Henning Bundgaard

Statens Serum Institut, København, Capital Region, Denmark

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Publications (148)766.98 Total impact

  • International journal of cardiology 11/2015; 203. DOI:10.1016/j.ijcard.2015.11.029 · 4.04 Impact Factor
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    ABSTRACT: Aims: A common underlying mechanism with a genetic component could link pregnancy losses with vascular disease. We examined whether pregnancy losses (miscarriages and stillbirths) and atherosclerotic outcomes co-aggregated in families. Methods and results: Using Danish registers, we identified women with pregnancies in 1977-2008, and their parents (>1 million) and brothers (>435 000). We followed parents for incident ischaemic heart disease (IHD), myocardial infarction (MI), and cerebrovascular infarction (CVI), and brothers for a broader combined atherosclerotic endpoint. Using Cox regression, we estimated hazard ratios (HRs) for each outcome by history of pregnancy loss in daughters/sisters. Overall, parents whose daughters had 1, 2, and ≥3 miscarriages had 1.01 [95% confidence interval (CI) 0.99-1.04], 1.07 (95% CI 1.02-1.11), and 1.10 (95% CI 1.02-1.19) times the rate of MI, respectively, as parents whose daughters had no miscarriages. For parents with ≥3 daughters, the HRs were 1.12 (95% CI 1.02-1.24), 1.29 (95% CI 1.13-1.48), and 1.33 (95% CI 1.12-1.57). Effect magnitudes did not differ for fathers and mothers. We observed similar patterns for IHD and CVI (parents) and the atherosclerotic endpoint (brothers). Parents whose daughters had stillbirths had 1.14 (95% CI 1.05-1.24) and 1.07 (95% CI 0.96-1.18) times the rates of MI and CVI, respectively, as parents whose daughters had no stillbirths. Conclusion: Certain pregnancy losses and atherosclerotic diseases in both heart and brain may have a common aetiologic mechanism. Women in families with atherosclerotic disease may be predisposed to pregnancy loss; conversely, pregnancy losses in first-degree relatives may have implications for atherosclerotic disease risk.
    European Heart Journal 10/2015; DOI:10.1093/eurheartj/ehv549 · 15.20 Impact Factor

