Georg Nickenig

University of Bonn - Medical Center, Bonn, North Rhine-Westphalia, Germany

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Publications (480)2575.19 Total impact

  • Journal of the American College of Cardiology 10/2015; 66(15):B26. DOI:10.1016/j.jacc.2015.08.107 · 16.50 Impact Factor
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    ABSTRACT: Background: Valve-in-valve transcatheter aortic valve replacement (TAVR) is becoming a valuable option with promising clinical results in failed bioprosthetic heart valves. Sizing recommendations are based on size compatibility rather than on broad clinical data, in vitro measurements, or biomechanical evidence. The hemodynamic performance of transcatheter heart valves within degenerated surgical heart valves is unknown. Methods: We evaluated the in vitro hydrodynamic performance of two commercially available transcatheter heart valves (Medtronic CoreValve [Medtronic, Minneapolis, MN] and Edwards SAPIEN XT [Edwards Lifesciences, Irvine, CA]) in two different bioprosthetic aortic valves (Edwards Perimount [Edwards Lifesciences] and St. Jude Trifecta [St. Jude Medical, St. Paul, MN]). Results: Within the Edwards Perimount (23 mm) prosthesis, pressure gradients were higher for the SAPIEN XT compared with the CoreValve (11.2 ± 0.1 mm Hg versus 10.1 ± 0.1 mm Hg, p < 0.01), whereas effective orifice area (1.99 ± 0.01 cm(2) versus 1.80 ± 0.01 cm(2), p < 0.01) and total paravalvular leakage (9.0% ± 1.0% versus 5.4% ± 1.3%, p < 0.01) were increased when using the CoreValve. Similarly, measurements in the St. Jude Trifecta revealed higher transvalvular pressure gradients (13.0 ± 0.2 mm Hg versus 10.9 ± 0.3 mm Hg, p < 0.01) and lower effective orifice area for the SAPIEN XT compared with the CoreValve. However, total relative regurgitation was higher with SAPIEN XT as compared with the CoreValve in St. Jude Trifecta prostheses (11.2% ± 1.4% versus 8.3% ± 0.9%, p < 0.01). Conclusions: Both transcatheter heart valve prostheses performed well in the described valve-in-valve settings. Hydrodynamic results were in line with the International Organization for Standardization standards for all configurations. The observed differences indicate a necessity for preclinical valve-in-valve tests in addition to clinical long-term data about longevity.
    The Annals of thoracic surgery 09/2015; DOI:10.1016/j.athoracsur.2015.06.047 · 3.85 Impact Factor
  • F W Horlbeck · G Nickenig · J O Schwab
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    ABSTRACT: A 65-year-old man with severe coronary artery disease and coronary artery bypass graft presented with an acute posterior ST-elevation myocardial infarction. Immediate percutaneous coronary intervention resulted in successful revascularisation of the culprit lesion (RCx) with several remaining coronary stenoses. Despite the reduced left ventricular ejection fraction, no primary prevention indication for an implantable cardioverter/defibrillator early after myocardial infarction existed. Due to the complex coronary anatomy with several remaining stenotic vessels we regarded the patient to be at a particularly high risk for lethal ventricular arrhythmias and provided him with a wearable cardioverter defibrillator (WCD). Twenty-six days later, he experienced spontaneous ventricular tachycardia and fibrillation which was successfully treated with high voltage therapy by the WCD. Subsequently, we decided to implant him an ICD following secondary prevention indication. Besides established indications for primary prevention ICD therapy, some patients early after myocardial infarction may be at a particularly high risk for sudden cardiac death. Temporary protection with a WCD in carefully selected patients can offer a safe opportunity for later reevaluation of permanent ICD implantation depending on the course of left ventricular ejection fraction and the occurrence of arrhythmia.
