Marc W Merx

Universitätsklinikum Düsseldorf, Düsseldorf, North Rhine-Westphalia, Germany

Are you Marc W Merx?

Claim your profile

Publications (81)457.63 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims: Introduction of a novel contrast injection protocol during rotational C-arm CT (RCT) in cardiac catheterisation of patients with aortic stenosis for aortic root assessment. Methods and results: Fifty-two patients underwent RCT imaging with contrast injection performed either into the aorta (Ao-RCT, n=25) or into the left ventricle (LV-RCT, n=27). Aortic annulus diameters were assessed in a multiplanar reconstruction view and compared with corresponding multidetector computed tomography (MDCT). LV contrast injection additionally enabled measurement of the left ventricular outflow tract (LVOT). LV-RCT improved the accuracy of annulus measurements and correlated well with MDCT data in comparison with Ao-RCT and MDCT (r=0.9 r=0.76, respectively). The Bland-Altman analysis showed smaller differences in MDCT and LV-RCT annulus measurements than between MDCT and Ao-RCT (LV-RCT: mean=0.4 mm, limits of agreement -1.5-2.3 mm vs. Ao-RCT: mean=0.1 mm, limits of agreement -3.4-3.6 mm). The inter-observer agreement for the annulus measurements was significantly increased for LV-RCT as calculated by the intra-class coefficient (ICC=0.85) in comparison with Ao-RCT (ICC=0.52). Conclusions: Cardiac catheterisation including LV-RCT offers complementary assessment of left ventricular function, aortic valve anatomy, coronary angiography and arterial access routes. LV-RCT for aortic root measurements shows better correlation to MDCT than standard Ao-RCT protocols.
    EuroIntervention: journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology 04/2014; · 3.17 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Nitric oxide (NO) derived from endothelial NO synthase (NOS3) plays a central role in myocardial ischemia/reperfusion (I/R)-injury. Subsets of circulating blood cells, including red blood cells (RBCs), carry a NOS3 and contribute to blood pressure regulation and RBC nitrite/nitrate formation. We hypothesized that the circulating blood born NOS3 also modulates the severity of myocardial infarction in disease models. We cross-transplanted bone marrow in wild-type and NOS3(-/-) mice with wild-type mice, producing chimeras expressing NOS3 only in vascular endothelium (BC-/EC+) or in both blood cells and vascular endothelium (BC+/EC+). After 60-min closed-chest coronary occlusion followed by 24 h reperfusion, cardiac function, infarct size (IS), NOx levels, RBCs NO formation, RBC deformability, and vascular reactivity were assessed. At baseline, BC-/EC+ chimera had lower nitrite levels in blood plasma (BC-/EC+: 2.13 ± 0.27 μM vs. BC+/EC+ 3.17 ± 0.29 μM; *p < 0.05), reduced DAF FM associated fluorescence within RBCs (BC-/EC+: 538.4 ± 12.8 mean fluorescence intensity (MFI) vs. BC+/EC+: 619.6 ± 6.9 MFI; ***p < 0.001) and impaired erythrocyte deformability (BC-/EC+: 0.33 ± 0.01 elongation index (EI) vs. BC+/EC+: 0.36 ± 0.06 EI; *p < 0.05), while vascular reactivity remained unaffected. Area at risk did not differ, but infarct size was higher in BC-/EC+ (BC-/EC+: 26 ± 3 %; BC+/EC+: 14 ± 2 %; **p < 0.01), resulting in decreased ejection fraction (BC-/EC+ 46 ± 2 % vs. BC+/EC+: 52 ± 2 %; *p < 0.05) and increased end-systolic volume. Application of the NOS inhibitor S-ethylisothiourea hydrobromide was associated with larger infarct size in BC+/EC+, whereas infarct size in BC-/EC+ mice remained unaffected. Reduced infarct size, preserved cardiac function, NO levels in RBC and RBC deformability suggest a modulating role of circulating NOS3 in an acute model of myocardial I/R in chimeric mice.
    Archiv für Kreislaufforschung 01/2014; 109(1):398. · 7.35 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The aim of our study was to develop a reproducible murine model of elastase-induced aneurysm formation combined with aortic transplantation.