  • Europace 10/2015; DOI:10.1093/europace/euv285 · 3.67 Impact Factor
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    ABSTRACT: Letter to the editor. In press
    International Journal of Legal Medicine 10/2015; DOI:10.1007/s00414-015-1282-3 · 2.69 Impact Factor
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    ABSTRACT: Objective: Cardiovascular implantable electronic device (CIED) infections are increasing in numbers. The objective was to review the clinical presentation and outcome in patients affected with CIED infections with either local pocket or systemic presentation. Design: All device removals due to CIED infection during the period from 2005 to 2012 were retrospectively reviewed. CIED infections were categorized as systemic or pocket infections. Treatment included complete removal of the device, followed by antibiotic treatment of six weeks. Results: Seventy-one device removals due to infection (32 systemic and 39 pocket infections) were recorded during the study period. Median follow-up time was 26 (IQR 9-41) months, 30 day and 12 month mortality were 4% and 14%, respectively. There was no long-term difference in mortality between patients with pocket vs. systemic infection (p = 0.48). During follow-up no relapses and two cases of new infections were noted (2.8%). Conclusions: CIED infection with systemic or pocket infection was difficult to distinguish in clinical presentation and outcome. Complete device removal and antibiotic treatment of long duration was safe and without relapses.
    Scandinavian cardiovascular journal: SCJ 10/2015; DOI:10.3109/14017431.2015.1091089 · 1.03 Impact Factor
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    ABSTRACT: The empiric treatment of infective endocarditis (IE) varies widely and, in some places, a regimen of penicillin in combination with an aminoglycoside is administered. The increasing incidence of Staphylococcus aureus IE, poor tissue penetration by aminoglycosides and low frequency of penicillin-susceptible S. aureus may potentially lead to functional tobramycin monotherapy. Therefore, this study aimed to evaluate tobramycin monotherapy in an experimental S. aureus IE rat model. Catheter-induced IE at the aortic valves were established with S. aureus (NCTC 8325-4) and rats were randomised into untreated (n = 22) or tobramycin-treated (n = 13) groups. The treatment group received tobramycin once-daily. Animals were evaluated at 1 day post infection (DPI), 2 DPI or 3 DPI. Quantitative bacteriology and cytokine expression were measured for valves, myocardium and serum. A decrease of bacterial load was observed in valves and the spleens of the treated (n = 6) compared to the untreated group at 2 DPI (n = 8) (p ≤ 0.02 and p ≤ 0.01, respectively), but not at 3 DPI (n = 7). Quantitative bacteriology in the myocardium was not different between the groups. Keratinocyte-derived chemokine (KC) in the aortic valves was significantly reduced at 2 DPI in the tobramycin-treated group (p ≤ 0.03). However, the expression of interleukin (IL)-1b, IL-6 and granulocyte-colony stimulating factor (G-CSF) in the valves was not different between the two groups. In the myocardium, a significant reduction in IL-1b was observed at 2 DPI (p ≤ 0.001) but not at 3 DPI. Tobramycin as functional monotherapy only reduced bacterial load and inflammation transiently, and was insufficient in most cases of S. aureus IE.
    European Journal of Clinical Microbiology 10/2015; 34(12). DOI:10.1007/s10096-015-2488-5 · 2.67 Impact Factor
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    ABSTRACT: Objectives: Diagnostics of patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) are complex, and based on the 2010 Task Force document including different diagnostic modalities. However, recommendations for clinical management and follow-up of patients with ARVC and their relatives are sparse. This paper aims to give a practical overview of management strategies, risk stratification, and selection of appropriate therapies for patients with ARVC and their family members. Design: This paper summarizes follow-up and treatment strategies in ARVC patients in the Nordic countries. The author group represents cardiologists who are actively involved in the Nordic ARVC Registry which was established in 2009, and contains prospectively collected clinical data from more than 590 ARVC patients from Denmark, Norway, Sweden, and Finland. Results: Different approaches of management and follow-up are required in patients with definite ARVC and in genetic-mutation-positive family members. Furthermore, ARVC patients with and without implantable cardioverter defibrillators (ICDs) require different follow-up strategies. Conclusion: Careful follow-up is required in patients with ARVC diagnosis to evaluate the need of anti-arrhythmic therapy and ICD implantation. Mutation-positive family members should be followed regularly for detection of early disease and risk stratification of ventricular arrhythmias.
