Ursula Müller-Werdan

University Hospital RWTH Aachen, Aachen, North Rhine-Westphalia, Germany

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Publications (189)426.79 Total impact

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    ABSTRACT: Objectives: Elevated heart rate can increase myocardial oxygen demand and reduce myocardial perfusion, provoking myocardial ischemia and angina symptoms. We evaluated adding ivabradine to the therapy of patients on metoprolol. Methods: ADDITIONS (prActical Daily efficacy anD safety of Procoralan® In combinaTION with betablockerS) was a multicenter, 4-month, noninterventional, prospective, open-label trial that involved stable-angina patients. Along with metoprolol, patients received ivabradine (5 or 7.5 mg, b.i.d.). We investigated the effect of ivabradine on heart rate, angina attacks, nitrate consumption, quality of life (QoL) and tolerability as well as the influence of baseline heart rate. Results: Heart rate fell by 19.7 ± 11.2 bpm, with an 8-fold decrease in weekly angina attacks (1.7 ± 2.2 to 0.2 ± 0.7) and nitrate consumption (2.4 ± 3.4 to 0.3 ± 0.9). Patient numbers in Canadian Cardiovascular Society class I more than doubled (i.e. from 29 to 65%) and QoL improved (the EQ-5D index and visual analog scale scores rose from 0.68 ± 0.27 to 0.84 ± 0.20 and 58.1 ± 18.4 to 72.2 ± 15.5 mm, respectively). The effect of ivabradine was greater in patients with a baseline heart rate ≥70 bpm (mean reduction in heart rate -21.2 ± 10.4 bpm, with a relative reduction in angina attacks and short-acting nitrate consumption of 87.1 and 87.2%, respectively). Conclusions: Ivabradine combined with metoprolol safely and effectively reduces heart rate, angina attacks and nitrate use, and improves QoL in stable-angina patients.
    No preview · Article · Oct 2015 · Cardiology
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    ABSTRACT: Arterial hypertension is a common disease with high prevalence in the general population. Left ventricular hypertrophy (LVH) is an independent risk factor in arterial hypertension. Electrocardiographic indices like the Sokolow-Lyon index (SLI) are recommended as diagnostic screening methods for LVH. We assessed the diagnostic performance of the SLI in a cohort of a large general population. We used electrocardiographic and echocardiographic data from the prospective, population-based cohort study CARdio-vascular Disease, Living and Ageing in Halle (CARLA). Linear and logistic regression models were used to assess the association of SLI with LVH. To assess the impact of the body-mass-index (BMI), we performed interaction analyses. AUC of SLI to predict LVH was 55.3 %, sensitivity of the SLI was 5 %, specificity 97 %. We found a significant association of SLI after covariate-adjustment with echocardiographically detected LVH (increase of left-ventricular mass index, LVMI 7.0 g/m(2) per 1 mV increase of SLI, p < 0.0001). However, this association was mainly caused by an association of SLI with the left-ventricular internal diameter (LVIDd, increase of 0.06 cm/m(2) per 1 mV increase of SLI, p < 0.0001). In obese (BMI > 30 kg/m(2)) we found the strongest association with an increase of 9.2 g/m(2) per 1 mV. Although statistically significant, relations of SLI and echocardiographic parameters of LVH were weak and mainly driven by the increase in LVIDd, implicating a more eccentric type of LVH in the collective. The relations were strongest when obese subjects were taken into account. Our data do not favour the SLI as a diagnostic screening test to identify patients at risk for LVH, especially in non-obese subjects without eccentric LVH.