    Der Internist 09/2015; 56(9):1062-8. DOI:10.1007/s00108-015-3782-0 · 0.31 Impact Factor
  • European Heart Journal 08/2015; DOI:10.1093/eurheartj/ehv384 · 15.20 Impact Factor
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    ABSTRACT: Non-alcoholic steatohepatitis (NASH) is characterised by hepatic steatosis, inflammation and fibrosis, which might progress to cirrhosis. Human NASH is associated with metabolic syndrome (MS). Currently, rodent NASH models either lack significant fibrosis or MS. ApoE(-/-) mice are a MS model used in cardiovascular research. The aim of this work was to establish and characterise a novel mouse NASH model with significant fibrosis and MS. ApoE(-/-) and wild-type mice (wt) were fed either a western-diet (WD), methionine-choline-deficient-diet (MCD) or normal chow. Liver histology, RT-PCR, hepatic hydroxyproline content, triglycerides and cholesterol levels, and fasting glucose levels assessed hepatic steatosis, inflammation and fibrosis. Further, portal pressure was measured invasively, and kidney pathology was assessed by histology. ApoE(-/-) mice receiving WD showed abnormal glucose tolerance, hepatomegaly, weight gain and full spectrum of NASH including hepatic steatosis, fibrosis and inflammation, with no sign of renal damage. MCD-animals showed less severe liver fibrosis, but detectable renal pathological changes, besides weight loss and unchanged glucose tolerance. This study describes a murine NASH model with distinct hepatic steatosis, inflammation and fibrosis, without renal pathology. ApoE(-/-) mice receiving WD represent a novel and fast model with all characteristic features of NASH and MS well suitable for NASH research.
    Scientific Reports 08/2015; 5:12931. DOI:10.1038/srep12931 · 5.58 Impact Factor
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    ABSTRACT: The angiotensin II type 1 receptor (AT1R) and the peroxisome proliferator-activated receptor γ (PPARγ) have been implicated in the pathogenesis of atherosclerosis. A number of studies have reported that AT1R inhibition or genetic AT1R disruption and PPARγ activation inhibit vascular inflammation and improve glucose and lipid metabolism, underscoring a molecular interaction of AT1R and PPARγ. We here analyzed the hypothesis that vasculoprotective anti-inflammatory and metabolic effects of AT1R inhibition are mediated by PPARγ. Female ApoE(-/-)/AT1R(-/-) mice were fedwith a high-fat and cholesterol-rich diet and received continuous treatment with the selective PPARγ antagonist GW9662 or vehicle at a rate of 700 ng/kg/min for 4 weeks using subcutaneously implanted osmotic mini-pumps. Additionally, one group of female ApoE(-/-) mice served as a control group. After treatment for 4 weeks mice were sacrificed and read-outs (plaque development, vascular inflammation and insulinsensitivity) were performed. Using AT1R deficient ApoE(-/-) mice (ApoE(-/-)/AT1R(-/-) mice) we found decreased cholesterol-induced endothelial dysfunction and atherogenesis compared to ApoE(-/-) mice. Inhibition of PPARγ by application of the specific PPARγ antagonist GW9662 significantly abolished the anti-atherogenic effects of AT1R deficiency in ApoE(-/-)/AT1R(-/-) mice (plaque area as % of control: ApoE(-/-): 39 ±5%; ApoE(-/-)/AT1R(-/-): 17 ±7%, p = 0.044 vs. ApoE(-/-); ApoE(-/-)/AT1R(-/-) + GW9662: 31 ±8%, p = 0.047 vs. ApoE(-/-)/AT1R(-/-)). Focusing on IL6 as a pro-inflammatory humoral marker we detected significantly increased IL-6 levels in GW9662-treated animals (IL-6 in pg/ml: ApoE(-/-): 230 ±16; ApoE(-/-)/AT1R(-/-): 117 ±20, p = 0.01 vs. ApoE(-/-); ApoE(-/-)/AT1R(-/-) + GW9662: 199 ±20, p = 0.01 vs. ApoE(-/-)/AT1R(-/-)), while the anti-inflammatory marker IL-10 was significantly reduced after PPARγ inhibition in GW9662 animals (IL-10 in pg/ml: ApoE(-/-): 18 ±4; ApoE(-/-)/AT1R(-/-): 55 ±12, p = 0.03 vs. ApoE(-/-); ApoE(-/-)/AT1R(-/-) + GW9662: 19 ±4, p = 0.03 vs. ApoE(-/-)/AT1R(-/-)). Metabolic parameters of glucose homeostasis (glucose and insulin tolerance test) were significantly deteriorated in ApoE(-/-)/AT1R(-/-) mice treated with GW9662 as compared to vehicle-treated ApoE(-/-)/AT1R(-/-) mice. Systolic blood pressure and plasma cholesterol levels were similar in all groups. Genetic disruption of the AT1R attenuates atherosclerosis and improves endothelial function in an ApoE(-/-) mouse model of hypercholesterolemia-induced atherosclerosis via PPARγ, indicating a significant role of PPARγ in reduced vascular inflammation, improvement of insulin sensitivity and atheroprotection of AT1R deficiency.