    Scandinavian cardiovascular journal: SCJ 09/2015; 49(6):1-9. DOI:10.3109/14017431.2015.1086017 · 1.03 Impact Factor
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    ABSTRACT: Background: In sudden, unexpected, non-traumatic death in young individuals, structural abnormalities of the heart are frequently identified at autopsy. However, the findings may be unspecific and cause of death may remain unclear. A significant proportion of these cases are most likely caused by inherited cardiac diseases, and the cases are categorized as sudden cardiac death (SCD). The purpose of this study was to explore the added diagnostic value of genetic testing by next-generation sequencing (NGS) of a broad gene panel, as a supplement to the traditional forensic investigation in cases with non-diagnostic structural abnormalities of the heart. Methods and results: We screened 72 suspected SCD cases (<50 years) using the HaloPlex Target Enrichment System (Agilent) and NGS (Illumina MiSeq) for 100 genes previously associated with inherited cardiomyopathies and channelopathies. Fifty-two cases had non-diagnostic structural cardiac abnormalities and 20 cases, diagnosed with a cardiomyopathy post-mortem (ARVC = 14, HCM = 6), served as comparators. Fifteen (29 %) of the deceased individuals with non-diagnostic findings had variants with likely functional effects based on conservation, computational prediction, allele-frequency and supportive literature. The corresponding frequency in deceased individuals with cardiomyopathies was 35 % (p = 0.8). Conclusion: The broad genetic screening revealed variants with likely functional effects at similar high rates, i.e. in 29 and 35 % of the suspected SCD cases with non-diagnostic and diagnostic cardiac abnormalities, respectively. Although the interpretation of broad NGS screening is challenging, it can support the forensic investigation and help the cardiologist's decision to offer counselling and clinical evaluation to relatives of young SCD victims.
    Deutsche Zeitschrift für die Gesamte Gerichtliche Medizin 09/2015; DOI:10.1007/s00414-015-1261-8 · 2.71 Impact Factor
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    ABSTRACT: -Recommendations for pre-symptomatic screening of relatives of cardiomyopathy patients are based on findings from tertiary centers. Cardiomyopathy inheritance patterns are fairly well understood, but how cardiomyopathy in younger persons (<50 years) aggregates in families at the population level is unclear. In a nationwide cohort, we examined the risk of cardiomyopathy by family history of premature death (<60 years) from cardiomyopathy. -By linking Danish national register data, we constructed a cohort of 3.9 million persons born from 1950 to 2008. We ascertained family history of premature (<60yrs) death from cardiomyopathy or other conditions, and cohort members were followed from 1977 to 2008 for cardiomyopathy diagnosed at <50 years. We identified 3,890 cardiomyopathies in 89 million person-years of follow-up. Using Poisson regression, we estimated incidence rate ratios for cardiomyopathy by family history of premature death. Premature cardiomyopathy deaths in first- and second-degree relatives were associated with 29- and 6-fold increases in the rate of cardiomyopathy, respectively. If the first-degree relative died aged <35yrs, the rate of cardiomyopathy increased 100-fold; given ≥2 premature deaths in first-degree relatives, the rate increased more than 400-fold. In contrast, a family history of premature death from other cardiac or non-cardiac conditions increased the rate of cardiomyopathy 3-fold at most. -A family history of premature cardiomyopathy death was associated with an increase in risk of cardiomyopathy ranging from 6- to 400-fold, depending on age, kinship, gender and number of affected family members. Our general population-based results support recommendations for pre-symptomatic screening of relatives of cardiomyopathy patients.