    Full-text · Article · Jul 2015 · BMC Cardiovascular Disorders
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    ABSTRACT: In critically ill patients regulation of heart-rate is often severely disturbed. Interaction of bacterial endotoxin (lipopolysaccharide, LPS) with hyperpolarization-activated cyclic nucleotide-gated cation-(HCN)-channels may interfere with heart-rate regulation. Here, we analyze the effect of LPS, the HCN-channel blocker ivabradine or Ca(2+) -channel blockers (nifedipine, verapamil) on pacemaking in spontaneously beating neonatal rat cardiomyocytes (CM) in vitro. In vivo, we analyze telemetrically the effect of LPS on the heart-rate of adult CD1-mice with and without autonomic blockade. LPS (100 ng/ml) and ivabradine (5 μg/ml) reduced the beating-rate of CM by 20.1 and 24.6%, respectively. Coincubation of CM with both, LPS and ivabradine, did not further reduce the beating-rate, indicating interaction of both compounds with HCN-channels, while coincubation with Ca(2+-) channel blockers and LPS caused additive beating-rate reduction. In CD1-mice with an active autonomic-nervous-system, injection of LPS (0.4 mg/kg) expectedly resulted in increased heart-rate. However, if the autonomic nervous system was blocked by propranolol and atropine, in line with the in vitro data, LPS induced a significant reduction of heart-rate, which was not additive to ivabradine. The in vivo and in vitro results indicate that endotoxin interacts with HCN-channels of cardiomyocytes. Thus, LPS indirectly sensitizes HCN-channels for sympathetic activation (tachycardic-effect), and in parallel directly inhibits channel activity (bradycardic-effect). Both effects may contribute to the detrimental effects of septic cardiomyopathy and septic autonomous dysfunction. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    No preview · Article · Apr 2015 · Clinical and Experimental Pharmacology and Physiology
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    ABSTRACT: The anti-anginal efficacy of ivabradine is well established. We describe a post hoc analysis in the ADDITIONS database to investigate effectiveness and tolerability of ivabradine in combination with beta-blocker in patients with angina who have had a percutaneous coronary intervention (PCI). ADDITIONS was a non-interventional, multicenter prospective study including 2,330 patients with stable angina. In addition to beta-blocker, patients were treated with ivabradine in approved dosages for 4 months. We divided the population according to whether they had previously had a PCI or not, and explored the effect of ivabradine on heart rate, number of weekly angina attacks, frequency of nitrate consumption, as well as quality of life (QoL) and tolerability. Data were available for 2,319 patients, of whom 51.4% had previously had a PCI. There was no difference in the effect of ivabradine on mean heart rate between patients with a previous PCI [64.4 ± 7.6 beats per minute (bpm)] than those without (66.8 ± 8.5 bpm) at 4 months (both P < 0.0001). Similarly, the number of angina attacks decreased from 1.9 ± 2.4 to 0.5 ± 1.5 per week in patients with a previous PCI and 1.5 ± 2.0 to 0.3 ± 1.0 per week in patients without a previous PCI (both P < 0.0001). The frequency of nitrate consumption fell from 2.7 ± 3.7 to 1.0 ± 1.9 per week and 1.8 ± 2.8 to 0.6 ± 1.5 per week (both P < 0.0001) in patients with and without a previous PCI, respectively. There was no difference in the improvements in Canadian Cardiovascular Society class of angina, QoL, and physicians' assessment of effectiveness and tolerability between patients with a previous PCI and those without. Ivabradine is an effective and well-tolerated anti-anginal treatment in patients with stable angina after PCI. Ivabradine reduced the frequency of weekly angina attacks and nitrate consumption, led to an improvement in Canadian Cardiovascular Society class and a substantial improvement in the QoL of stable angina patients.
