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Cyprus College
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The college was founded in 1961 with the purpose to provide a well rounded education of high calibre where students can acquire the necessary academic knowledge.
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Wroclaw University
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Founded in 1702 by Leopold I Habsburg. Since the beginning of 20th century the university has produced 9 Nobel Prize winners.
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Volyn University
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The history dates back to 1940. At present, the university includes 4 institutes, 14 faculties and 73 departments.
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Berkeley College
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Through the power of internet, Berkeley college online brings the classroom to you anywhere in the world with the same high level of support as On-Campus classes.
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AIS
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New Zealand's largest international degree provider. The programmes are focused on the global marketplace.
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WORLD UNIVERSITY DIRECTORY
Medical Education European Heart Journal - current issue
<span class="paragraphSection"> <span style="font-style:italic;">For the podcast associated with this article, please visit https://academic.oup.com/eurheartj/pages/Podcasts</span>.</span>
<span class="paragraphSection">Evidence-based medicine relies on large, well-designed, randomized controlled trials (RCTs) to generate reliable results. To achieve this, RCTs must be meticulously planned, executed, and analysed. However, training opportunities for aspiring clinical trialists are often limited. The University of Oxford Master of Science (MSc) in Clinical Trials addresses this gap by offering comprehensive training in both the theoretical and practical aspects of trial methodology. The programme covers a range of trial types and clinical conditions, with a special focus on large, streamlined outcome trials in cardiovascular disease. The MSc provides clinicians with the expertise needed to design and conduct trials that address critical questions, produce reliable answers, and ultimately save lives.</span>
<span class="paragraphSection">A 49-year-old man presented with chest tightness, palpitations, and post-activity syncope was referred to our clinic. He underwent a Bentall procedure 8 years ago for aortic root aneurysm and severe aortic valve regurgitation. Physical examination revealed a systolic murmur in the apex and marfanoid signs (see Supplementary data onlineSupplementary data online, <span style="font-style:italic;">Figure S1</span>). Transthoracic echocardiography showed a chordae tendineae rupture in A2 and severe mitral regurgitation (<span style="font-style:italic;">Panel A</span>). Enhanced computed tomography showed markedly dilated left heart (left atrium: 76 × 84 mm, left ventricle: 104 ×95 mm, mitral annular: 45 × 49 mm) and anterior mitral valve leaflet prolapse (<span style="font-style:italic;">Panel B</span>, black arrow). And the right ventricle was tightly adhered to the posterior sternal border (<span style="font-style:italic;">Panels B–D</span>, arrows; Supplementary data onlineSupplementary data online, <span style="font-style:italic;">Video S1</span>). Whole exome sequencing identified a heterozygous deleterious variant in <span style="font-style:italic;">FBN1</span> gene (NM_000138.5:c.2306G>A), and he was diagnosed with Marfan syndrome (MFS).</span>
<span class="paragraphSection"><div class="boxTitle">Abstract</div>The increasing prevalence of diabetes, obesity, and their cardiometabolic sequelae present major global health challenges and highlight shortfalls of current approaches to the prevention and treatment of these conditions. Representing the largest global burden of morbidity and mortality, the pathobiological processes underlying cardiometabolic diseases are in principle preventable and, even when disease is manifest, sometimes reversable. Nevertheless, with current clinical and public health strategies, goals of widespread prevention and remission remain largely aspirational. Application of precision medicine approaches that reduce errors and improve accuracy in medical and health recommendations has potential to accelerate progress towards these goals. Precision medicine must also maintain safety and ideally be cost-effective, as well as being compatible with an individual’s preferences, capabilities, and needs. Initial progress in precision medicine was made in the context of rare diseases, with much focus on pharmacogenetic studies, owing to the cause of these diseases often being attributable to highly penetrant single gene mutations. By contrast, most obesity and type 2 diabetes are heterogeneous in aetiology and clinical presentation, underpinned by complex interactions between genetic and non-genetic factors. The heterogeneity of these conditions can be leveraged for development of approaches for precision therapies. Adequate characterization of the heterogeneity in cardiometabolic disease necessitates diversity of and synthesis across data types and research methods, ideally culminating in precision trials and real-world application of precision medicine approaches. This State-of-the-Art Review provides an overview of the current state of the science of precision medicine, as well as outlining a roadmap for study designs that maximise opportunities and address challenges to clinical implementation of precision medicine approaches in obesity and diabetes.</span>
