European Heart Journal (Eur Heart J )

Publisher: European Society of Cardiology, Oxford University Press


European Heart Journal is an international, English language, peer-reviewed journal of cardiology. European Heart Journal is an official professional journal of the European Society of Cardiology and is published twice monthly by W.B. Saunders, a Harcourt Health Sciences Company. European Heart Journal aims to publish the highest quality material, both clinical and scientific, on all aspects of cardiology. European Heart Journal includes research findings, technical evaluations, review articles, and in addition provides a forum for the exchange of information and views on all professional cardiology issues including education. European Heart Journal promotes excellence in the profession of cardiology by its commitment to the publication of research, by its support for education, and by its encouragement and dissemination of best practice. The European Heart Journal is cited in : Science Citiation Index, SCISearch, Research Alert, Medical Documentation Sevice, Current Contents/Clinical Medicine, Chemical Abstracts, EMBASE and Index Medicus. Harcourt Home

  • Impact factor
  • 5-year impact
  • Cited half-life
  • Immediacy index
  • Eigenfactor
  • Article influence
  • Website
    European Heart Journal website
  • Other titles
    European heart journal (Online), European heart journal
  • ISSN
  • OCLC
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Oxford University Press

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 month embargo on science, technology, medicine articles
    • 24 month embargo on arts and humanities articles
    • Some titles may have different embargoes
  • Conditions
    • Pre-print can only be posted prior to acceptance
    • Pre-print must be accompanied by set statement (see link)
    • Pre-print must not be replaced with post-print, instead a link to published version with amended set statement should be made
    • Pre-print on personal website, employer website, free public server or pre-prints in subject area
    • Post-print on Institutional or Central repositories
    • Publisher version cannot be used except for Nucleic Acids Research articles
    • Published source must be acknowledged
    • Must link to publisher version
    • Set phrase to accompany archived copy (see policy)
    • Articles in some journals can be made Open Access on payment of additional charge
    • Eligible UK authors may deposit in OpenDepot
    • Publisher will deposit on behalf of NIH funded authors to PubMed Central, Nucleic Acids Research authors must pay their fee first
    • Some titles may use different policies
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Purpose: Currently, an echocardiogram presents the left ventricle (LV) based on images obtained from ultrasound methods. Utilizing mathematical equations, specific echocardiographic data may provide more detailed, valuable and practical information for physicians. In our project using appropriate mathematically based softwares, we have attempted to create a novel software capable of demonstrate LV model in normal hearts. Methods: Echocardiography was performed on 50 healthy volunteers. Data evaluated included: velocity (radial, longitudinal, rotational and vector point), displacement (longitudinal and rotational), strain rate (longitudinal and circumferential) and strain (radial, longitudinal and circumferential) of all 16 LV myocardial segments. Using these data, force vectors of myocardial samples were estimated by MATLAB and LSDYNA softwares, interfaced in the echocardiograph system. Dynamic orientation contraction (through the cardiac cycle) of every individual myocardial fiber could be created by adding together the sequential steps of the multiple fragmented sectors of that fiber. This way we attempted to mechanically illustrate the global LV model. Results: LV Myocardial modeling: Our study shows that in normal cases myocardial fibers initiate from the posterior-basal region of the heart, continues through the LV free wall, reaches the septum, loops around the apex, ascends, and ends at the superior-anterior edge of LV. Conclusion: We were able to define the whole LV myocardial model mathematically, for the first time, by MATLAB software and LSDYNA software in normal subjects. This will enable physicians to diagnose and follow-up many cardiac diseases when this software is interfaced within echocardiographic machines.
    European Heart Journal 10/2014;
  • European Heart Journal 05/2014;