    Full-text · Article · Feb 2015 · Advances in Therapy
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    ABSTRACT: Abstract BACKGROUND: Clinical trials have proven the anti-anginal and anti-ischemic efficacy of the pacemaker current inhibitor ivabradine in combination with beta-blockers in patients with stable angina pectoris (AP). This retrospective subgroup analysis of the ADDITIONS study evaluated the effectiveness and tolerability of ivabradine combined with beta-blockers, and its effects on angina symptoms and quality of life in elderly patients ≥ 75 years in everyday practice. METHODS: In the non-interventional, multicenter, prospective, open-label ADDITIONS study 2330 patients with stable AP of different age groups were treated with a flexible dose of ivabradine twice daily in addition to beta-blockers for 4 months. Heart rate (HR), number of angina attacks, nitrate consumption, tolerance, and quality of life (QoL) were evaluated. A subgroup analysis was performed, focusing on 479 patients (21%) ≥ 75 years. RESULTS: In these 479 patients ≥ 75 years ivabradine (mean dose 11.61 ± 3.18 mg per day) after 4 months of treatment reduced HR by 19.2 ± 11.6 bpm to 65.4 ± 8.3 bpm. The average number of angina attacks per week was decreased by 1.6 ± 1.8 to 0.4 ± 1.3 and the average consumption of short-acting nitrates per week was reduced by 2.2 ± 3.2 to 0.6 ± 1.8 units (both p < 0.0001). There was a marked shift in Canadian Cardiovascular Society (CCS) grade distribution with most patients (57%) now classified as CCS grade I, and 42% as CCS grades II and III. This was accompanied by an improvement in EQ-5D QoL index to 0.75 ± 0.22 (p < 0.0001). Tolerability of ivabradine treatment was rated by the physicians as “very good/good” for 72%/28% of elderly patients. CONCLUSIONS: In daily clinical practice, addition of ivabradine to beta-blockers was effective in reducing HR, angina attacks and nitrate consumption in elderly patients (≥ 75 years) with stable angina pectoris. In addition, a marked improvement of CCS symptom scores and QoL was demonstrated. Treatment was generally well tolerated.
    No preview · Article · Nov 2014 · Experimental Gerontology
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    ABSTRACT: BACKGROUND: Clinical trials have proven the anti-anginal and anti-ischemic efficacy of the pacemaker current inhibitor ivabradine in combination with beta-blockers in patients with stable angina pectoris (AP). This retrospective subgroup analysis of the ADDITIONS study evaluated the effectiveness and tolerability of ivabradine combined with beta-blockers, and its effects on angina symptoms and quality of life in elderly patients ≥ 75 years in everyday practice. METHODS: In the non-interventional, multicenter, prospective, open-label ADDITIONS study 2330 patients with stable AP of different age groups were treated with a flexible dose of ivabradine twice daily in addition to beta-blockers for 4 months. Heart rate (HR), number of angina attacks, nitrate consumption, tolerance, and quality of life (QoL) were evaluated. A subgroup analysis was performed, focusing on 479 patients (21%) ≥ 75 years. RESULTS: In these 479 patients ≥ 75 years ivabradine (mean dose 11.61 ± 3.18 mg per day) after 4 months of treatment reduced HR by 19.2 ± 11.6 bpm to 65.4 ± 8.3 bpm. The average number of angina attacks per week was decreased by 1.6 ± 1.8 to 0.4 ± 1.3 and the average consumption of short-acting nitrates per week was reduced by 2.2 ± 3.2 to 0.6 ± 1.8 units (both p < 0.0001). There was a marked shift in Canadian Cardiovascular Society (CCS) grade distribution with most patients (57%) now classified as CCS grade I, and 42% as CCS grades II and III. This was accompanied by an improvement in EQ-5D QoL index to 0.75 ± 0.22 (p < 0.0001). Tolerability of ivabradine treatment was rated by the physicians as “very good/good” for 72%/28% of elderly patients. CONCLUSIONS: In daily clinical practice, addition of ivabradine to beta-blockers was effective in reducing HR, angina attacks and nitrate consumption in elderly patients (≥ 75 years) with stable angina pectoris. In addition, a marked improvement of CCS symptom scores and QoL was demonstrated. Treatment was generally well tolerated.
