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European Heart Journal
Journal Prestige (SJR): 9.315
Citation Impact (citeScore): 9
Number of Followers: 78  
 
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 0195-668X - ISSN (Online) 1522-9645
Published by Oxford University Press Homepage  [415 journals]
  • The growing role of genetics in the understanding of cardiovascular
           diseases: towards personalized medicine

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      Authors: Crea F.
      Pages: 1929 - 1933
      Abstract: With thanks to Amelia Meier-Batschelet, Johanna Huggler, and Martin Meyer for help with compilation of this article.
      PubDate: Fri, 21 May 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehab279
      Issue No: Vol. 42, No. 20 (2021)
       
  • Broaden your horizons with the latest addition to the journal family, EHJ
           Open

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      Authors: Ozkan J.
      Pages: 1934 - 1935
      PubDate: Fri, 14 May 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehab203
      Issue No: Vol. 42, No. 20 (2021)
       
  • Powerful tributes to pioneering cardiologist Bernard Lown

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      Authors: Nicholls M.
      Pages: 1935 - 1936
      Abstract: Mark Nicholls speaks to Russian cardiologist Eugene Chazov and International Physicians for the Prevention of Nuclear War (IPPNW) co-President Ira Helfand about how Bernard Lown will be remembered as a cardiologist, educator, and peace activist
      PubDate: Fri, 02 Apr 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehab178
      Issue No: Vol. 42, No. 20 (2021)
       
  • Cardiovascular Genetics in the European Heart Journal

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      Authors: Tofield A.
      Pages: 1937 - 1937
      Abstract: The team of Deputy and Associate Editors Heribert Schunkert, Sharlene Day and Peter Schwartz
      PubDate: Mon, 25 Oct 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehaa705
      Issue No: Vol. 42, No. 20 (2021)
       
  • A most remarkable person: Dr Bernard Lown

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      Authors: Kowey P.
      Pages: 1938 - 1939
      PubDate: Mon, 05 Apr 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehab202
      Issue No: Vol. 42, No. 20 (2021)
       
  • Leveraging clinical epigenetics in heart failure with preserved ejection
           fraction: a call for individualized therapies

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      Authors: Hamdani N; Costantino S, Mügge A, et al.
      Pages: 1940 - 1958
      Abstract: Described as the ‘single largest unmet need in cardiovascular medicine’, heart failure with preserved ejection fraction (HFpEF) remains an untreatable disease currently representing 65% of new heart failure diagnoses. HFpEF is more frequent among women and associates with a poor prognosis and unsustainable healthcare costs. Moreover, the variability in HFpEF phenotypes amplifies complexity and difficulties in the approach. In this perspective, unveiling novel molecular targets is imperative. Epigenetic modifications—defined as changes of DNA, histones, and non-coding RNAs (ncRNAs)—represent a molecular framework through which the environment modulates gene expression. Epigenetic signals acquired over the lifetime lead to chromatin remodelling and affect transcriptional programmes underlying oxidative stress, inflammation, dysmetabolism, and maladaptive left ventricular remodelling, all conditions predisposing to HFpEF. The strong involvement of epigenetic signalling in this setting makes the epigenetic information relevant for diagnostic and therapeutic purposes in patients with HFpEF. The recent advances in high-throughput sequencing, computational epigenetics, and machine learning have enabled the identification of reliable epigenetic biomarkers in cardiovascular patients. Contrary to genetic tools, epigenetic biomarkers mirror the contribution of environmental cues and lifestyle changes and their reversible nature offers a promising opportunity to monitor disease states. The growing understanding of chromatin and ncRNAs biology has led to the development of several Food and Drug Administration approved ‘epidrugs’ (chromatin modifiers, mimics, anti-miRs) able to prevent transcriptional alterations underpinning left ventricular remodelling and HFpEF. In the present review, we discuss the importance of clinical epigenetics as a new tool to be employed for a personalized management of HFpEF.
      PubDate: Wed, 05 May 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehab197
      Issue No: Vol. 42, No. 20 (2021)
       