    Circulation 08/2015; 132(11). DOI:10.1161/CIRCULATIONAHA.114.013478 · 14.43 Impact Factor
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    ABSTRACT: A rare genetic variant in the desmosomal gene plakophilin-2 (PKP2) c.419C>T(p.(S140F)) has repeatedly been identified in patients with dilated cardiomyopathy (DCM) and arrhythmogenic right ventricular cardiomyopathy (ARVC). Whether this is a disease-causing variant remains highly controversial. We tested this hypothesis using three approaches. Initially, in a prospective study of 10 407 individuals from the general population, including 2688 who developed heart failure or arrhythmias during >14 years of follow-up, PKP2 c.419C>T was identified in 98 individuals (0.94%). PKP2 genotype was not associated with electrocardiographic or echocardiographic changes, or with plasma levels of probrain natriuretic peptide (all P≥0.05). In c.419C>T carriers versus non-carriers, multifactorially adjusted hazard ratios were 1.26 (95% confidence interval: 0.77–2.07) for heart failure, 1.40 (0.90–2.17) for arrhythmias, 1.15 (0.78–1.71) for end points combined, and 1.33 (0.98–1.80) for all-cause mortality. The cumulative survival as a function of age and PKP2 genotype was similar among carriers and non-carriers (P=0.14). Second, comparing 517 patients referred for genetic testing with 1918 matched controls, odds ratios as a function of c.419C>T genotype were 2.11 (0.50–8.99) for ARVC, 0.72 (0.16–3.28) for hypertrophic cardiomyopathy (HCM)/DCM, and 1.28 (0.46–3.54) for end points combined. Third, in in vitro studies cellular localization of plakophilin-2, plakoglobin, connexin-43, or N-cadherin were similar in cells transfected with wild-type or mutant plakophilin-2. In conclusion, combining epidemiological data, with data on patients referred for genetic testing for ARVC or HCM/DCM, and data from in vitro studies, PKP2 c.419C>T did not associate with heart failure, arrhythmias, or premature death, with ARVC or HCM/DCM, or with effects in vitro, suggesting that this is not a disease-causing variant.
    European journal of human genetics: EJHG 08/2015; DOI:10.1038/ejhg.2015.171 · 4.35 Impact Factor
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    ABSTRACT: Identification of the first echocardiographic manifestations of hypertrophic cardiomyopathy may be important for clinical management and our understanding of the pathogenesis. We studied the development of pre-diagnostic echocardiographic changes in young relatives to HCM patients during long-term years follow-up. HCM-relatives not fulfilling the diagnostic criteria for HCM and age of <18 years were included in this study. We performed echocardiographic evaluations at inclusion and after 12 ± 1 years follow-up. Based on family screening of 11 sarcomere genes, CRYAB, α-GAL, and titin, we evaluated: (1) non-carriers (known family mutation ruled out-controls), (2) carriers (phenotype negative gene mutation carriers) and (3) phenotype negative relatives with unknown genetic status (relatives from families without identified mutations). At inclusion (age 11 ± 5 years), there were no differences in echocardiographic chamber dimensions, systolic or diastolic function between the three groups. During follow-up (age 23 ± 5 years), carriers (n = 8) developed lower left ventricular end-diastolic dimension (LVEDd) compared to non-carriers (n = 23) (41 ± 4 vs. 46 ± 4 mm; p = 0.04) and a higher ratio of early left ventricular filling velocity and early diastolic velocity of lateral mitral annulus (E/e' 6 ± 1 vs. 5 ± 1; p = 0.003). No significant differences in LVEDd or E/e' were found between relatives with unknown genetic status (n = 24) and non-carriers though Z-scores for these parameters were >2 in a subset of relatives with unknown genetic status. Children carrying pathogenic sarcomere gene mutations develop reduced LVEDd and increased E/e' as first pre-diagnostic echocardiographic manifestations during follow-up into adulthood.
    The international journal of cardiovascular imaging 08/2015; 31(8). DOI:10.1007/s10554-015-0723-x · 1.81 Impact Factor