    Full-text · Article · Nov 2014 · Experimental Gerontology
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    ABSTRACT: Objectives: Inflammation is essential for atherogenesis. Cholesterol, a cardiovascular risk factor, may activate inflammation in the vessel wall during this process. Cytokine-mediated interactions of human monocytes with vascular smooth muscle cells (SMCs) may perpetuate this process. Methods: We investigated the capacity of the cholesterol metabolite 25-hydroxycholesterol to induce inflammatory mediators in cocultures of freshly isolated monocytes with SMCs. We determined the role of interleukin-(IL)-1 in this interaction using qPCR, bioassays, ELISA and western blot. Cocultures with SMC to monocyte ratios from 1:4 to 1:20 were tested. Results: In separate SMC and monocyte cultures (monocultures) 25-hydroxycholesterol only poorly activated IL-1, IL-6 and MCP-1 production, whereas LPS stimulated much higher cytokine levels than unstimulated cultures. In contrast, cocultures of SMCs and monocytes stimulated with 25-hydroxycholesterol produced hundredfold higher cytokine levels than the corresponding monocultures. Blocking experiments with IL-1-receptor antagonist showed that IL-1 decisively contributed to the 25-hydroxycholesterol-induced synergistic IL-6 and MCP-1 production. The presence of intracellular IL-1β precursor, released mature IL-1β, and caspase-1 p10 indicated that the inflammasome was involved in this process. Determination of IL-1-mRNA in Transwell experiments indicated that the monocytes are the major source of IL-1, which subsequently activates the SMCs, the primary source of IL-6 in the coculture. Conclusion: Taken together, these interactions between local vessel wall cells and invading monocytes may multiply cholesterol-triggered inflammation in the vessel wall, and IL-1 may play a key role in this process. The data also indicate that lower cholesterol levels than expected from monocultures may suffice to initiate inflammation in the tissue. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
    No preview · Article · Oct 2014 · Atherosclerosis

  • No preview · Article · Aug 2014 · Atherosclerosis
  • Bernhard Maisch · Karl Werdan · Ursula Müller-Werdan · Naranjan S Dhalla

    No preview · Article · May 2014 · Canadian Journal of Physiology and Pharmacology
  • J. Abraham · R. Reichstein · C. Richter · K. Sadowski · U. Müller-Werdan
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    ABSTRACT: Die kardiovaskulären Erkrankungen zählen zu den häufigsten stationären Behandlungsanlässen älterer Menschen. Dennoch finden die Besonderheiten geriatrischer Patienten in der akutstationären Versorgung bisher kaum Beachtung. Ziel dieser Untersuchung war die deskriptive Darstellung klinischer Versorgungsverläufe geriatrischer und nichtgeriatrischer Patienten mit akutem Myokardinfarkt (AMI).Im Rahmen einer Vollerhebung wurden 83 Patientenakten aus dem Jahr 2009 im Hinblick auf pflegerische, therapeutische sowie sozialberatende und medizinische Maßnahmen untersucht. Die retrospektive Dokumentenanalyse stützt sich auf die Daten der kardiologischen Fachabteilung eines Universitätsklinikums. Die Eingruppierung in geriatrische und nichtgeriatrische Patienten erfolgte anhand einer im Vorfeld entwickelten Kriterienliste.Es konnten 48 geriatrische und 35 nichtgeriatrische Patienten identifiziert werden. Es zeigten sich bei den geriatrischen Patienten ein umfassender pflegerischer und therapeutischer Unterstützungsbedarf, eine hohe Komplikationshäufigkeit und lange Verweildauer sowie Besonderheiten bezüglich des Entlassungsorts.Aufgezeigt wurden die komplexen Problemstellungen und besonderen Versorgungsbedürfnisse geriatrischer Patienten mit akutem Myokardinfarkt. Diese vulnerable Patientengruppe sollte in der Akutversorgung stärker Beachtung finden. Weiterführende Studien mit einem prospektiven Ansatz sind notwendig, um die spezifischen Bedürfnisse geriatrischer Patienten in der Akutversorgung zu erfassen.