    Archives of Medical Science 08/2015; 11(4):877-85. DOI:10.5114/aoms.2015.53309 · 2.03 Impact Factor
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    ABSTRACT: Recent studies have demonstrated the feasibility of measuring heart rate turbulence (HRT) as a marker of baroreflex function in healthy mice. The aim of this investigation was to measure HRT in a mouse model with induced structural heart defects and to determine if there were threshold values of HRT for inducible ventricular tachycardias (VTs). HRT was measured during electrophysiological investigations two weeks after transverse aortic constriction (TAC, n = 13) or myocardial cryoinfarction (MCI, n = 14). Sham operated mice served as controls (n = 8 for TAC-controls and n = 9 for MCI-controls). Mice with heart disease lacked an early acceleration (turbulence onset [TO]) in heart rate after extrastimulus pacing (heart disease: 0.39% [0.19% - 0.59%] vs. all controls: -0.04% [-0.25% - 0.19%]; p<0.01). At a cutoff value of >0.25%, TO could be used to classify mice with induced heart disease with a sensitivity of 64.0% and specificity of 88.2% (p<0.01) but did not identify mice at higher risk of induced VTs. Animals that were susceptible to VTs (n = 8) had lower values for turbulence slope (TS) compared with non-inducible mice (6.2ms/beat [3.1ms/beat - 9.5ms/beat] vs. 10.1ms/beat [7.2ms/beat - 14.2ms/beat]; p = 0.03). TS <7.8ms/beat identified mice with inducible VTs with a sensitivity of 75.0% and specificity of 75.8% (p = 0.02). Measurement of HRT is feasible in mouse models with induced structural heart disease. More abnormal values for TO were found in the presence of structural heart disease but did not predict susceptibility to VTs. Decreased TS was associated with VTs induced by programmed stimulation. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Journal of Cardiovascular Electrophysiology 07/2015; DOI:10.1111/jce.12766 · 2.96 Impact Factor
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    ABSTRACT: Background: Unlike the well-established association between sleep disordered breathing (SDB) and chronic heart failure, the relationship between SDB and severe aortic stenosis (AS) is not well investigated. Given the increasing prevalence of AS, and the improving prognosis of high risk AS patients attributable to transcatheter aortic valve implantation (TAVI), the prevalence and impact of SDB needs to be better understood. Methods and results: In this study, 140 patients with severe AS underwent polygraphy prior to TAVI. Clinical and hemodynamic parameters were recorded. Patients were followed for 573±405 days. We found that 99/140 patients (71%) had SDB with a mean apnoea-hypopnoea-index of 24±17/h. SDB was mild in 27%, moderate in 23% and severe in 21% of patients. In addition, 35 patients (25%) had obstructive sleep apnoea (OSA), whereas 64 patients (46%) had central sleep apnoea (CSA). Patients with OSA had predominantly mild SDB (20/38 pts.), and patients with CSA mostly had severe SDB (24/29 pts.). The prevalence and distribution of OSA and CSA were independent of left ventricular function. Overall, 1 and 2 year survival rates (74% and 71%, resp.) did not differ significantly between patients without SDB or those with OSA and CSA (p=0.81). Conclusions: SDB, with a preponderance of CSA, was found to be highly prevalent in patients with high-grade AS scheduled for TAVI. SDB prevalence was independent of left ventricular function. Mortality after TAVI was not influenced by the type or severity of SDB.