<span class="paragraphSection">There are no better examples in contemporary medicine illustrating the fusion and cross-fertilization of conservative and surgical disciplines than cardiovascular surgery and cardiology. The boundaries of the two medical specialties are almost unrecognizable not only in dedicated hospital facilities such as heart centres but also in tertiary institutions with different levels of expertise. A patient-centred approach presumes close cooperation between clinical cardiologists, imaging specialists, interventional cardiologists, and cardiovascular surgeons working together to evaluate clinical conditions, symptoms, and pathological imaging findings. They assess indications and modes of treatment according to individual patient characteristics (<span style="font-style:italic;">Figure 1</span>).</span>
<span class="paragraphSection"><div class="boxTitle">Abstract</div>Pregnancy complicated by maternal obesity contributes to an increased cardiovascular risk in offspring, which is increasingly concerning as the rates of obesity and cardiovascular disease are higher than ever before and still growing. There has been much research in humans and preclinical animal models to understand the impact of maternal obesity on offspring health. This review summarizes what is known about the offspring cardiovascular phenotype, describing a mechanistic role for oxidative stress, metabolic inflexibility, and mitochondrial dysfunction in mediating these impairments. It also discusses the impact of secondary postnatal insults, which may reveal latent cardiovascular deficits that originated <span style="font-style:italic;">in utero</span>. Finally, current interventional efforts and gaps of knowledge to limit the developmental origins of cardiovascular dysfunction in offspring of obese pregnancy are highlighted.</span>
<span class="paragraphSection"><div class="boxTitle">Abstract</div><div class="boxTitle">Background and Aims</div>Hyperglycaemia during gestational diabetes (GD) predisposes women and their offspring to later cardiometabolic disease. The hyperglycaemia-mediated epigenetic changes remain to be elucidated. Methyltransferase MLL1-induced trimethylation of histone 3 at lysine 4 (H3K4me3) activates inflammatory and oxidative phenotype. This epigenetic mark in GD women and its transmission to the offspring were investigated.<div class="boxTitle">Methods</div>Peripheral blood mononuclear cells (PBMC) were collected from GD and control (C) women and also from adolescents born to women of both groups. Endothelial human umbilical vein endothelial cells (HUVEC) and cord blood mononuclear cells (CBMC) were from umbilical cords. The NF-κBp65 and NOX4 expressions were investigated by reverse transcription quantitative polymerase chain reaction and immunofluorescence (IF). MLL1 and H3K4me3 were investigated by immunoblotting and IF. H3K4me3 on NF-κBp65 and NOX4 promoters was studied by chromatin immunoprecipitation. Superoxide anion generation was measured by electron spin resonance spectroscopy. Plasma cytokines were measured by enzyme-linked immunosorbent assay. To investigate the role of MLL1, HUVEC were exposed to inhibitor MM102 or siRNA transfection.<div class="boxTitle">Results</div>PBMC, CBMC, and HUVEC showed an increase of <span style="font-style:italic;">NF-κBp65</span>, <span style="font-style:italic;">IL-6</span>, <span style="font-style:italic;">ICAM-1</span>, <span style="font-style:italic;">MCP-1</span>, and <span style="font-style:italic;">VCAM-1</span> mRNAs. These findings were associated with H3K4me3 enrichment in the promoter of <span style="font-style:italic;">NF-κBp65</span>. Elevated H3K4me3 and cytokine levels were observed in GD adolescents. MLL1 drives H3K4me3 not only on <span style="font-style:italic;">NF-kB p65</span>, but also on <span style="font-style:italic;">NOX4</span> promoter. Inhibition of MLL1 blunted <span style="font-style:italic;">NF-κBp65</span> and <span style="font-style:italic;">NOX4</span> by modulating inflammatory and oxidative phenotype.<div class="boxTitle">Conclusions</div>Such proof-of-concept study shows persistence of MLL1-dependent H3K4me3 in offspring born to GD women, suggesting an epigenetic-driven transmission of maternal phenotype. These findings may pave the way for pharmacological reprogramming of adverse histone modifications to mitigate abnormal phenotypes underlying early ASCVD.</span>
<span class="paragraphSection"><div class="boxTitle">Abstract</div><div class="boxTitle">Background and Aims</div>Observational studies have highlighted that gestational diabetes mellitus is associated with a higher risk of cardiovascular diseases, but the causality remains unclear. Herein, the causality between genetic predisposition to gestational diabetes mellitus and the risk of cardiovascular diseases was investigated using sex-specific Mendelian randomization analysis.<div class="boxTitle">Methods</div>Linkage disequilibrium score regression analysis and two-sample Mendelian randomization analysis were applied to infer the genetic correlation and causality, respectively. Mediation analysis was conducted using a two-step Mendelian randomization approach. Sensitivity analyses were performed to differentiate causality from pleiotropy. The genome-wide association study summary statistics for gestational diabetes mellitus were obtained from FinnGen consortium, while for cardiovascular diseases were generated based on individual-level genetic data from the UK Biobank.