  • European Heart Journal 05/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Whether prasugrel plus bivalirudin is a superior strategy to unfractionated heparin plus clopidogrel in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) has never been assessed in specifically designed randomized trials. The Bavarian Reperfusion Alternatives Evaluation (BRAVE) 4 study is an investigator-initiated, randomized, open-label, multicentre trial, designed to test the hypothesis that in STEMI patients with planned primary PCI a strategy based on prasugrel plus bivalirudin is superior to a strategy based on clopidogrel plus heparin in terms of net clinical outcome. Owing to slow recruitment, the trial was stopped prematurely after enrolment of 548 of 1240 planned patients. At 30 days, the primary composite endpoint of death, myocardial infarction, unplanned revascularization of the infarct related artery, stent thrombosis, stroke, or bleeding was observed in 42 patients (15.6%) randomized to prasugrel plus bivalirudin and 40 patients (14.5%) randomized to clopidogrel plus heparin [relative risk, 1.09; one-sided 97.5% confidence interval (CI) 0-1.79, P = 0.680]. The composite ischaemic endpoint of death, myocardial infarction, unplanned revascularization of the infarct-related artery, stent thrombosis, or stroke occurred in 13 patients (4.8%) in the prasugrel plus bivalirudin group and 15 patients (5.5%) in the clopidogrel plus heparin group (relative risk, 0.89; 95% CI 0.40-1.96, P = 0.894). Bleeding according to the HORIZONS-AMI definition was observed in 38 patients (14.1%) in the prasugrel plus bivalirudin group and 33 patients (12.0%) in the clopidogrel plus heparin group (relative risk, 1.18; 95% CI 0.74-1.88, P = 0.543). Results were consistent across various subgroups of patients. In this randomized trial of STEMI patients, we were unable to demonstrate significant differences in net clinical outcome between prasugrel plus bivalirudin and clopidogrel plus heparin. Neither the composite of ischaemic complications nor bleeding were favourably affected by prasugrel plus bivalirudin compared with a regimen of clopidogrel plus unfractionated heparin. However, the results must be interpreted in view of the premature termination of the trial. Unique identifier NCT00976092 (
    European Heart Journal 05/2014;
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    ABSTRACT: Cardiovascular magnetic resonance (CMR) has improved diagnostic and management strategies in hypertrophic cardiomyopathy (HCM) by expanding our appreciation for the diverse phenotypic expression. We sought to characterize the prevalence and clinical significance of a recently identified accessory left ventricular (LV) muscle bundle extending from the apex to the basal septum or anterior wall (i.e. apical-basal). CMR was performed in 230 genotyped HCM patients (48 ± 15 years, 69% male), 30 genotype-positive/phenotype-negative (G+/P-) family members (32 ± 15 years, 30% male), and 126 controls. Left ventricular apical-basal muscle bundle was identified in 145 of 230 (63%) HCM patients, 18 of 30 (60%) G+/P- family members, and 12 of 126 (10%) controls (G+/P- vs. controls; P < 0.01). In HCM patients, the prevalence of an apical-basal muscle bundle was similar among those with disease-causing sarcomere mutations compared with patients without mutation (64 vs. 62%; P = 0.88). The presence of an LV apical-basal muscle bundle was not associated with LV outflow tract obstruction (P = 0.61). In follow-up, 33 patients underwent surgical myectomy of whom 22 (67%) were identified to have an accessory LV apical-basal muscle bundle, which was resected in all patients. Apical-basal muscle bundles are a unique myocardial structure commonly present in HCM patients as well as in G+/P- family members and may represent an additional morphologic marker for HCM diagnosis in genotype-positive status.
    European Heart Journal 05/2014;
  • European Heart Journal 05/2014;
  • European Heart Journal 05/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Long-term anticoagulation treatment with warfarin has been associated with a number of limitations in clinical practice and there is a need for more convenient long-term anticoagulation treatment. One of the non-vitamin K oral anticoagulants in development is edoxaban, a factor Xa inhibitor that is administered once daily. The pharmacological properties of edoxaban have various advantages in anticoagulant therapy. Edoxaban quickly reaches peak plasma concentrations in 1.5 h, has a half-life of 10-14 h, has relatively high bioavailability of 62% and exhibits highly selective, competitive, concentration-dependent inhibition of human factor Xa. The plasma concentrations of edoxaban are also closely correlated with suppression of thrombin generation and a range of platelet activation parameters (fragment 1+2, thrombin-antithrombin complex, and β-thromboglobulin), which edoxaban has been shown to rapidly inhibit. The anticoagulant activity of edoxaban is not affected by food intake or ethnicity and a number of drug-drug interaction studies have been performed. Co-administration of edoxaban with strong P-glycoprotein inhibitors, such as dronedarone, quinidine, and verapamil requires edoxaban dose-reduction by 50% to avoid the risk of over-exposure. The exposure of edoxaban may also increase in patients with a body weight ≤60 kg and moderate renal impairment. This meant a dose-reduction strategy in patients at risk of over-exposure was utilized in Phase III clinical studies. In conclusion, the pharmacological properties of edoxaban provide rapid and specific inhibition of factor Xa, which is closely related to plasma concentrations. Given the limitations with long-term warfarin therapy, once-daily edoxaban may provide a convenient long-term alternative for patients.