    PLoS ONE 07/2015; 10(7):e0133176. DOI:10.1371/journal.pone.0133176 · 3.23 Impact Factor
  • Vedat Tiyerili · Georg Nickenig · Christoph Hammerstingl
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    ABSTRACT: Transcatheter left atrial appendage (LAA) closure has proven to be an effective method to reduce the risk of thromboembolic events in patients who have nonvalvular atrial fibrillation (AF) that is unsuitable for chronic oral anticoagulation. In this case report, we describe the rare case of a late LAA occluder (28-mm Amplatzer cardiac plug) embolization, which was treated uneventfully with interventional device capture. Special interventional and device specific characteristics must be taken into account when planning such a complex procedure as descirbed in our case.
    Clinical Research in Cardiology 07/2015; DOI:10.1007/s00392-015-0887-3 · 4.56 Impact Factor
  • Felipe C. Fuchs · Eberhard Grube · Georg Nickenig
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    ABSTRACT: Endothelial microparticles (EMP) are released from activated or apoptotic endothelial cells (ECs) and can be taken up by adjacent ECs, but their effect on vascular inflammation after engulfment is largely unknown. We sought to determine the role of EMP in EC inflammation. In vitro, EMP treatment significantly reduced tumour necrosis factor-α-induced endothelial intercellular adhesion molecule (ICAM)-1 expression on mRNA and protein level, whereas there was no effect on vascular cell adhesion molecule-1 expression. Reduced ICAM-1 expression after EMP treatment resulted in diminished monocyte adhesion in vitro. In vivo, systemic treatment of ApoE-/- mice with EMP significantly reduced murine endothelial ICAM-1 expression. To explore the underlying mechanisms, Taqman microRNA array was performed and microRNA (miR)-222 was identified as the strongest regulated miR between EMP and ECs. Following experiments demonstrated that miR-222 was transported into recipient ECs by EMP and functionally regulated expression of its target protein ICAM-1 in vitro and in vivo. After simulating diabetic conditions, EMP derived from glucose-treated ECs contained significantly lower amounts of miR-222 and showed reduced anti-inflammatory capacity in vitro and in vivo. Finally, circulating miR-222 level was diminished in patients with coronary artery disease (CAD) compared to patients without CAD. EMPs promote anti-inflammatory effects in vitro and in vivo by reducing endothelial ICAM-1 expression via the transfer of functional miR-222 into recipient cells. In pathological hyperglycaemic conditions, EMP-mediated miR-222-dependent anti-inflammatory effects are reduced. © 2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
    Journal of Cellular and Molecular Medicine 06/2015; 19(9). DOI:10.1111/jcmm.12607 · 4.01 Impact Factor
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    ABSTRACT: Ion channels involved in cardiac excitation-contraction coupling are linked to the cytoskeleton. Therefore changes in the cytoskeletal actin filaments may influence cardiac membrane currents and electro-mechanical coupling. Depolymerization of actin filaments by gelsolin (gsn) is involved in the organisation of the cytoskeleton by leading to a lower polymerization state. Gsn is activated by Ca(2+) and inhibited by phosphoinositol-bisphosphate (PIP2). Furthermore, gsn has been linked to pathological conditions with reduced contractility like heart failure, amyloidosis and apoptosis. Thus, we hypothesize, that gsn deficiency may change electromechanical properties of freshly isolated ventricular cardiomyocytes. We recorded L-type Ca(2+) current (ICa,L) in whole-cell patch clamp mode in freshly isolated ventricular cardiomyocytes from gsn deficient ((-/-)) and control (gsn(+/+)) mice. Sarcomere shortening was monitored in field-stimulated myocytes from 0.5 Hz to 10 Hz by video microscopy. Shortening-frequency relation, post-rest potentiation and β-adrenergic stimulation were investigated. ICa,L was increased in gsn(-/-) vs. gsn(+/+) myocytes. Sarcomere shortening amplitude and velocity were enhanced in gsn(-/-) vs. gsn(+/+) at all frequencies. Shortening-frequency relationship showed a biphasic pattern with decay in shortening amplitude between 0.5 and 2 Hz and an increase at higher frequencies in both genotypes. Post-rest characteristics revealed a frequency-dependent decay of post-rest potentiation in gsn(+/+) while it remained stable in gsn(-/-). In gsn(-/-) a reduced response to β-adrenergic stimulation was observed. Resting sarcomere length was shorter in gsn(-/-) but neither increasing frequency nor β-adrenergic stimulation induced further decay in any of the genotypes. In summary, gsn deficiency had a profound effect on excitiation-contraction properties and improved systolic function while not affecting diastolic function in unloaded isolated cardiomyocytes. Therefore, gsn mediated effects on contractility may play a role in patients with heart failure and cancer, where gsn levels are known to be elevated.