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Biomedical subjects

G Ertl

Publications and source records attributed to G Ertl.

At least 19 recordsLinked to original sources

[Therapy of chronic left heart failure].

Chronic heart failure is an increasingly frequent clinical syndrome, characterized by reduced physical performance, dyspnea and an adverse prognosis. It is associated with age, indicating that it will become more common. Diagnosis requires the characterization of cardiac dysfunction and a precise definition of the underlying cardiac disease. Treatment guidelines of the cardiac societies, which were updated 2005, recommend therapy with ACE-inhibitors, AT1 receptor antagonists, beta-blockers, aldosterone antagonists and digitalis. It is essential, however, to consider the individual circumstances such as underlying disease, age as well as the frequent complications and comorbidities.

Adrenergic beta-Antagonists↗

Role of p38 mitogen-activated protein kinase in cardiac remodelling.

BACKGROUND AND PURPOSE: Mitogen-activated protein kinases (MAPK) are centrally involved in several mechanisms important for heart failure such as apoptosis, activation of inflammatory responses and cell proliferation. We therefore evaluated the effect of the selective p38 MAPK inhibitor SB 239063 on progression of left ventricular remodelling after myocardial infarction (MI) in rats. EXPERIMENTAL APPROACH: Rats were treated for 9 weeks with placebo or SB 239063 by gavage (15 mg kg(-1)) twice daily starting 7 days after ligation of the left anterior descending artery. Serial transthoracic echocardiography was performed at days 7, 36 and 70. KEY RESULTS: Over the 9 weeks, mortality was not different between the groups. On echocardiography, animals after myocardial infarction exhibited significant left ventricular dilatation as expected (week 10, end-systolic diameter, placebo sham 5.21+/- 0.34 vs. placebo MI 8.44+/- 0.57 mm). However, there was no difference between placebo and SB 239063-treated rats (week 10, end-systolic diameter, SB MI 7.76+/- 0.74 mm, not significantly different from placebo MI). Haemodynamics changed accordingly. Moreover, SB 239063 had no effect on left ventricular hypertrophy. Treatment with SB 239063 significantly reduced cytokine expression of tumour necrosis factor and interleukin-1beta after myocardial infarction. However, collagen content was not influenced by the treatment. CONCLUSION: Despite a reduction of inflammation, treatment with the p38 inhibitor SB 239063 does not affect cardiac remodelling and cardiac function when treatment is started 7 days after myocardial infarction.

Animals↗

Interaction of hydrogen with RuO2(110) surfaces: activity differences between various oxygen species.

The interaction of hydrogen with RuO(2)(110) surfaces was studied by means of thermal desorption and vibration spectroscopies. The stoichiometric surface exposes two types of coordinatively unsaturated atoms: double-bonded O-bridge and five-fold-bonded Ru-cus, while at the O-rich surface the Ru-cus atoms are covered with single-bonded O-cus. On the stoichiometric RuO(2)(110) surface at 90 K, H(2) either adsorbs molecularly on Ru-cus sites or dissociates and forms with O-bridge an H(2)O-like surface group. If, in addition, also O-cus is present at the surface, hydrogen interacts exclusively with this species forming H(2)O-cus. This demonstrates that hydrogen reacts much more readily with O-cus than with O-bridge as expected from the reduced bond order and smaller binding energy of O-cus. It is furthermore shown that at surface temperatures below 90 K free coordinatively unsaturated Ru-cus sites are needed to activate the incoming H(2) molecules prior to any reaction with O-cus or O-bridge. Generally, Ru-cus sites play a key role for reactions of a number of molecules at the RuO(2)(110) surface. These findings are supported by recent DFT-based calculations but are at variance with other reports.

Journal Article↗

[Differential diagnosis of dyspnea - significance of clinic aspects, imaging and biomarkers for the diagnosis of heart failure].