  • Genetic insight into sick sinus syndrome

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      Authors: Thorolfsdottir R; Sveinbjornsson G, Aegisdottir H, et al.
      Pages: 1959 - 1971
      Abstract: AimsThe aim of this study was to use human genetics to investigate the pathogenesis of sick sinus syndrome (SSS) and the role of risk factors in its development.Methods and resultsWe performed a genome-wide association study of 6469 SSS cases and 1 000 187 controls from deCODE genetics, the Copenhagen Hospital Biobank, UK Biobank, and the HUNT study. Variants at six loci associated with SSS, a reported missense variant in MYH6, known atrial fibrillation (AF)/electrocardiogram variants at PITX2, ZFHX3, TTN/CCDC141, and SCN10A and a low-frequency (MAF = 1.1–1.8%) missense variant, p.Gly62Cys in KRT8 encoding the intermediate filament protein keratin 8. A full genotypic model best described the p.Gly62Cys association (P = 1.6 × 10−20), with an odds ratio (OR) of 1.44 for heterozygotes and a disproportionally large OR of 13.99 for homozygotes. All the SSS variants increased the risk of pacemaker implantation. Their association with AF varied and p.Gly62Cys was the only variant not associating with any other arrhythmia or cardiovascular disease. We tested 17 exposure phenotypes in polygenic score (PGS) and Mendelian randomization analyses. Only two associated with the risk of SSS in Mendelian randomization, AF, and lower heart rate, suggesting causality. Powerful PGS analyses provided convincing evidence against causal associations for body mass index, cholesterol, triglycerides, and type 2 diabetes (P > 0.05).ConclusionWe report the associations of variants at six loci with SSS, including a missense variant in KRT8 that confers high risk in homozygotes and points to a mechanism specific to SSS development. Mendelian randomization supports a causal role for AF in the development of SSS.
      PubDate: Sat, 13 Feb 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehaa1108
      Issue No: Vol. 42, No. 20 (2021)
       
  • Genetic insight into sick sinus syndrome. Is there a pill for it or how
           far are we on the translational road to personalized medicine'

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      Authors: Tomsits P; Clauss S, Kääb S.
      Pages: 1972 - 1975
      PubDate: Fri, 16 Apr 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehab209
      Issue No: Vol. 42, No. 20 (2021)
       
  • Association between prophylactic angiotensin-converting enzyme inhibitors
           and overall survival in Duchenne muscular dystrophy—analysis of registry
           data

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      Authors: Porcher R; Desguerre I, Amthor H, et al.
      Pages: 1976 - 1984
      Abstract: AimsTo estimate the effect of prophylactic angiotensin-converting enzyme inhibitors (ACEi) on survival in Duchenne muscular dystrophy (DMD).Methods and resultsWe analysed the data from the French multicentre DMD Heart Registry (ClinicalTrials.gov: NCT03443115). We estimated the association between the prophylactic prescription of ACEi and event-free survival in 668 patients aged 8 to 13 years, with normal left ventricular function, using (i) a Cox model with intervention as a time-dependent covariate, (ii) a propensity-based analysis comparing ACEi treatment vs. no treatment, and (iii) a set of sensitivity analyses. The study outcomes were overall survival and hospitalizations for heart failure (HF) or acute respiratory failure. Among the 668 patients included in the DMD Heart Registry, 576 (mean age 6.1 ± 2.8 years) were eligible for this study, of whom 390 were treated with ACEi prophylactically. Death occurred in 53 patients (13.5%) who were and 60 patients (32.3%) who were not treated prophylactically with ACEi, respectively. In a Cox model with intervention as a time-dependent variable, the hazard ratio (HR) associated with ACEi treatment was 0.49 [95% confidence interval (CI) 0.34–0.72] and 0.47 (95% CI 0.31–0.17) for overall mortality after adjustment for baseline variables. In the propensity-based analysis, 278 patients were included in the treatment group and 834 in the control group, with 18.5% and 30.4% 12-year estimated probability of death, respectively. ACEi were associated with a lower risk of death (HR 0.39; 95% CI 0.17–0.92) and hospitalization for HF (HR 0.16; 95% CI 0.04–0.62). All other sensitivity analyses yielded similar results.ConclusionProphylactic ACEi treatment in DMD was associated with a significantly higher overall survival and lower rates of hospitalization for HF.
      PubDate: Mon, 22 Mar 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehab054
      Issue No: Vol. 42, No. 20 (2021)
       