    No preview · Article · Jan 2014 · Zeitschrift für Gerontologie + Geriatrie
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    ABSTRACT: We investigated the relationship of impaired autonomic function and severity of illness in chronic heart failure (CHF) and multiple-organ dysfunction syndrome (MODS) as an end stage of CHF. Furthermore, we assessed the link of parasympathetic modulation of the heart rate and inflammatory activation in CHF and MODS. Sixty-five patients admitted for worsening of CHF were retrospectively enrolled in this study. In addition, 65 age- and sex-matched patients with pronounced MODS were assigned for comparison of autonomic function and C-reactive protein in patients with CHF or MODS, respectively. Heart rate variability (HRV) parameters of the time and frequency domain as markers of autonomic function were analyzed from 24-hour Holter electrocardiograms. The more pronounced the severity of illness as expressed by the Acute Physiology and Chronic Health Evaluation score, the more the HRV was impaired. This effect was particularly seen for overall variability (SD of RR intervals) and HRV parameters characterizing the parasympathetic modulations of the heart rate (high, very low frequency power). C-reactive protein levels as markers of inflammation were inversely related to high and very low frequencies. Our results allow for speculation that autonomic dysfunction in CHF indicates a beginning of uncoupled interorgan communication potentially leading to MODS as characterized by disruption of communication between the organs.
    No preview · Article · Dec 2013 · Journal of critical care
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    ABSTRACT: Depressed heart rate variability in severe inflammatory diseases can partially be explained by the lipopolysaccharide (LPS)-dependent modulation of cardiac pacemaker channels. Recently, we showed that LPS inhibits pacemaker current in sino-atrial node cells and in HEK293 cells expressing cloned pacemaker channels, respectively. The present study was designed to verify whether this inhibition involves LPS-dependent intracellular signaling and to identify structures of LPS responsible for pacemaker current modulation. We examined the effect of LPS on the activity of human hyperpolarization-activated cyclic nucleotide-gated channel 2 (hHCN2) stably expressed in HEK293 cells. In whole-cell recordings bath-application of LPS decreased pacemaker current (IhHCN2) amplitude. The same protocol had no effect on channel activity in cell-attached patch recordings, where channels are protected from the LPS-containing bath solution. This demonstrates that LPS has to interact directly with or close to the channel protein. After cleavage of LPS into lipid A and the polysaccharide chain, neither of them alone impaired IhHCN2, suggesting that modulation of channel activity critically depends on the integrity of the entire LPS molecule. We furthermore showed that β-cyclodextrin interfered with LPS-dependent channel modulation predominantly via scavenging of lipid A, thereby abrogating the capability of LPS to intercalate into target cell membranes. We conclude that LPS impairs IhHCN2 by a local mechanism that is restricted to the vicinity of the channels. Furthermore, intercalation of lipid A into target cell membranes is a prerequisite for the inhibition that is suggested to depend on direct interaction of the LPS polysaccharide chain with cardiac pacemaker channels.
    Full-text · Article · Dec 2013 · The Journal of Physiology
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    ABSTRACT: Patients with infective endocarditis (IE) form a heterogeneous group, ranging from those who are successfully treated with no adverse events, to those with severe complications and a high mortality. In this Review, we highlight pathogen-host interactions and the mechanisms underlying various risk factors for patients with IE. A temporal trend in the pattern of IE has been observed in high-income countries within the past 5 decades, with patients contracting IE at an increasingly old age, and a growing incidence of health-care-associated staphylococcal IE. Consequently, prevention strategies should no longer focus on prophylaxis of streptococcal bacteraemia during dental procedures, but instead encourage a more-general approach to reduce the incidence of health-care-associated IE. Much knowledge has been gained about the mechanisms of vegetation formation, growth, and embolization on damaged or inflamed cardiac valves, and on cardiac devices. Improved understanding of these mechanisms will help to combat the increasing problem of antimicrobial resistance. Two mechanisms of IE should increasingly be the focus of future research: the role of immunosenescence in elderly patients with IE, particularly after transcatheter aortic valve implantation, and the mechanisms that trigger septic shock, a condition that leads to a substantial increase in the risk of death in patients with IE.