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 06/2015; 66(3):373-83. · 2.39 Impact Factor
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    ABSTRACT: The aim of the CoreValve prospective, international, post-market ADVANCE-II study was to define the rates of conduction disturbances and permanent pacemaker implantation (PPI) after transcatheter aortic valve replacement with the Medtronic CoreValve System (Minneapolis, Minnesota) using optimized implantation techniques and application of international guidelines on cardiac pacing. Conduction disturbances are a frequent complication of transcatheter aortic valve replacement. The rates of PPI in the published reports vary according to bioprosthesis type and the indications for PPI. The primary endpoint was the 30-day incidence of PPI with Class I/II indications when the Medtronic CoreValve System was implanted at an optimal depth (≤6 mm below the aortic annulus). The timing and resolution of all new-onset conduction disturbances were analyzed. A total of 194 patients were treated. The overall rate of PPI for Class I/II indications was 18.2%. An optimal depth was reached in 43.2% of patients, with a nonsignificantly lower incidence of PPI in patients with depths ≤6 mm, compared with those with deeper implants (13.3% vs. 21.1%; p = 0.14). In a paired analysis, new-onset left bundle branch block and first-degree atrioventricular block occurred in 45.4% and 39.0% of patients, respectively, and resolved spontaneously within 30 days in 43.2% and 73.9%, respectively. In patients with new PPI, the rate of intrinsic sinus rhythm increased from 25.9% at 7 days to 59.3% at 30 days (p = 0.004). Optimal Medtronic CoreValve System deployment and adherence to international guidelines on cardiac pacing are associated with a lower rate of new PPI after transcatheter aortic valve replacement, compared with results reported in previous studies. (CoreValve Advance-II Study: Prospective International Post-Market Study [ADVANCE II]; NCT01624870). Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
    JACC. Cardiovascular Interventions 05/2015; 8(6). DOI:10.1016/j.jcin.2015.02.005 · 7.35 Impact Factor
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    ABSTRACT: To investigate the influence of non-cardiac comorbidities on outcomes of patients enrolled in the German transcatheter mitral valve interventions (TRAMI) registry. Intrahospital and 30-day MACCE rates (death of all causes, stroke and myocardial infarction) of 828 patients from the TRAMI registry were stratified by the number of non-cardiac comorbidities. The following non-cardiac comorbidities were prospectively recorded in the registry: diabetes, renal insufficiency, extracardiac arteriopathy, chronic lung disease, neurological disease or malignancy on palliative care. The 375 (45.3 %) patients with multiple (≥2) non-cardiac comorbidities presented with higher NYHA classes, higher logistic Euroscores, higher levels of NT-proBNP and a shorter 6-min walk distance. Rates of intraprocedural death (0.3 vs. 0.0 %, p = 0.41) and intrahospital MACCE (3.6 vs. 1.9 %, p = 0.16) were not significantly higher in patients with multiple non-cardiac comorbidities, but 30-day MACCE rate was significantly enhanced (6.4 vs. 3.6 %, p = 0.049). However, both patient groups showed a similar clinical improvement after 30 days. Renal insufficiency was the only non-cardiac comorbidity which was independently associated with the 30-day MACCE rate. MitraClip device placement is feasible and safe in patients with multiple non-cardiac comorbidities resulting in a significant clinical improvement and acceptable intrahospital and 30-day event rates. Renal failure is an independent predictor of outcome.