    PLoS ONE 01/2014; 9(7):e102648. · 3.53 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Dietary interventions with flavan-3-ols have shown beneficial effects on vascular function. The translation of these findings into the context of the health of the general public requires detailed information on habitual dietary intake. However, only limited data are currently available for European populations. Therefore, in the present study, we assessed the habitual intake of flavan-3-ol monomers, proanthocyanidins (PA) and theaflavins in the European Union (EU) and determined their main food sources using the EFSA (European Food Safety Authority) Comprehensive European Food Consumption Database. Data for adults aged 18-64 years were available from fourteen European countries, and intake was determined using the FLAVIOLA Flavanol Food Composition Database, developed for the present study and based on the latest US Department of Agriculture and Phenol-Explorer databases. The mean habitual intake of flavan-3-ol monomers, theaflavins and PA ranged from 181 mg/d (Czech Republic) to 793 mg/d (Ireland). The highest intakes of flavan-3-ol monomers and theaflavins were observed in Ireland (191/505 mg/d) and the lowest intakes in Spain (24/9 mg/d). In contrast, the daily intake of PA was highest in Spain (175 mg/d) and lowest in The Netherlands (96 mg/d). Main sources were tea (62 %), pome fruits (11 %), berries (3 %) and cocoa products (3 %). Tea was the major single contributor to monomer intake (75 %), followed by pome fruits (6 %). Pome fruits were also the main source of PA (28 %). The present study provides important data on the population-based intake of flavanols in the EU and demonstrates that dietary intake amounts for flavan-3-ol monomers, PA and theaflavins vary significantly across European countries. The average habitual intake of flavan-3-ols is considerably below the amounts used in most dietary intervention studies.
    The British journal of nutrition 12/2013; · 3.45 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Pulmonary vein isolation (PVI) as a cornerstone for catheter ablation of atrial fibrillation (AF) remains a complex and time consuming procedure. The purpose of this study was to assess feasibility, safety and acute efficacy of a novel irrigated multielectrode ablation catheter guided by an electroanatomical mapping system for PVI in patients with paroxysmal AF. 25 consecutive patients (60 ± 10 years) with paroxysmal AF underwent PVI by using a novel decapolar mapping and ablation catheter (NMARQ). Ablation was guided by electroanatomical mapping allowing radiofrequency (RF) energy delivery in the antral region of pulmonary veins (PV) from 10 irrigated electrodes simultaneously. The day after ablation, cardiac magnetic resonance imaging (MRI) was performed routinely in order to assess for potential acute PV-stenosis. Overall, 97 of 97 targeted PV (100 %) could be isolated with a mean of 27 ± 11 RF applications and a mean total burning time of 15 ± 6 minutes per patient. The total procedure time from femoral vein access to catheter withdrawal was 110 ± 31 minutes including a mean total fluoroscopy time of 23 ± 9 minutes. On average, 6 ± 3 RF impulses with a maximum of 25 Watt were applied per vein. After a short learning curve procedure, fluoroscopy and total burning time decreased to 94 ± 16 minutes, 16 ± 3 minutes and 9 ± 2 minutes respectively (p<0.05). Entrance and exit block could be verified by placing the ablation catheter into 90 of 97 (93%) PVs in 18 of 25 (72%) patients. No procedure-related complications were observed, especially no acute PV stenosis could be detected. Use of a novel irrigated multielectrode ablation system for PVI is feasible and safe, resulting in acute isolation of all targeted PVs with no complications and short procedure times. Sustainability of these initial results has to be confirmed in long term efficacy and follow up trials.