    No preview · Article · Nov 2013 · Nature Reviews Cardiology
  • J. Schröder · S. Nuding · S. Dietz · S. Gielen · K. Werdan · U. Müller-Werdan

    No preview · Article · Oct 2013 · Intensiv- und Notfallbehandlung
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    K. Werdan · H. Ebelt · G. Stoeckl · S. Nuding · F. Hoepfner · U. Mueller-Werdan
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    ABSTRACT: Objectives: The non-interventional multicenter ADDITIONS study follow-up evaluated the effectiveness, safety, and effect on quality of life (QoL) of ivabradine (iva) in combination with betablockers over one year. Methods: Resting heart rate (HR), the number of angina attacks, nitrate consumption, and concomitant medications were documented in 901 patients with chronic stable angina treated with iva twice daily in flexible doses in combination with betablockers for one year. QoL was evaluated by the EQ-5D patient questionnaire at each visit. A descriptive statistical analysis was performed. Results: 901 patients (intention to treat, mean age 65.4±10.6 years, 58% male) with chronic stable angina were analyzed. 53% of the patients had undergone a PCI or CABG before and 35% had a history of myocardial infarction. All patients received betablockers (e.g. Metoprolol 41%, mean daily dose (mdd) 109.6 mg; Bisoprolol 39%, mdd 6.9 mg; Nebivolol 13%, mdd 4.9 mg; Carvedilol 7%, mdd 28.9 mg) and concomitant standard medication. At baseline, most patients (49%) were classified CCS grade II, mean HR was 86.1±12.6 bpm, a mean of 1.7±2.2 angina attacks per week were reported, consumption of short-acting nitrates was 2.3±3.2 units per week, and the EQ-5D index was 0.66±0.28. After one year, iva (mean dose 12.53±2.84 mg per day) had reduced HR by 20.7±14.0 bpm to 65.4±8.8 bpm, the number of angina attacks by 1.4±2.5 per week (p<0.0001, Wilcoxon signed rank test), and nitrate consumption by 1.9±3.1 units per week (p<0.0001), had improved EQ-5D index by 0.18±0.27 (p<0.0001), and most patients (63%) were classified CCS grade I. HR reduction and improvement of angina symptoms by iva was similar in three subgroups defined by betablocker background dose (<50%, 50% to 99%, and ≥100% of recommended target dose): see table. View this table:Enlarge table
    Full-text · Article · Aug 2013 · European Heart Journal
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    K. Werdan · H. Ebelt · G. Stoeckl · S. Nuding · F. Hoepfner · U. Mueller-Werdan
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    ABSTRACT: Objectives: A stratified analysis of the effectiveness of ivabradine in combination with betablockers was performed for angina patients with and without left ventricular dysfunction (LVD) from the non-interventional multicenter ADDITIONS follow-up study over one year. Methods: 901 patients with chronic stable angina were treated with ivabradine bid in flexible doses in combination with betablockers for one year. Among other parameters, resting heart rate (HR), LVD, ejection fraction (EF), and severity of symptoms (CCS score) were evaluated. LVD diagnosis was based on a qualitative assessment by the physician. Descriptive statistics were performed. Results: Of 901 patients (intention to treat, mean age 65.4±10.6 years, 58% male) with chronic stable angina analyzed, 53% had undergone a PCI/CABG before and 35% had