    Clinical Research in Cardiology 05/2015; DOI:10.1007/s00392-015-0872-x · 4.56 Impact Factor
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    ABSTRACT: Intermittent hypoxia seems to be a major pathomechanism of obstructive sleep apnea-associated progression of atherosclerosis. The goal of the present study was to assess the influence of hypoxia on endothelial function depending on the initial stage of vasculopathy. We used 16 ApoE-/- mice were exposed to a 6-week-intermittent hypoxia either immediately (early preatherosclerosis) or after 5 weeks of high-cholesterol diet (advanced preatherosclerosis). Another 16 ApoE-/- mice under normoxia served as corresponding controls. Endothelial function was measured by an organ bath technique. Blood plasma CD31+/annexin V+ endothelial microparticles as well as sca1/flk1+ endothelial progenitor cells in blood and bone marrow were analyzed by flow cytometry. The findings were that intermittent hypoxia impaired endothelial function (56.6 ± 6.2 % of maximal phenylephrine-induced vasoconstriction vs. 35.2 ± 4.1 % in control) and integrity (increased percentage of endothelial microparticles: 0.28 ± 0.05 % vs. 0.15 ± 0.02 % in control) in early preatherosclerosis. Peripheral repair capacity expressed as the number of endothelial progenitor cells in blood was attenuated under hypoxia (2.0 ± 0.5 % vs. 5.3 ± 1.9 % in control), despite the elevated number of these cells in the bone marrow (2.0 ± 0.4 % vs. 1.1 ± 0.2 % in control). In contrast, endothelial function, as well as microparticle and endothelial progenitor cell levels were similar under hypoxia vs. control in advanced preatherosclerosis. We conclude that hypoxia aggravates endothelial dysfunction and destruction in early preatherosclerosis.
    Advances in Experimental Medicine and Biology 05/2015; 858. DOI:10.1007/5584_2015_114 · 1.96 Impact Factor
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    European Heart Journal 05/2015; 36(31). DOI:10.1093/eurheartj/ehv167 · 15.20 Impact Factor
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    ABSTRACT: Left ventricular conduction disturbances (VCD) with or without need for pacemaker (PM) implantation are common after transcatheter aortic valve replacement (TAVR). Its effect on patients' functional recovery after TAVR is unclear. 212 patients (Age 80.8 ± 6.4 years, logEuroscore 28.95 ± 17.37 %) underwent TAVR with the self-expanding CoreValve prosthesis and completed 9-month follow-up (FU). After TAVR 125 (59 %) patients were diagnosed with VCD. This group consists of 41 (19 %) patients with a new PM after TAVR, 33 (16 %) patients with PM prior TAVR and markedly increased ventricular stimulation rate, 48 (23 %) patients with new LBBB post-TAVR and three (1 %) patients with LBBB prior TAVR. After FU, the presence of VCD alone was associated with worse recovery of left ventricular ejection fraction (LVEF) (VCD: LVEFbaseline 51.7 ± 18.2 %, LVEFFU 53.9 ± 13.0 %; p = 0.8; noVCD: LVEFbaseline 53.8 ± 12.9 %, LVEFFU 63.4 ± 10.1 %; p < 0.01) but had no impact on functional outcomes after TAVR (p > 0.05). Especially patients with VCD caused by permanent RV pacing showed worse functional outcomes presenting with higher functional NYHA classes (p < 0.05), and higher NT-proBNP levels (p < 0.05). 20.4 % of patients with need for PM after TAVR remained in NYHA class ≥3, as compared to 5 % of patients without PM (VCD but no PM: 4.7 %, p < 0.001; noVCD: 5.3 %, p < 0.001). VCD with or without need for PM had no impact on survival after FU. The occurrence of VCD after TAVR is common and associated with unfavorable left ventricular functional recovery. However, only the combination of VCD with permanent right ventricular pacing has adverse impact on heart failure-related symptoms after TAVR.