    Heart rhythm: the official journal of the Heart Rhythm Society 12/2013; · 4.56 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Endothelial nitric oxide synthase (NOS)3-derived nitric oxide (NO) modulates inotropic response and diastolic interval for optimal cardiac performance under non-inflammatory conditions. In sepsis, excessive NO production plays a key role in severe hypotension and myocardial dysfunction. We aimed to determine the role of NOS3 on myocardial performance, NO production, and time course of sepsis development. NOS3(-/-) and C57BL/6 wildtype mice were rendered septic by cecum ligation and puncture (CLP). Cardiac function was analyzed by serial echocardiography, in vivo pressure and isolated heart measurements. Cardiac output (CO) increased to 160 % of baseline at 10 h after sepsis induction followed by a decline to 63 % of baseline after 18 h in wildtype mice. CO was unaltered in septic NOS3(-/-) mice. Despite the hyperdynamic state, cardiac function and mean arterial pressure were impaired in septic wildtype as early as 6 h post CLP. At 12 h, cardiac function in septic wildtype was refractory to catecholamines in vivo and respective isolated hearts showed impaired pressure development and limited coronary flow reserve. Hemodynamics remained stable in NOS3(-/-) mice leading to significant survival benefit. Unselective NOS inhibition in septic NOS3(-/-) mice diminished this survival benefit. Plasma NO( x )- and local myocardial NO( x )- and NO levels (via NO spin trapping) demonstrated enhanced NO( x )- and bioactive NO levels in septic wildtype as compared to NOS3(-/-) mice. Significant contribution by inducible NOS (NOS2) during this early phase of sepsis was excluded. Our data suggest that NOS3 relevantly contributes to bioactive NO pool in developing sepsis resulting in impaired cardiac contractility.
    Archiv für Kreislaufforschung 03/2013; 108(2):330. · 7.35 Impact Factor
  • Source
    Journal of Cardiovascular Magnetic Resonance 01/2013; 15(1). · 4.44 Impact Factor
  • Source
    Journal of Cardiovascular Magnetic Resonance 01/2013; 15(1). · 4.44 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Introduction Murine arterial graft models are being used to uncover the inflammatory reactions of the vessel wall after surgery and the herein involved mediators. The aim of this study was to establish a model of transplantation-induced atherosclerosis after aortic transplantation. Methods Mice on a C57BL/6-background (n = 14) underwent infrarenal, orthotopic aortic transplantation. A group of sham animals (n = 10) served as controls. These groups of mice were kept on normal chow. In addition, apolipoprotein E-deficient (ApoE-/-) mice were employed (n = 5) that were fed a high fat diet immediately after surgery for 4 weeks. Results Ultrasound analyses and immunohistochemical analyses of the transplanted aorta revealed no major changes in morphology and function of C57BL/6 mice. In contrast, ApoE-/- mice developed marked intimal hyperplasia, with signs of monocyte/macrophage and smooth muscle cell infiltrations. Conclusion While C57BL/6 mice showed no significant changes in the aorta after transplantation, ApoE-/- mice on a high fat diet displayed signs of transplant atherosclerosis. Hence, this model provides an experimental basis for studying the pathogenesis of chronic atherosclerotic vessel wall remodeling after transplantation. This may also be useful for elucidating new therapeutic targets for the treatment of this disease.
    Gefässchirurgie 12/2012; · 0.24 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Transcatheter aortic valve implantation (TAVI) using the Medtronic CoreValve (MCV) system might represent an alternative to conventional redo surgery in older high-risk patients with a failing aortic valve bioprosthesis. Symptomatic patients with failing aortic valve bioprosthesis, aged ≥65 years with a logistic EuroSCORE ≥10 % were considered for treatment. Local anesthesia was used to retrogradely implant the MCV system into the failing bioprosthetic valve. Clinical events were recorded and a transthoracic echocardiography was performed to evaluate the impact of MCV on hemodynamics after transcatheter aortic valve implantation. A total of 27 patients (aged 74.8±8 years, logistic EuroSCORE of 31±17%) were treated. In those with AS and AS and AR (n=25), the mean gradient declined from 42±16 mm Hg before to 18±8 mm Hg after MCV implantation (P<0.001), in those with AR the level declined by 2. There was no intraprocedural death and no procedural myocardial infarction. On the basis of the definitions of the Valvular Academic Research Consortium, the rate of major stroke was 7.4 %, of life-threatening bleeding 7.4%, of kidney failure stage III 7.4%, and of major access site complication 11.1 %, respectively. Within 30 days after the procedure, 2 patients died; 1 from stroke and 1 from cardiac failure (30-day mortality: 7.4%). THESE RESULTS SUGGEST THAT TRANSFEMORAL MCV IMPLANTATION INTO A WIDE RANGE OF DEGENERATED AORTIC BIOPROSTHETIC VALVES: IRRESPECTIVE OF THE FAILURE MODE: is feasible, safe, and improves hemodynamics in older patients with higher risk for conventional aortic valve redo surgery.