Dyspnea is a frequent reason for emergency consultations in hospitals or community medical facilities. Besides heart failure, a wide variety of other disorders may cause this symptom. Thus, early and accurate differential diagnosis is mandatory in order to facilitate rapid institution of appropriate therapy. This CME article elaborates on the specific usefulness of traditional diagnostic tools as history, symptomatology and physical signs along with chest X-ray and ECG and the more recently introduced natriuretic peptides to discriminate heart failure from other causes of dyspnea in the emergency setting. According to a systematic search and meta-analysis of the respective literature, several features from history and physical examination as well as pulmonary congestion on chest X-ray, atrial fibrillation and a high level of confidence of the initial clinical judgment indicate a cardiac cause of dyspnea with high specificity, but less sensitivity. Thus, in patients presenting with one or several of these characteristic features, little further diagnostic yield is to be expected from natriuretic peptides. If, however, the suspicion of heart failure remains unsettled by these means, determination of biomarkers may be helpful, although it needs to be considered that moderately elevated levels have only a limited specificity in particular in elderly patients with comorbidities. As also recognized by the European Guidelines for diagnosis and treatment of chronic heart failure, a BNP level of <100 pg/ml has proven particularly useful for excluding heart failure. Thus, a directed history, symptoms, physical findings, chest-X-ray and ECG remain the diagnostic mainstay. If the diagnosis cannot be established by these traditional tools, BNP or NT-proBNP testing may be very helpful, especially for ruling out heart failure.

Diagnosis, Differential↗

Catalytic oxidation of ammonia on RuO2(110) surfaces: mechanism and selectivity.

The selective oxidation of ammonia to either N2 or NO on RuO2(110) single-crystal surfaces was investigated by a combination of vibrational spectroscopy (HREELS), thermal desorption spectroscopy (TDS) and steady-state rate measurements under continuous flow conditions. The stoichiometric RuO2(110) surface exposes coordinatively unsaturated (cus) Ru atoms onto which adsorption of NH3 (NH3-cus) or dissociative adsorption of oxygen (O-cus) may occur. In the absence of O-cus, ammonia desorbs completely thermally without any reaction. However, interaction between NH3-cus and O-cus starts already at 90 K by hydrogen abstraction and hydrogenation to OH-cus, leading eventually to N-cus and H2O. The N-cus species recombine either with each other to N2 or with neighboring O-cus leading to strongly held NO-cus which desorbs around 500 K. The latter reaction is favored by higher concentrations of O-cus. Under steady-state flow condition with constant NH3 partial pressure and varying O2 pressure, the rate for N2 formation takes off first, passes through a maximum and then decreases again, whereas that for NO production exhibits an S-shape and rises continuously. In this way at 530 K almost 100% selectivity for NO formation (with fairly high reaction probability for NH3) is reached.

Ammonia↗

Adsorption and interaction of ethylene on RuO2(110) surfaces.

Ethylene (C2H4) adsorbed on the stoichiometric and oxygen-rich RuO2(110) surfaces, exposing coordinatively unsaturated Ru-cus and O-cus atoms, is investigated by applying high-resolution electron energy-loss spectroscopy and thermal desorption spectroscopy in combination with isotope labeling experiments. On the stoichiometric RuO2(110) surface C2H4 adsorbs and desorbs molecularly. In contrast, on the oxygen-rich RuO2(110) surface ethylene adsorbs molecularly at 85 K and is completely oxidized through interaction with O-cus and O-bridge upon annealing to 500 K. The first couple of reactions are observed at 200 K taking place on Ru-cus: A change from pi- to sigma-bonding, formation of -C=O and -C-O groups, and dehydrogenation giving rise to H2O adsorbed at Ru-cus. Maximum reaction rate is reached for C2H4 chemisorbed at Ru-cus with O-cus neighbors on each side. A model for the first couple of reactions is sketched. For the final combustion, C2H4 reacts both with O-cus and O-bridge. Ethylene oxide is not detected under any circumstance.

Journal Article↗

[Acute heart failure and cardiogenic shock: pathophysiology, clinical aspects and management strategies].