  • Cardioprotection in Duchenne muscular dystrophy

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      Authors: Owens A; Jessup M.
      Pages: 1985 - 1987
      PubDate: Mon, 22 Mar 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehab152
      Issue No: Vol. 42, No. 20 (2021)
       
  • Clinical characteristics and outcomes in childhood-onset hypertrophic
           cardiomyopathy

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      Authors: Marston N; Han L, Olivotto I, et al.
      Pages: 1988 - 1996
      Abstract: AimsChildhood-onset hypertrophic cardiomyopathy (HCM) is far less common than adult-onset disease, thus natural history is not well characterized. We aim to describe the characteristics and outcomes of childhood-onset HCM.Methods and resultsWe performed an observational cohort study of 7677 HCM patients from the Sarcomeric Human Cardiomyopathy Registry (SHaRe). Hypertrophic cardiomyopathy patients were stratified by age at diagnosis [<1 year (infancy), 1–18 years (childhood), >18 years (adulthood)] and assessed for composite endpoints reflecting heart failure (HF), life-threatening ventricular arrhythmias, atrial fibrillation (AF), and an overall composite that also included stroke and death. Stratifying by age of diagnosis, 184 (2.4%) patients were diagnosed in infancy; 1128 (14.7%) in childhood; and 6365 (82.9%) in adulthood. Childhood-onset HCM patients had an ∼2%/year event rate for the overall composite endpoint, with ventricular arrhythmias representing the most common event in the 1st decade following baseline visit, but HF and AF becoming more common by the end of the 2nd decade. Sarcomeric variants were more common in childhood-onset HCM (63%) and carried a worse prognosis than non-sarcomeric disease, including a greater than two-fold increased risk of HF [HRadj 2.39 (1.36–4.20), P = 0.003] and 67% increased risk of the overall composite outcome [HRadj 1.67 (1.16–2.41), P = 0.006]. When compared with adult-onset HCM, childhood-onset was 36% more likely to develop life-threatening ventricular arrhythmias [HRadj 1.36 (1.03–1.80)] and twice as likely to require transplant or ventricular assist device [HRadj 1.99 (1.23–3.23)].ConclusionPatients with childhood-onset HCM are more likely to have sarcomeric disease, carry a higher risk of life-threatening ventricular arrythmias, and have greater need for advanced HF therapies. These findings provide insight into the natural history of disease and can help inform clinical risk stratification.
      PubDate: Fri, 26 Mar 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehab148
      Issue No: Vol. 42, No. 20 (2021)
       
  • Childhood-onset hypertrophic cardiomyopathy research coming of age

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      Authors: Kaski J.
      Pages: 1997 - 1999
      PubDate: Fri, 26 Mar 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehab093
      Issue No: Vol. 42, No. 20 (2021)
       
  • Genome-wide association analysis in dilated cardiomyopathy reveals two new
           players in systolic heart failure on chromosomes 3p25.1 and 22q11.23

