiological functions in the human body and its bioresorbable alloy has the strength-to-weight ratio comparable with that of strong aluminum alloys and alloy steels. The aim of this review is to present the new developments in Magnesium BRS technology, to describe its clinical application and to discuss the future prospects of this innovative therapy.

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Summary Plaque rupture and subsequent thrombotic occlusion of the coronary artery account for as many as three quarters of myocardial infarctions. The concept of plaque stabilisation emerged about 20 years ago to explain the discrepancy between the reduction of cardiovascular events in patients receiving lipid lowering therapy and the small decrease seen in angiographic evaluation of atherosclerosis. Since then, the concept of a vulnerable plaque has received a lot of attention in basic and clinical research leading to a better understanding of the pathophysiology of the vulnerable plaque and acute coronary syndromes. From pathological and clinical observations, plaques that have recently ruptured have thin fibrous caps, large lipid cores, exhibit outward remodelling and invasion by vasa vasorum. Ruptured plaques are also focally inflamed and this may be a common denominator of the other pathological features. Plaques with similar characteristics, but which have not yet ruptured, are believed to be vulnerable to rupture. Experimental studies strongly support the validity of anti-inflammatory approaches to promote plaque stability. Unfortunately, reliable non-invasive methods for imaging and detection of such plaques are not yet readily available. There is a strong biological basis and supportive clinical evidence that low-density lipoprotein lowering with statins is useful for the stabilisation of vulnerable plaques. There is also some clinical evidence for the usefulness of antiplatelet agents, beta blockers and renin-angiotensin-aldosterone system inhibitors for plaque stabilisation. Determining the causes of plaque rupture and designing diagnostics and interventions to prevent them are urgent priorities for current basic and clinical research in cardiovascular area.

Introduction: Cardiovascular disease (CVD) is a major cause of death in COPD. Numerous studies describe clinical evidence of endothelial dysfunction in COPD but the molecular pathways which link COPD and CVD remain unclear. Late outgrowth endothelial progenitor cells (EPC) could serve as a research tool to investigate endothelial defects in COPD patients. Aim and objectives: To examine whether EPC from COPD patients exhibit dysfunctional characteristics, illustrating the underlying molecular process of endothelial dysfunction in COPD. Methods: EPC were isolated from peripheral blood samples received from 16 healthy non smoking volunteers (age ± SEM, 57±2.7yr), 10 healthy smokers (57±2.6yr) and 16 COPD patients (67±1.6yr). The mononuclear fraction was placed in culture in the presence of endothelial growth factors. Late outgrowth colonies of EPC appeared between day 7 and 24, as characteristic cobblestone monolayers. The cells were grown to confluence in T-25 or T-75 flasks and used at passages 4 to 6 for all experiments. Endothelial senescence was measured by senescence-associated β-galactosidase (SA-β-Gal) activity and sirtuin (SIRT) 1 protein levels by Western blotting. Results: EPC from healthy smokers and COPD patients displayed significantly increased senescence and reduced SIRT1 protein levels compared to healthy non smoking subjects. SIRT1 protein levels negatively correlated with endothelial senescence. Conclusions: The results from our study demonstrate that EPC from smokers and COPD patients display epigenetic molecular dysfunctions linked to increased senescence. These defects may contribute to endothelial dysfunction and cardiovascular events.

<b>Background:</b> COPD is a disease of accelerated ageing, that may result from cellular senescence. MicroRNA-34a induces cellular senescence in small airway epithelial cells (SAEC) by inhibiting sirtuin-1 (SIRT1), an anti-ageing molecule. Extracellular vesicles (EVs) may contain microRNAs that can be modified in senescent cells. Senescent cells influence their environment and induce cellular senescence in neighbouring cells, thereby spreading senescence. The role of EVs in spreading senescence is currently unknown. <b>Aim:</b> To compare the effect of EVs produced by SAEC from COPD patients and non-smoker (NS) donors on cellular senescence of healthy SAEC <b>Methods:</b> Primary SAEC were cultured in submerged culture. EVs were isolated by ultracentrifugation. Recipient cells were treated with EVs, and senescence markers were measured by RT-qPCR and Western blot <b>Results:</b> Healthy cells treated with COPD EVs showed increased expression of miR-34a within 3h (1.3-fold increase in treated cells compared to non-treated, n=5, p&lt;0.05). Consequently, decreased expression of the protein SIRT1 (3.3-fold, n=5, p=0.01) and increased expression of p21CIP1 (3.6-fold, n=6, p&lt;0.05) was detected 48h after treatment with COPD EVs compared to NS EVs. This effect was specific to miR-34a, as pre-treatment of EVs with a detergent or pre-treatment of recipient cells with antagomir against miR-34a blocked this effect <b>Conclusion:</b> These data suggest that vesicular miR-34a is involved in cellular senescence and may contribute to senescence propagation and ageing acceleration observed in COPD lungs. Further exploration of EVs in senescence may provide useful biomarkers and targets for future COPD therapy

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No abstract is provided for this article.