    Clinical Research in Cardiology 05/2015; DOI:10.1007/s00392-015-0865-9 · 4.56 Impact Factor
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    ABSTRACT: While idiopathic pulmonary arterial hypertension (PAH) is a rare disease, it is seen more frequently in patients with HIV infection. The aim of this study was to evaluate the prevalence of pulmonary hypertension (PH) in patients with HIV infection by echocardiographic screening. Echocardiography and N-terminal of the prohormone brain natriuretic peptide measurement were used to examine the prevalence of PH prospectively in HIV-positive patients (n = 374) during routine follow-up visits for HIV disease. In echocardiographic screening, PH was detected in a total of 23 of 374 HIV-infected patients (6.1%). Of these, three patients (13%) presented with symptoms of dyspnoea and fatigue, and diagnosis of PAH was confirmed by right heart catheterization. Patients with systolic pulmonary artery pressure (sPAP) > 30 mmHg were more likely to be female, to have a history of injecting drug use and to originate from high-prevalence countries (HPCs). Echocardiographic screening detected PH in a substantial proportion of HIV-positive patients. Female gender, a history of injecting drug use and HPC origin were associated with a higher prevalence of HIV-associated PH. The relevance and long-term outcome of these findings need to be validated in follow-up studies, which are ongoing. © 2015 British HIV Association.
    HIV Medicine 05/2015; 16(9). DOI:10.1111/hiv.12261 · 3.99 Impact Factor
  • Journal of the American College of Cardiology 05/2015; 65(17):S60. DOI:10.1016/j.jacc.2015.03.184 · 16.50 Impact Factor

Publication Stats

16k Citations
2,575.19 Total Impact Points


  • 2008–2015
    • University of Bonn - Medical Center
      Bonn, North Rhine-Westphalia, Germany
  • 2006–2015
    • University of Bonn
      • Medizinische Klinik und Poliklinik II
      Bonn, North Rhine-Westphalia, Germany
    • Karolinska University Hospital
      • Department of Cardiology
      Tukholma, Stockholm, Sweden
    • Centre Hospitalier Universitaire de Toulouse
      Tolosa de Llenguadoc, Midi-Pyrénées, France
  • 2013
    • Heart & Vascular Center
      Göttingen, Lower Saxony, Germany
  • 2001–2008
    • Universität des Saarlandes
      Saarbrücken, Saarland, Germany
  • 2007
    • Deutsche Sporthochschule Köln
      Köln, North Rhine-Westphalia, Germany
    • Deutsches Herzzentrum München
      München, Bavaria, Germany
  • 2005
    • Humboldt-Universität zu Berlin
      • Department of Biology
      Berlín, Berlin, Germany
  • 2001–2005
    • Universitätsklinikum des Saarlandes
      Homburg, Saarland, Germany
  • 1997–2000
    • University of Cologne
      • • Division of Cardiology, Pneumology, Angiology and Intensive Care
      • • Department of Internal Medicine
      Köln, North Rhine-Westphalia, Germany
  • 1994–1997
    • Emory University
      • • Department of Pharmacology
      • • Division of Cardiology
      Atlanta, Georgia, United States