<div class="boxTitle">Results</div>Linkage disequilibrium score regression analyses revealed that gestational diabetes mellitus had a significant genetic correlation with coronary artery disease and myocardial infarction after Benjamini–Hochberg correction in ever-pregnant women. In Mendelian randomization analyses, odds ratios (95% confidence interval) for coronary artery disease and myocardial infarction were 1.09 (1.01–1.17) and 1.12 (.96–1.31) per unit increase in the log-odds of genetic predisposition to gestational diabetes mellitus in ever-pregnant women, respectively. Further, Type 2 diabetes and hypertension were identified as mediators for the causality of genetic predisposition to gestational diabetes mellitus on coronary artery disease. In sensitivity analyses, the direction of odds ratio for the association between instrumental variables with gestational diabetes mellitus-predominant effects and the risk of coronary artery disease was consistent with the primary results in ever-pregnant women, although not statistically significant.<div class="boxTitle">Conclusions</div>This study demonstrated a suggestive causal relationship between genetic predisposition to gestational diabetes mellitus and the risk of coronary artery disease, which was mainly mediated by Type 2 diabetes and hypertension. These findings highlight targeting modifiable cardiometabolic risk factors may reduce the risk of coronary artery disease in women with a history of gestational diabetes mellitus.</span>
<span class="paragraphSection"><strong>This commentary refers to ‘Ticagrelor monotherapy for acute coronary syndrome: an individual patient data meta-analysis of TICO and T-PASS trials’, by Y.-J. Lee <span style="font-style:italic;">et al.</span>, <a href="https://doi.org/10.1093/eurheartj/ehae249">https://doi.org/10.1093/eurheartj/ehae249</a> and the discussion piece ‘Subgroup effects of ticagrelor treatment strategies: credibility considerations in an individual patient data meta-analysis', by T. Li <span style="font-style:italic;">et al.</span>, <a href="https://doi.org/10.1093/eurheartj/ehae683">https://doi.org/10.1093/eurheartj/ehae683</a>.</strong></span>
<span class="paragraphSection"><strong>This commentary refers to ‘Ticagrelor monotherapy for acute coronary syndrome: an individual patient data meta-analysis of TICO and T-PASS trials’, by Y.-J. Lee <span style="font-style:italic;">et al.</span>, <a href="https://doi.org/10.1093/eurheartj/ehae249">https://doi.org/10.1093/eurheartj/ehae249</a> and the discussion piece ‘Subgroup effects of ticagrelor monotherapy for acute coronary syndrome using individual patient data from the TICO and T-PASS trials’, by Y.-J. Lee <span style="font-style:italic;">et al.</span>, <a href="https://doi.org/10.1093/eurheartj/ehae685">https://doi.org/10.1093/eurheartj/ehae685</a>.</strong></span>
<span class="paragraphSection">Comment on the article ‘Transcatheter Repair versus Mitral-Valve Surgery for Secondary Mitral Regurgitation’ which was published in the <span style="font-style:italic;">New England Journal of Medicine</span>, <a href="https://doi.org/10.1056/NEJMoa2408739">https://doi.org/10.1056/NEJMoa2408739</a>.</span>
<span class="paragraphSection"><div class="boxTitle">Abstract</div>With the increasing burden of diabetes as a cause of macro- and microvascular disease linked to the epidemics of obesity, attention is being paid to dysglycaemic states that predict and precede the development of type 2 diabetes. Such conditions, termed pre-diabetes, are characterized by fasting plasma glucose, or plasma glucose levels on an oral glucose tolerance test, or values of glycated haemoglobin intermediate between ‘normal’ values and those characterizing diabetes. These last are by definition associated, in epidemiological terms, with a higher incidence of microvascular disease—mostly retinopathy. Pre-diabetes overlaps with the components of the ‘metabolic syndrome’—among which are excess visceral adiposity; hypertension; hypertriglyceridaemia; high levels of small, dense low-density lipoproteins; and metabolic-associated fatty liver disease. There is little doubt that pre-diabetes has important prognostic implications, especially for the occurrence of myocardial infarction, ischaemic stroke, and peripheral arterial disease. It is disputed, however, whether pre-diabetes is itself an actionable disease entity, in addition to the risk factors characterizing it. Because of this uncertainty, the latest European Society of Cardiology guidelines chose not to include pre-diabetes as a treatment target for atherosclerotic cardiovascular disease, at variance from the three previous editions of such guidelines. This is spurring a debate, the Pro and Contra arguments featured in the present debate article.</span>
<span class="paragraphSection">This is a correction to: Mathieu Echivard <span style="font-style:italic;">et al.</span>, Prognostic value of ventricular arrhythmia in early post-infarction left ventricular dysfunction: the French nationwide WICD-MI study, <span style="font-style:italic;">European Heart Journal</span>, 2024; ehae575, <a href="https://doi.org/10.1093/eurheartj/ehae575">https://doi.org/10.1093/eurheartj/ehae575</a></span>
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