    Circulation Cardiovascular Interventions 10/2012; 5(5):689-97. · 6.54 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: To characterize the time course of tumor necrosis factor-α (TNF-α) serum levels along with myocardial perfusion and contractile function in patients with ST-segment elevation myocardial infarction (STEMI) and successful primary percutaneous coronary intervention (PCI). Serum levels of TNF-α, interleukin 6 (IL-6), and C-reactive protein (CRP) were measured in 42 patients with STEMI before, one and 6 days after successful PCI. Myocardial perfusion was assessed by contrast-enhanced echocardiography (ceEcho), contractile function by unenhanced two-dimensional (2DE) and real-time three-dimensional echocardiography. In a subset of 18 patients, infarct size was quantified by late gadolinium enhancement cardiovascular magnetic resonance imaging (LGE-CMR) on day six. TNF-α serum levels were in the upper normal range within the first 12 h from symptom onset and increased continuously until day six, while IL-6 and CRP increased subsequently with a peak on day one after STEMI. Serum TNF-α on day one after PCI correlated with perfusion defects, wall motion abnormalities, and infarct size (ceEcho: r = 0.52, p = 0.005; 2DE: r = 0.56, p = 0.002; LGE-CMR: r = 0.83-0.86; p < 0.0001). Using multiple regression linear analysis, infarct size on day six was predicted by serum TNF-α 1 day after PCI (p = 0.006, adjusted R (2) 0.638). Our data reflect the clinical significance of early TNF-α elevation in patients with STEMI and primary PCI (Controlled Clinical Trials number, NCT00529607).
    Clinical Research in Cardiology 05/2012; 101(10):815-27. · 3.67 Impact Factor
  • Source
    Journal of Cardiovascular Magnetic Resonance 02/2012; 14 Suppl 1:P97. · 4.44 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Here we assess the intrinsic functions of the chemokine receptor CXCR4 in remodeling after myocardial infarction (MI) using Cxcr4 heterozygous (Cxcr4(+/-)) mice. Myocardial necrosis triggers complex remodeling and inflammatory changes. The chemokine CXCL12 has been implicated in protection and therapeutic regeneration after MI through recruiting angiogenic outgrowth cells, improving neovascularization and cardiac function, but the endogenous role of its receptor CXCR4 is unknown. MI was induced by ligation of the left descending artery. Langendoff perfusion, echocardiography, quantitative immunohistochemistry, flow cytometry, angiogenesis assays, and cardiomyocyte analysis were performed. After 4 weeks, infarct size was reduced in Cxcr4(+/-) mice compared with wild-type mice and in respective bone marrow chimeras compared with controls. This was associated with altered inflammatory cell recruitment, decreased neutrophil content, delayed monocyte infiltration, and a predominance of Gr1(low) over classic Gr1(high) monocytes. Basal coronary flow and its recovery after MI were impaired in Cxcr4(+/-)mice, paralleled by reduced angiogenesis, myocardial vessel density, and endothelial cell count. Notably, no differences in cardiac function were seen in Cxcr4(+/-)mice compared with wild-type mice. Despite defective angiogenesis, Cxcr4(+/-) mouse hearts showed no difference in CXCL12, vascular endothelial growth factor or apoptosis-related gene expression. Electron microscopy revealed lipofuscin-like lipid accumulation in Cxcr4(+/-) mouse hearts and analysis of lipid extracts detected high levels of phosphatidylserine, which protect cardiomyocytes from hypoxic stress in vitro. CXCR4 plays a crucial role in endogenous remodeling processes after MI, contributing to inflammatory/progenitor cell recruitment and neovascularization, whereas its deficiency limits infarct size and causes adaptation to hypoxic stress. This should be carefully scrutinized when devising therapeutic strategies involving the CXCL12/CXCR4 axis.