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    ABSTRACT: Background Family history of myocardial infarction (MI) is an independent risk factor for MI. Several genetic variants are associated with increased risk of MI and family history of MI in a first-degree relative doubles MI risk. However, although family history of MI is not a simple dichotomous risk factor, the impact of specific, detailed family histories has not received much attention, despite its high clinical relevance. We examined risk of MI by MIs in first- and second-degree relatives and by number and age of affected relatives. Methods and Findings Using Danish national registers, we established a nationwide cohort of persons born between 1930 and 1992 with identifiable first- or second-degree relatives. Incident MIs in both cohort members and relatives aged ≥20 years were identified. We calculated incidence rate ratios (IRRs) for MI by family history of MI, by Poisson regression. In 4.4 million persons followed for 104 million person-years, we identified 128,384 incident MIs. IRRs with 95% confidence intervals [CIs] for MI by history of MI in 1, 2 or ≥3 first-degree relatives were 1.46 (1.42-1.49), 2.38 (2.22-2.56) and 3.58 (2.66-4.81), respectively. Corresponding estimates for second-degree relatives were 1.17 (1.05-1.30), 1.87 (1.46-2.38) and 2.18 (1.09-4.36). A history of MI in combinations of first- and second-degree relatives increased risks 1.8- to 7-fold in middle-aged persons (36 to 55 years). Estimates were robust to adjustment for diabetes, hypertension, dyslipidemia and use of cardiovascular medications. Conclusion A detailed family history, particularly number of affected first- and second-degree relatives, contributes meaningfully to risk assessment, especially in middle-aged persons. Future studies should test for potential improvement of risk algorithm prediction using detailed family histories.
    PLoS ONE 05/2015; 10(5). DOI:10.1371/journal.pone.0125896 · 3.23 Impact Factor
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    ABSTRACT: Hypertrophic cardiomyopathy (HCM) is a genetic cardiac disease primarily caused by mutations in genes coding for sarcomeric proteins. A molecular-genetic etiology can be established in ~60% of cases. Evolutionarily conserved mitochondrial DNA (mtDNA) haplogroups are susceptibility factors for HCM. Several polymorphic mtDNA variants are associated with a variety of late-onset degenerative diseases and affect mitochondrial function. We examined the role of private, non-haplogroup associated, mitochondrial variants in the etiology of HCM. In 87 Danish HCM patients, full mtDNA sequencing revealed 446 variants. After elimination of 312 (69.9%) non-coding and synonymous variants, a further 109 (24.4%) with a global prevalence > 0.1%, three (0.7%) haplogroup associated and 19 (2.0%) variants with a low predicted in silico likelihood of pathogenicity, three variants: MT-TC: m.5772G>A, MT-TF: m.644A>G, and MT-CYB: m.15024G>A, p.C93Y remained. A detailed analysis of these variants indicated that none of them are likely to cause HCM. In conclusion, private mtDNA mutations are frequent, but they are rarely, if ever, associated with HCM.
    PLoS ONE 04/2015; 10(4):e0124540. DOI:10.1371/journal.pone.0124540 · 3.23 Impact Factor
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    ABSTRACT: Transcatheter aortic valve implantation (TAVI) is an advancing mode of treatment for inoperable or high-risk patients with aortic stenosis. Prosthetic valve endocarditis (PVE) after TAVI is a serious complication, but only limited data exist on its incidence, outcome, and procedural risk factors. Observational single-center study of 509 consecutive patients treated with a transcatheter implanted self-expandable aortic valve prosthesis (Medtronic CoreValve). We identified 18 patients diagnosed with TAVI-PVE during a median follow-up period of 1.4 years (interquartile range, 0.5-2.5 years; longest follow-up was 6.3 years). TAVI-PVE was most frequent in the first year after implantation (first-year incidence, 3.1% [confidence interval, 1.4%-4.8%]); the overall annualized rate was 2.1% per patient-year (confidence interval, 1.2%-3.3%). Seventeen patients (94%) were treated conservatively and 1 with surgery. Four patients (22%) died from endocarditis or complications to treatment, 2 of those (11%) during initial hospitalization for PVE. An increased risk of TAVI-PVE was seen in patients with low implanted valve position (hazard ratio, 2.8 [1.1-7.2]), moderate or worse postprocedural paravalvular regurgitation (hazard ratio, 4.0 [1.5-11]), implantation of >1 prosthesis (hazard ratio, 5.2 [1.5-18]), and any vascular complication (hazard ratio, 3.8 [1.5-9.8]). TAVI-PVE occurred at a slightly higher rate than reported for surgically implanted valves. Conservative treatment was associated with an acceptable outcome. Suboptimal valve deployment and vascular complications were associated with an increased risk of TAVI-PVE. © 2015 American Heart Association, Inc.
    Circulation Cardiovascular Interventions 04/2015; 8(4). DOI:10.1161/CIRCINTERVENTIONS.114.001939 · 6.22 Impact Factor