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      Authors: Garnier S; Harakalova M, Weiss S, et al.
      Pages: 2000 - 2011
      Abstract: Aims Our objective was to better understand the genetic bases of dilated cardiomyopathy (DCM), a leading cause of systolic heart failure.Methods and results We conducted the largest genome-wide association study performed so far in DCM, with 2719 cases and 4440 controls in the discovery population. We identified and replicated two new DCM-associated loci on chromosome 3p25.1 [lead single-nucleotide polymorphism (SNP) rs62232870, P = 8.7 × 10−11 and 7.7 × 10−4 in the discovery and replication steps, respectively] and chromosome 22q11.23 (lead SNP rs7284877, P = 3.3 × 10−8 and 1.4 × 10−3 in the discovery and replication steps, respectively), while confirming two previously identified DCM loci on chromosomes 10 and 1, BAG3 and HSPB7. A genetic risk score constructed from the number of risk alleles at these four DCM loci revealed a 3-fold increased risk of DCM for individuals with 8 risk alleles compared to individuals with 5 risk alleles (median of the referral population). In silico annotation and functional 4C-sequencing analyses on iPSC-derived cardiomyocytes identify SLC6A6 as the most likely DCM gene at the 3p25.1 locus. This gene encodes a taurine transporter whose involvement in myocardial dysfunction and DCM is supported by numerous observations in humans and animals. At the 22q11.23 locus, in silico and data mining annotations, and to a lesser extent functional analysis, strongly suggest SMARCB1 as the candidate culprit gene.Conclusion This study provides a better understanding of the genetic architecture of DCM and sheds light on novel biological pathways underlying heart failure.
      PubDate: Wed, 03 Mar 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehab030
      Issue No: Vol. 42, No. 20 (2021)
       
  • Corrigendum to: Genome-wide association analysis in dilated cardiomyopathy
           reveals two new players in systolic heart failure on chromosomes 3p25.1
           and 22q11.23

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      Pages: 2011 - 2011
      Abstract: Eur Heart J 2021; doi:10.1093/eurheartj/ehab030
      PubDate: Sat, 24 Apr 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehab192
      Issue No: Vol. 42, No. 20 (2021)
       
  • Genome-wide association for heart failure: from discovery to clinical use

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      Authors: Fullenkamp D; Puckelwartz M, McNally E.
      Pages: 2012 - 2014
      PubDate: Wed, 21 Apr 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehab172
      Issue No: Vol. 42, No. 20 (2021)
       
  • Influenza vaccination: a ‘shot’ at INVESTing in cardiovascular
           health

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      Authors: Bhatt A; Vardeny O, Udell J, et al.
      Pages: 2015 - 2018
      Abstract: The link between viral respiratory infection and non-pulmonary organ-specific injury, including cardiac injury, has become increasingly appreciated during the current coronavirus disease 2019 (COVID-19) pandemic. Even prior to the pandemic, however, the association between acute infection with influenza and elevated cardiovascular risk was evident. The recently published results of the NHLBI-funded INfluenza Vaccine to Effectively Stop CardioThoracic Events and Decompensated (INVESTED) trial, a 5200 patient comparative effectiveness study of high-dose vs. standard-dose influenza vaccine to reduce cardiopulmonary events and mortality in a high-risk cardiovascular population, found no difference between strategies. However, the broader implications of influenza vaccine as a strategy to reduce morbidity in high-risk patients remain extremely important, with randomized controlled trial and observational data supporting vaccination in high-risk patients with cardiovascular disease. Given a favourable risk-benefit profile and widespread availability at generally low cost, we contend that influenza vaccination should remain a centrepiece of cardiovascular risk mitigation and describe the broader context of underutilization of this strategy. Few therapeutics in medicine offer seasonal efficacy from a single administration with generally mild, transient side effects, and exceedingly low rates of serious adverse effects. Infection control measures such as physical distancing, hand washing, and the use of masks during the COVID-19 pandemic have already been associated with substantially curtailed incidence of influenza outbreaks across the globe. Appending annual influenza vaccination to these measures represents an important public health and moral imperative.
      PubDate: Mon, 22 Mar 2021 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehab133
      Issue No: Vol. 42, No. 20 (2021)
       
  • Management of acute coronary syndromes in patients presenting without
           persistent ST-segment elevation and coexistent atrial fibrillation

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      Authors: Verdecchia P; Angeli F, Cavallini C.
      Pages: 2019 - 2019
      Abstract: This commentary refers to ‘2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation’, by J.P. Collet et al., doi: 10.1093/eurheartj/ehaa575 and the discussion piece 'Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation and coexistent atrial fibrillation – Dual versus triple antithrombotic therapy', by J-P. Collet and H. Thiele, doi:10.1093/eurheartj/ehaa909.
      PubDate: Mon, 09 Nov 2020 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehaa575 and the discussion piece 'management of acute coronary syndromes in patien
      Issue No: Vol. 42, No. 20 (2020)
       