    Journal of the American College of Cardiology 11/2011; 58(23):2415-23. · 14.09 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cell-based therapy is considered a novel and potentially new strategy in regenerative medicine. But the efficacy of cell-based therapy has been limited by the poor survival of the transplanted cells in an ischaemic environment. The goal of the present study is to present a possibility to increase survival of the transplanted cardiomyocytes, by increasing the vascularization of the infarcted area. First, we injected endothelial progenitor cells (EPCs) to augment the vascular density in infarcted areas and to improve the benefit of a subsequent Tx of foetal cardiomyocytes. Serial echocardiography indeed showed significant improvement of the left ventricular function after application of EPC and a significant additive improvement after Tx of foetal cardiomyocytes. In contrast, repetitive EPC transplantation as a control group did not show an additional improvement after the second transplantation. Histologically, cells could be readily detected after Tx by BrdU-staining for EPC and by carboxy-fluorescein diacetate succinimidyl ester (CFSE)-staining for foetal cardiomyocytes. Staining for CD31 revealed a significant increase in vessel density in the infarction area compared with medium controls, possibly contributing to the benefit of transplanted foetal cardiomyocytes. Notably, a significant increase in the number of apoptotic cells was observed in cell-transplanted hearts accompanied by an increase in proliferation, collagen content and neutrophil infiltration, suggesting an active remodelling concomitant with sustained inflammatory processes. In conclusion, repetitive Tx of different cell types after myocardial infarction in rat hearts significantly improved left ventricular function and could represent a feasible option to enhance the benefit of cell therapy.
    Journal of Cellular and Molecular Medicine 11/2011; 16(7):1640-7. · 4.75 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Desmosomes are cell-cell adhesion sites and part of the intercalated discs, which couple adjacent cardiomyocytes. The connection is formed by the extracellular domains of desmosomal cadherins that are also linked to the cytoskeleton on the cytoplasmic side. To examine the contribution of the desmosomal cadherin desmoglein 2 to cardiomyocyte adhesion and cardiac function, mutant mice were prepared lacking a part of the extracellular adhesive domain of desmoglein 2. Most live born mutant mice presented normal overall cardiac morphology at 2 weeks. Some animals, however, displayed extensive fibrotic lesions. Later on, mutants developed ventricular dilation leading to cardiac insufficiency and eventually premature death. Upon histological examination, cardiomyocyte death by calcifying necrosis and replacement by fibrous tissue were observed. Fibrotic lesions were highly proliferative in 2-week-old mutants, whereas the fibrotic lesions of older mutants showed little proliferation indicating the completion of local muscle replacement by scar tissue. Disease progression correlated with increased mRNA expression of c-myc, ANF, BNF, CTGF and GDF15, which are markers for cardiac stress, remodeling and heart failure. Taken together, the desmoglein 2-mutant mice display features of dilative cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy, an inherited human heart disease with pronounced fibrosis and ventricular arrhythmias that has been linked to mutations in desmosomal proteins including desmoglein 2.
    Archiv für Kreislaufforschung 04/2011; 106(4):617-33. · 7.35 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: As yet, murine aortic grafts have merely been monitored histopathologically. The aim of our study was to examine how these grafts can be monitored in vivo and non-invasively by using high-resolution ultrasound microimaging to evaluate function and morphology. A further aim was to prove if this in vivo monitoring can be correlated to immunohistological data that indicates graft integrity. Murine infrarenal aortic isografts were orthotopically transplanted into 14 female mice (C57BL/6-Background) whereas a group of sham-operated animals (n = 10) served as controls. To assess the graft morphology and hemodynamics, we examined the mice over a post-operative period of 8 weeks with a sophisticated ultrasound system (Vevo 770, Visual Sonics). The non-invasive graft monitoring was feasible in all transplanted mice. We could demonstrate a regular post-transplant graft function and morphology, such as anterior/posterior wall displacement and wall thickness. Mild alterations of anterior wall motion dynamics could only be observed at the site of distal graft anastomosis (8 weeks after grafting (transplant vs. sham mice: 0.02 mm ± 0.01 vs. 0.03 mm ± 0.01, p<0.05). However, the integrity of the entire graft wall could be confirmed by histopathological evaluation of the grafts. With regard to graft patency, function and morphology, high resolution ultrasound microimaging has proven to be a valuable tool for longitudinal, non-invasive, in vivo graft monitoring in this murine aortic transplantation model. Consequently, this experimental animal model provides an excellent basis for molecular and pharmacological studies using genetically engineered mice.