  • Journal of the American College of Cardiology 03/2015; 65(10):A857. DOI:10.1016/S0735-1097(15)60857-9 · 16.50 Impact Factor

  • Journal of the American College of Cardiology 03/2015; 65(10):A978. DOI:10.1016/S0735-1097(15)60978-0 · 16.50 Impact Factor

  • ACC 2015; 03/2015
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    ABSTRACT: To assess the degree and progression of cardiac involvement in patients with limb-girdle type 2 (LGMD2) and Becker muscular dystrophies (BMD). A follow-up study of 100 LGMD2 (types A-L) and 30 BMD patients assessed by electrocardiogram (ECG) and echocardiography, supplemented by Holter-monitoring at follow-up. After a median of 8.9years (range 0.4-13.7), twelve patients had died: LGMD2 (n=10, mean age 61±11years), BMD (n=2, age 43 and 45years). Of the remaining 118 patients, 89 completed follow-up: LGMD2 (n=64, age 48±13years) and BMD (n=25, age 40±13years). In BMD, LVEF decreased from 60% (10-62) to 50% (10-64), p=0.02 corresponding to a one percentage drop annually. Among patients with LGMD2, LVEF decreased significantly in patients with LGMD type 2I (n=28) from 59% (15-72) to 55% (20-61), p=0.03, i.e. a 0.4 percentage drop annually, and LVEF≤50% was associated with increased mortality in this subgroup. In LGMD2E, 3/5 patients (60%) at baseline and 4/5 (80%) at follow-up had LVEF≤50%. ECG abnormalities were non-progressive in BMD and in all subgroups of LGMD2. SVT and NSVT were present in both groups: BMD (3/14 (21%) and (2/14 (14%)), LGMD2 (16/51 (31%) and 8/51 (16%)), respectively, all asymptomatic. LVEF decreased significantly in patients with BMD and LGMD2I, and the majority of patients with LGMD2E had left ventricular systolic dysfunction. This study emphasizes the need for tailored regular cardiac assessments according to molecular diagnosis with special focus on BMD and LGMD types 2I and 2E. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    International Journal of Cardiology 12/2014; 182C:403-411. DOI:10.1016/j.ijcard.2014.12.090 · 4.04 Impact Factor
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    ABSTRACT: No medical treatment has been reliably shown to halt or reverse disease progression in hypertrophic cardiomyopathy, but the results of several pilot studies have suggested beneficial effects of angiotensin II receptor blockers on left ventricular hypertrophy and fibrosis, which are predictive of an adverse outcome. We aimed to assess the effect of the angiotensin II receptor blocker losartan on left ventricular hypertrophy and fibrosis in patients with hypertrophic cardiomyopathy. In this single-centre, randomised, double-blind, placebo-controlled trial, adult patients (aged 18 years and older) with obstructive or non-obstructive hypertrophic cardiomyopathy were randomly assigned via computer-based system to losartan (100 mg per day) or placebo for 12 months. Patients and investigators were masked to assigned treatment. The primary endpoint was change in left ventricular mass as assessed by cardiac magnetic resonance imaging (CMR) or CT. Efficacy analyses were done in the modified intention-to-treat population (all patients with data available at the 12-month follow-up). The trial is registered with ClinicalTrials.gov, number NCT01447654. Between Dec 1, 2011, and May 1, 2013, 318 patients were screened. 133 patients (mean age 52 years [SD 13], 35% women) consented and were randomly assigned to placebo (n=69) or losartan (n=64). 124 (93%) patients completed the study and were included in the modified intention-to-treat analysis for the primary endpoint. After 12 months we noted no significant difference in the change in left ventricular mass between the placebo group and the losartan group (mean difference 1 g/m(2), 95% CI -3 to 6; p=0·60). A decrease in systolic blood pressure in the losartan group (from mean 127 mm Hg [SD 12] to 121 mm Hg [14]; p=0·0001) confirmed drug compliance; blood pressure did not decrease in the placebo group. Two (2%) patients, both in the placebo group, died from sudden cardiac death during follow-up. In the losartan group, one (1%) patient had angioedema, one (1%) had deterioration of renal function, and one (1%) had hyperkalaemia. Treatment was well tolerated by patients with left ventricular outflow obstruction at baseline. Our findings challenge the generally held view that angiotensin II receptor blockers reduce cardiac hypertrophy. Treatment with losartan was safe, suggesting that it can be used for other indications in patients with hypertrophic cardiomyopathy, irrespective of obstructive physiology. Additional studies are needed to assess the effect of angiotensin II receptor blockers in preclinical hypertrophic cardiomyopathy-eg, in genotype-positive but phenotype-negative individuals. Capital Region of Denmark, Rigshospitalet Research Fund, Danish Heart Association, Heart Centre Research Foundation, P A Messerschmidt and Wife Foundation, Westerberg Foundation, Beckett Foundation, Soren Segel and Wife Johanne Segel Research Foundation, and A P Møller and Chastine Mc-Kinney Møller Foundation. Copyright © 2014 Elsevier Ltd. All rights reserved.
    The Lancet Diabetes & Endocrinology 12/2014; 3(2). DOI:10.1016/S2213-8587(14)70241-4 · 9.19 Impact Factor

Publication Stats

2k Citations
766.98 Total Impact Points


  • 2011-2015
    • Statens Serum Institut
      • • Department of Epidemiology Research
      • • Department of Clinical Biochemistry and Immunology
      København, Capital Region, Denmark
  • 2000-2015
    • Children's Heart Center
      Las Vegas, Nevada, United States
  • 1997-2014
    • Copenhagen University Hospital
      København, Capital Region, Denmark
  • 1995-2014
    • IT University of Copenhagen
      København, Capital Region, Denmark
  • 2013
    • University of Copenhagen Herlev Hospital
      Herlev, Capital Region, Denmark
  • 2012-2013
    • Rigshospitalet
      • Department of Cardiology
      København, Capital Region, Denmark
  • 2000-2013
    • National University (California)
      San Diego, California, United States
  • 2007
    • University of Sydney
      Sydney, New South Wales, Australia
  • 2005
    • Royal North Shore Hospital
      Sydney, New South Wales, Australia
  • 2001
    • Slovak Academy of Sciences
      Presburg, Bratislavský, Slovakia