    European Heart Journal 05/2014;
  • European Heart Journal 05/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: The author reviews statistical methods commonly applied in economic evaluations that rely on individual patient-level data. The paper includes a review of foundational concepts, unique characteristics of health economic data, and methods developed to address them. The paper then highlights issues that should be considered in the interpretation of findings from economic evaluations.
    European Heart Journal 05/2014;
  • European Heart Journal 05/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: A genetic variant (rs20417) of the PTGS2 gene, encoding for COX-2, has been associated with decreased COX-2 activity and a decreased risk of cardiovascular disease (CVD). However, this genetic association and the role of COX-2 in CVD remain controversial. The association of rs20417 with CVD was prospectively explored in 49 232 subjects (ACTIVE-A, CURE, epiDREAM/DREAM, ONTARGET, RE-LY, and WGHS) and the effect of potentially modifiable risk factors on the genetic association was further explored in 9363 INTERHEART participants. The effect of rs20417 on urinary thromboxane and prostacyclin metabolite concentrations was measured in 117 healthy individuals. Carriage of the rs20417 minor allele was associated with a decreased risk of major CVD outcomes (OR = 0.78, 95% CI: 0.70-0.87; P = 1.2 × 10(-5)). The genetic effect was significantly stronger in aspirin users (OR: 0.74, 95% CI: 0.64-0.84; P = 1.20 × 10(-5)) than non-users (OR: 0.87, 95% CI: 0.72-1.06; P = 0.16) (interaction P-value: 0.0041). Among patients with previous coronary artery disease (CAD), rs20417 carriers had a stronger protective effect on risk of major adverse events when compared with individuals without previous CAD (interaction P-value: 0.015). Carriers had significantly lower urinary levels of thromboxane (P = 0.01) and prostacyclin (P = 0.01) metabolites when compared with non-carriers. The rs20417 polymorphism is associated with a reduced risk of major cardiovascular events and lower levels of thromboxane and prostacyclin. Our results suggest that a genetic decrease in COX-2 activity may be beneficial with respect to CVD risk, especially, in higher risk patients on aspirin.
    European Heart Journal 05/2014;
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    ABSTRACT: Delcasertib is a selective inhibitor of delta-protein kinase C (delta-PKC), which reduced infarct size during ischaemia/reperfusion in animal models and diminished myocardial necrosis and improved reperfusion in a pilot study during primary percutaneous coronary intervention (PCI) for ST elevation myocardial infarction (STEMI). A multicentre, double-blind trial was performed in patients presenting within 6 h and undergoing primary PCI for anterior (the primary analysis cohort, n = 1010 patients) or inferior (an exploratory cohort, capped at 166 patients) STEMI. Patients with anterior STEMI were randomized to placebo or one of three doses of delcasertib (50, 150, or 450 mg/h) by intravenous infusion initiated before PCI and continued for ∼2.5 h. There were no differences between treatment groups in the primary efficacy endpoint of infarct size measured by creatine kinase MB fraction area under the curve (AUC) (median 5156, 5043, 4419, and 5253 ng h/mL in the placebo, delcasertib 50, 150, and 450 mg/mL groups, respectively) in the anterior STEMI cohort. No treatment-related differences were seen in secondary endpoints of infarct size, electrocardiographic ST-segment recovery AUC or time to stable ST recovery, or left ventricular ejection fraction at 3 months. No differences in rates of adjudicated clinical endpoints (death, heart failure, or serious ventricular arrhythmias) were observed. Selective inhibition of delta-PKC with intravenous infusion of delcasertib during PCI for acute STEMI in a population of patients treated according to contemporary standard of care did not reduce biomarkers of myocardial injury. Identifier: NCT00785954.
    European Heart Journal 05/2014;

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