Primary percutaneous coronary intervention (PPCI) preserves function and improves survival. The late effects of PPCI on left ventricular remodeling, however, have not yet been investigated on cardiac magnetic resonance imaging (CMRI).Twenty-five patients with acute myocardial infarction (AMI) treated with PPCI underwent CMRI within 10 days, at 4 months and at 5 years. Left ventricular ejection fraction (LVEF), end-diastolic volume (EDV) and end-systolic volume were quantified on cine images. Infarct mass and transmural extent of infarction were quantified on contrast-enhanced imaging. In all patients EDV increased significantly in the early phase (192 ± 40 ml to 211 ± 49 ml, P ≤ 0.01) and LVEF improved significantly (42 ± 9% to 46 ± 9%, P=0.02). In the late phase (>4 months) no significant changes were observed (LVEF 44 ± 9%, P=0.07; EDV 216 ± 68 ml, P=0.38). Three different groups could be identified. One-third (32%) had no dilatation at all; one-third (32%) had limited dilatation at 4 months without progression later; and 36% had progressive dilatation both at 4 months and at late follow-up. This third group had an average increase in EDV of 20% in the acute phase followed by an additional 13%. The strongest predictor for progressive dilatation was infarct mass.Even in the era of PPCI for AMI followed by optimal medical therapy, one-third of patients had progressive dilatation, which was best predicted by infarct mass.

‘The European Society of Cardiology is a manifest success’—this is what Desmond G. Julian, as the newly appointed Editor-in-Chief, wrote in his first Editorial in the very first issue of the European Heart Journal that appeared in February 1980.1 He was referring to the tremendous support given by its members to the then 4-yearly (!) Congress of the Society and to the many meetings of the Working Groups—but obviously this was just the beginning of what we experience today. Shortly thereafter, thanks to visionary leaders such as Paul Hugenholtz, Henry Denolin, and others, the European Society of Cardiology grew considerably in the following 30 years—despite the scepticism of many—into one of the most influential and prestigious bodies in medicine. Today, the European Society of Cardiology holds a highly successful annual congress with a growing number of participants, currently >30 000, and its flagship, the European Heart Journal , has turned from a Cinderella of medical literature to centre stage. Over the last three decades, the number of manuscript submissions initially grew slowly, then steadily, and recently markedly from 500 to >3500 a year ( Figure 1A ). Accordingly, the acceptance rate fell from >50% to currently 12%, allowing the selection of the best manuscripts for readers of the journal. As a consequence, the impact factor of the European Heart Journal grew from 1.0 slowly, but then considerably to its current 9.8 ( Figure 1B ). The European Heart Journal now, together with Circulation and the Journal of the American College of Cardiology , belongs to the top three of 95 journals in the field of cardiovascular medicine—what a birthday present! Figure 1 Manuscript submissions ( A ) and impact factor ( B ) of the European Heart Journal over the last 30 years. This success was possible only with the help of dedicated editors and reviewers. After … *Corresponding author. Tel: +41 44 634 55 38, Fax: +41 44 634 55 30, Email: cardiotfl{at}gmx.ch

Royal Brompton Grand RoundsHeart-lung transplantation for cystic fibrosis Can be successful despite contraindications About 6500 people in Britain have cystic fibrosis and only half of patients reach 19 years of age.'Despite recent improvements in treatment there is still a considerable morbidity and mortality.2The main cause of death is respiratory failure from chronic respiratory infection.Heart-lung transplantation for cystic fibrosis was first successfully carried out in 1985, and over 100 patients have now received transplants in Britain.34Case history A 29 year old man-had had cystic fibrosis c at the age of 4 years when he presented v absorption.At 14 years he had developed Royal Brompton National chest infections.Clinical treatment con, Heart and Lung Hospital, pancreatic enzymes, vitamins, chest physi London SW3 6HP antibiotics, and bronchodilators.In 1975 he I left abrasion pleurodesis and in 1981 a right Case presented by: pleurodesis for recurrent pneumothoraces.H(

Background Outcomes data for a durable-polymer everolimus-eluting stent (EES) at extended long-term follow-up in patients with ST-segment elevation myocardial infarction (STEMI) are unknown. Objectives The aim of this study was to assess the 10-year outcomes of patients enrolled in the EXAMINATION (A Clinical Evaluation of Everolimus Eluting Coronary Stents in the Treatment of Patients With ST-Segment Elevation Myocardial Infarction) trial. Methods The EXAMINATION-EXTEND (10-Years Follow-Up of the EXAMINATION Trial) study is an investigator-driven 10-year follow-up of the EXAMINATION trial, which randomly assigned 1,498 patients with STEMI in a 1:1 ratio to receive either EES (n = 751) or bare-metal stents (n = 747). The primary endpoint was a patient-oriented composite endpoint of all-cause death, any myocardial infarction, or any revascularization. Secondary endpoints included a device-oriented composite endpoint of cardiac death, target vessel myocardial infarction, or target lesion revascularization; the individual components of the combined endpoints; and stent thrombosis. Results Complete 10-year clinical follow-up was obtained in 94.5% of the EES group and 95.9% of the bare-metal stent group. Rates of the patient-oriented composite endpoint and device-oriented composite endpoint were significantly reduced in the EES group (32.4% vs. 38.0% [hazard ratio: 0.81; 95% confidence interval: 0.68 to 0.96; p = 0.013] and 13.6% vs. 18.4% [hazard ratio: 0.72; 95% confidence interval: 0.55 to 0.93; p = 0.012], respectively), driven mainly by target lesion revascularization (5.7% vs. 8.8%; p = 0.018). The rate of definite stent thrombosis was similar in both groups (2.2% vs. 2.5%; p = 0.590). No differences were found between the groups in terms of target lesion revascularization (1.4% vs. 1.3%; p = 0.963) and definite or probable stent thrombosis (0.6% vs. 0.4%; p = 0.703) between 5 and 10 years. Conclusions At 10-year follow-up, EES demonstrated confirmed superiority in combined patient- and device-oriented composite endpoints compared with bare-metal stents in patients with STEMI requiring primary percutaneous coronary intervention. Between 5- and 10-year follow-up, a low incidence of adverse cardiovascular events related to device failure was found in both groups. (10-Years Follow-Up of the EXAMINATION Trial; NCT04462315)