a history of myocardial infarction. All patients received betablockers (Metoprolol 41%, mean daily dose (mdd) 109.6 mg; Bisoprolol 39%, mdd 6.9 mg; Nebivolol 13%, mdd 4.9 mg; Carvedilol 7%, mdd 28.9 mg) and concomitant standard medication. Of the 901 patients, 39% (n=342) were diagnosed with LVD (+LVD) and 61% (n=559) without (-LVD). EF could be documented for 55% of all patients (n= 404). At baseline, mean HR was 85.6±12.4 bpm in the +LVD group and 86.3±12.6 bpm in the -LVD group. Overall, +LVD patients had a mean EF of 48.7±10.9% and a mean CCS grade of 2.2±0.7. Mean EF and CCS grade for -LVD patients were 61.2±11.2% and 1.7±0.7, respectively. Most patients in both groups were in CCS grade II (+LVD: 50%; -LVD: 49%) at baseline. After one year of treatment with ivabradine (mean dose 12.53±2.84 mg per day), HR reduction was comparable in the two groups (+LVD: 20.6±14.4 bpm; -LVD: 20.8±13.5 bpm). Mean EF increased by 4.5±10.6% (p<0.0001, Wilcoxon signed rank test) in +LVD patients and by 1.3±9.9% (p=0.26) in -LVD patients. Mean CCS grade improved by -0.7±0.9 to 1.5±0.6 (p<0.0001) and by -0.3±0.7 to 1.4±0.5 (p<0.0001) in +LVD and -LVD patients, respectively. Following treatment with ivabradine most patients in both groups were classified CCS grade I (+LVD: 57%; -LVD: 67%). Marked reductions were obvious in the number of patients with CCS III grading in the +LVD group (24%), with a smaller decrease in the -LVD group (7%). Reductions in patients with CCS II were similar in the two groups (15-20%). Conclusion: Over one year, in clinical practice the combination of ivabradine with betablockers was equally effective in reducing HR in stable angina patients with and without LVD. Moreover, treatment with ivabradine improved EF and mean CCS symptom score more in patients with LVD than in patients without.
    Full-text · Article · Aug 2013 · European Heart Journal
  • J Abraham · R Reichstein · C Richter · K Sadowski · U Müller-Werdan
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    ABSTRACT: Background: Although cardiovascular diseases belong to the most frequent causes of inpatient treatment of older people the specific characteristics of geriatric patients in the acute care unit still receive marginal attention. The aim of this study was the descriptive representation of clinical health care processes of geriatric and non-geriatric patients with acute myocardial infarction. Patients and methods: Using a retrospective document analysis 83 medical patient records were examined with regard to nursing, therapeutic as well as medical measures and social counseling. The classification in geriatric and non-geriatric patients was based on a predefined list of criteria. Results: In the study a total of 48 geriatric and 35 non-geriatric patients could be identified. There was a comprehensive need for support of nursing and therapeutic care, a high frequency of complications and a long length of stay as well as specifics concerning the place of discharge in geriatric patients. Conclusions: Complex problems and special care needs of geriatric patients with acute myocardial infarction were shown. This vulnerable group of patients should be given more attention in acute care. Further investigations with a prospective character are necessary in order to detect the specific needs of geriatric patients in acute care.