  • Management of acute coronary syndromes in patients presenting without
           persistent ST-segment elevation and coexistent atrial fibrillation –
           Dual versus triple antithrombotic therapy

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      Authors: Collet J; Thiele H.
      Pages: 2020 - 2021
      Abstract: This commentary refers to ‘2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation’, by J.-P. Collet et al., doi: 10.1093/eurheartj/ehaa575 and the discussion piece 'Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation and coexistent atrial fibrillation', by P. Verdecchia et al., doi:10.1093/eurheartj/ehaa906.
      PubDate: Fri, 13 Nov 2020 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehaa575 and the discussion piece 'management of acute coronary syndromes in patien
      Issue No: Vol. 42, No. 20 (2020)
       
  • A bleeding Blalock–Taussig shunt

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      Authors: Chin C; Huang S, Wang J, et al.
      Pages: 2022 - 2022
      Abstract: An 8-month-old girl was diagnosed with truncus arteriosus, left pulmonary artery sling (Panel A) and tracheal stenosis since birth. Because of complex pulmonary artery anatomy and bilateral pulmonary artery hypoplasia, she underwent operation for main pulmonary artery division from truncus, right modified Blalock-Taussig (mBT) shunt and sliding tracheoplasty at the age of 13 days. However, cardiogenic shock due to mBT shunt occlusion happened 2 weeks after surgery. After extracorporeal cardiopulmonary resuscitation, right mBT shunt revision, and new left mBT shunt implantation were performed. After prolonged hospitalization for post-resuscitation sequelae, she was discharged home at the age of 7 months with a tracheostomy.
      PubDate: Tue, 17 Nov 2020 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehaa887
      Issue No: Vol. 42, No. 20 (2020)
       
  • Percutaneous transmyocardial ablation of a metastatic adrenocortical
           carcinoma invading the interventricular septum

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      Authors: Xie X; Zhou Y, Wu B, et al.
      Pages: 2023 - 2023
      Abstract: A 52-year-old woman presented with exertional chest tightness for 3 months. She had undergone resection of left adrenocortical adenoma 9 years ago. A 5.5 cm × 4.1 cm mass was found on echocardiography in the interventricular septum (IVS) (Panel A, Supplementary material online, Video S1Supplementary material online, Video S1) that obstructed the right ventricular outflow tract (Panels B and C, Supplementary material online, Videos S2 and S3Supplementary material online, Videos S2 and S3). The mass was non-homogenously enhanced on contrast echocardiography (Panel D, Supplementary material online, Video S4Supplementary material online, Video S4) and computerized tomography (Panel E), and highly up took 18F-fluorodeoxyglucose on positron emission tomography (Panel F). Since its massive invasion into the IVS made complete surgical resection impossible, we performed percutaneous interventricular tumour biopsy and transmyocardial radiofrequency ablation. Under transthoracic echocardiography guidance, a biopsy needle was inserted percutaneously at the heart apex and was advanced into the IVS and then the body of tumour to obtain tissue sample. After biopsy, a radiofrequency ablation electrode needle was inserted and directed intramyocardially into the IVS and then into the tumour. The ablation power was increased from 20 W to 60 W with a duration of up to 20 min until visible hyperechoic regions were formed on the echocardiogram (Panel E, Supplementary material online, Video S5Supplementary material online, Video S5). Three rounds of ablation were performed along the centreline of the tumour. Her symptoms were significantly relieved after the procedure. Immunohistochemistry of the specimen was positive for neuroendocrine (synaptophysin, chromogranin A) and adrenocortical (Melan A) markers (Panels H–K), indicating adrenocortical carcinoma.
      PubDate: Tue, 15 Dec 2020 00:00:00 GMT
      DOI: 10.1093/eurheartj/ehaa911
      Issue No: Vol. 42, No. 20 (2020)
       
 
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