    European journal of radiology 02/2011; 81(2):244-9. · 2.65 Impact Factor
  • Source
    01/2011;
  • 12/2010: pages 92-105; , ISBN: 9783899677225
  • [Show abstract] [Hide abstract]
    ABSTRACT: Peripheral chemoreceptors residing predominantly in the carotid body monitor changes in arterial blood oxygen and are mechanistically linked to the cardiorespiratory control by the autonomic nervous system. Enhanced sympathetic activation is common in end-stage renal disease and kidney transplantation has been shown to improve cardiorespiratory reflex measures of autonomic function. The aim of the present study was to test whether improvement in renal function following kidney transplantation is related to an improvement in chemosensory function. We compared hyperoxic chemoreflex sensitivity (CHRS) in patients after renal transplantation (RTX) to that in patients on maintenance hemodialysis (HD), and that of age- and gender-matched healthy controls. In addition, we investigated the impact of common confounding factors including pharmacological neurohumoral modulation and diabetes mellitus. The difference in the R-R intervals divided by the difference in the oxygen pressures before and after deactivation of the chemoreceptors by 5-min inhalation of 7 L oxygen was calculated as the hyperoxic CHRS. Autonomic activity was characterized by 24-h time-domain heart rate variability (HRV) parameters. CHRS was improved in RTX patients as compared to HD patients being related to HRV. CHRS was related to the concomitant presence of diabetes and medication with cyclosporine. Our findings indicate that chemosensory activity following kidney transplantation is related to cardiac autonomic control, but functional testing might only be useful to characterize the time course and extent of sympathetic activation in selected patients due to existing co-morbidities and immunosuppressive medication in this population.
    European journal of medical research 11/2010; 15 Suppl 2:83-7. · 1.10 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cardiovascular mortality is markedly increased in chronic kidney disease (CKD) and may be explained in part by sympathetic hyperactivity. Impaired hyperoxic chemoreflex sensitivity (CHRS) has been attributed to an increased sympathetic tone. The aim of the present study was to examine whether chemosensor function is altered in patients with CKD. We assessed CHRS in 20 patients with stage 3 CKD [glomerular filtration rate (GFR) 30-59 ml/min/1.73 m(2)], in 15 patients with stage 4 CKD [GFR 15-29 ml/min/1.73 m(2)], as well as in 35 age and gender matched patients without any evidence of CKD. The difference in the R-R intervals divided by the difference in the oxygen pressures before and after deactivation of the chemoreceptors by inhalation of pure oxygen was calculated as the CHRS. A CHRS below 3.0 ms/mmHg was defined as pathological. CHRS was significantly depressed in patients with stage 3 CKD (2.9 ± 0.9 ms/mmHg, P=0.005) and in patients with stage 4 CKD (2.1 ± 0.6 ms/mmHg, P<0.001), as compared with patients without CKD (6.7 ± 0.9 ms/mmHg). There was a negative correlation between serum creatinine and CHRS (r=-0.51; P<0.001). In patients with CKD, chemosensor deactivation decreased mean arterial pressure from 91 ± 4 mmHg to 87 ± 3 mmHg (P=0.03). Multivariate analysis showed that GFR (P=0.001) was the only independent predictor of a pathological CHRS. Using a relatively non-invasive bedside test we provide evidence for a blunted peripheral chemosensor function in chronic kidney disease. We thereby lay the basis for interventional studies assessing chemosensor function in chronic kidney disease.
    International journal of cardiology 10/2010; 155(2):201-5. · 6.18 Impact Factor

Publication Stats

2k Citations
457.63 Total Impact Points

Institutions

  • 2010–2014
    • Universitätsklinikum Düsseldorf
      Düsseldorf, North Rhine-Westphalia, Germany
  • 2001–2013
    • Heinrich-Heine-Universität Düsseldorf
      • Institut für Herz- und Kreislaufphysiologie
      Düsseldorf, North Rhine-Westphalia, Germany
  • 1999–2012
    • University Hospital RWTH Aachen
      • Department of Neurology
      Aachen, North Rhine-Westphalia, Germany
  • 1995–2009
    • RWTH Aachen University
      • • Institute of Medical Statistics
      • • Institute for Molecular Cardiovascular Research
      Aachen, North Rhine-Westphalia, Germany
  • 2004
    • University of Rostock
      • Institut für Chemie
      Rostock, Mecklenburg-Vorpommern, Germany