    No preview · Article · Jun 2013 · Zeitschrift für Gerontologie + Geriatrie
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    ABSTRACT: Introduction: In sepsis, the reduced systemic vascular resistance (SVR) can lead to a compensatory increase in cardiac output (CO). This may mimic a normal cardiac function although there is already a sepsis-induced myocardial depression. On a cohort of patients with septic multi-organ dysfunction syndrome, we have recently developed a method to correlate the actual CO to the afterload (estimated by SVR) and introduced the parameter "afterload-related cardiac performance" (ACP), which indicates if the rise of CO is adequate for the particular SVR. In this present study it was to be investigated, if ACP can reveal septic cardiomyopathy in patients with community-acquired sepsis in the early state soon after admission to the emergency department (ED), and if there is a prognostic relevance of septic cardiomyopathy defined by ACP. Results were compared to cardiac index (CI) and cardiac power index (CPI). Methods: Adults presenting at the ED with sepsis were included. ACP, CI and CPI were calculated at the time of admission, after 24, and 72 h. They were correlated to severity of disease and the prognostic values were analyzed. Results: A total of 141 patients were included. Only ACP was significantly influenced by severity of sepsis, whereas CI and CPI were not. ACP was the only hemodynamic parameter predicting mortality: nonsurvivors had lower ACP values at the time of admission to the ED (66.9 vs. 88.9 %, p < 0.05) and ACP predicted non-survival with an AUC value of 0.72, p = 0.003. Cardiac impairment defined by an ACP value of 80 % or below determined worse prognosis. Conclusions: Septic cardiomyopathy occurs already at the early stage of disease and is of prognostic relevance. It might be recognized best, if cardiac function is correlated to afterload.
    No preview · Article · Jun 2013 · Clinical Research in Cardiology
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    ABSTRACT: Various strategies have been devised to reduce the clinical consequences of myocardial infarction including acute medical care, revascularization, stem cell transplantations and, more recently, prevention of cardiomyocyte cell death. Activation of embryonic signaling pathways is a particularly interesting option to complement these strategies and to improve the functional performance and survival rate of cardiomyocytes. Here, we have concentrated on Bone Morphogenetic Protein 2 (BMP-2), which induces ectopic formation of beating cardiomyocytes during development in the mesoderm and protects neonatal cardiomyocytes from ischemia-reperfusion injury.In a mouse model of acute myocardial infarction an i.v.-injection of BMP-2 reduced infarct size in mice when given after LAD-ligation. BMP-2 treated mice are characterized by a reduced rate of apoptotic cardiomyocytes both in the border zone of the infarcts and in the remote myocardium. In vitro, BMP2 increases the frequency of spontaneously beating neonatal cardiomyocytes and the contractile performance under electrical pacing at 2 Hz and at the same time preserves cellular ATPstores and decreases the rate of apoptosis despite the increased workload. BMP-2 specifically induced phosphorylation of Smad1/5/8 proteins and protects adult cardiomyocytes from long-lasting hypoxia-induced cellular damage and oxidative stress without activation of the cardiodepressant TGFß-pathway.Our data suggest that BMP-2 treatment may have considerable therapeutic potential in individuals with acute and chronic myocardial ischemia by improving the contractility of cardiomyocytes and preventing cardiomyocyte cell death.
    No preview · Article · Jan 2013 · Shock (Augusta, Ga.)
  • J. Schröder · H. Ebelt · K. Werdan · U. Müller-Werdan
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    ABSTRACT: This article presents clinically relevant papers, trials and guidelines from the field of intensive care and emergency medicine published 2011 and 2012.
    No preview · Article · Jan 2013 · Intensiv- und Notfallbehandlung

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Institutions

  • 2015
    • University Hospital RWTH Aachen
      Aachen, North Rhine-Westphalia, Germany
  • 1970-2015
    • Martin Luther University Halle-Wittenberg
      • • Institute for Physiological Chemistry
      • • Clinic for Internal Medicine III
      • • Institute for Human Genetics and Medical Biology
      • • Clinic for Ophthalmology
      • • Institute for Pathology
      Halle-on-the-Saale, Saxony-Anhalt, Germany
  • 2004-2013
    • Universitätsklinikum Halle (Saale)
      Halle-on-the-Saale, Saxony-Anhalt, Germany
  • 2012
    • Diakonissenkrankenhaus Dessau
      Dessau, Saxony-Anhalt, Germany
  • 2001
    • Hannover Medical School
      Hanover, Lower Saxony, Germany
  • 1995-1996
    • Ludwig-Maximilians-University of Munich
      • Department of Internal Medicine I
      München, Bavaria, Germany
    • Karl-Franzens-Universität Graz
      Gratz, Styria, Austria