Irrespective of improved medical and interventional therapeutic options, mortality among patients with acute heart failure and cardiogenic shock has remained disappointingly high. Early diagnosis and rapid initiation of basic treatment measures to improve hemodynamics and metabolism are of vital importance until causal therapy, e. g. revascularization, is initiated. Due to the principal difficulty to set up larger clinical trials, in patients with cardiogenic shock empirical rather than firm evidence supports the various treatment and management strategies currently in use. Continuous hemodynamic monitoring to tailor fluid therapy, new drugs, and prognostic markers have been developed for the treatment and monitoring of cardiogenic shock, all of which await testing in larger-scale studies. Ongoing challenges remain the right ventricular pump failure or hemodynamically compromising arrhythmia which may be either cause or consequence of cardiogenic shock.

Combined Modality Therapy↗

Morbus Fabry of the heart. Why should cardiologists care?

Fabry Disease is an X-linked lysosomal storage disorder leading to the accumulation of glycosphingolipids, mainly globotriaosylceramides in all tissues and solid organs of the body. The disease was described by Johannes Fabry and William Anderson coevally in 1898. Beside the involvement of the central nervous system, peripheral nerves, kidneys, skin and endovascular endothelium, the heart plays a major role in the disease. Left ventricular hypertrophy is one hallmark initially presenting with preserved ventricular function. However, with progression of the disease patients die due to heart failure. Though angina is often reported, the incidence of epicardial coronary stenosis is not a dominant feature, if at all small vessel disease can occur. In respect of arrhythmias a broad spectrum can be seen including shortened or prolonged PR-intervals, AV blocks of different degrees and sometimes malignant ventricular arrhythmias. In the past, women were considered to be carriers of the disease but hardly to develop clinical symptoms. In recent years there is evidence that female carriers may more often be affected with severe symptoms. In addition, a group of Fabry patients displaying mainly cardiac involvement were described as having a cardiac variant of the disease. This implied the hypothesis that some of those patients with unexplained myocardial hypertrophy do suffer from Fabry disease. Since 2002 enzyme replacement therapy is available and there is first evidence for its efficacy to reduce hypertrophy and increase myocardial function. If this is associated with a prognostic improvement has to be determined in future studies.

Cardiology↗

Cardiac regeneration by progenitor cells--bedside before bench?

Recent experimental and clinical trials give rise to the hope that progenitor cells could replace scar tissue after myocardial infarction with healthy functional myocardium. However, while a significant increase in left ventricular ejection fraction has been described after progenitor cell transplantation in several clinical trials, long-term results are lacking, and the mechanisms underlying the improvement of ejection fraction are unclear. Therefore, the efficacy of progenitor cell transplantation after myocardial infarction has not been established, and potential problems may have been underestimated. In-depth laboratory and animal studies are needed to determine the best cell type, optimal amount of cells, and time point for transplantation. Treatment of patients with progenitor cells outside well controlled prospective trials should be avoided.

Humans↗

Anaemia and the heart.

Anaemia is common in patients with congestive heart failure (CHF). Its prevalence increases with disease severity as a consequence of renal insufficiency, cytokine production, blood loss, iron deficiency, malnutrition and/or plasma volume overload. Anaemia can contribute to worsening of CHF. There is a nonlinear relationship (U-shaped curve) between haemoglobin and survival. Prevalence of anaemia among elderly people with acute myocardial infarction is high and is associated with more frequent in-hospital events, including death. Anaemia is also associated with higher in-hospital mortality rate after coronary bypass surgery and with all-cause and cardiac mortality after percutaneous coronary interventions. Patients with anaemia and cardiovascular disease have a higher mortality rate after cardiac/noncardiac surgery as compared to those with anaemia but without cardiovascular disease or those with cardiovascular disease but without anaemia. However, not all authors confirmed these findings. Therefore, multicentre trials to clarify this issue are urgently needed. Pleiotropic effects of recombinant human erythropoietin include reduction of myocardial and cerebral infarct size without an increase in haematocrit, neovascularization as well as mobilization of endothelial progenitor cells.

Aged↗

Inhibition of CO oxidation on RuO2(110) by adsorbed H2O molecules.

Catalytic CO oxidation on the RuO(2)(110) surface was studied at 300 K by scanning tunneling microscopy (STM), high-resolution electron-energy-loss spectroscopy (HREELS), and thermal desorption spectroscopy (TDS). Upon repeatedly exposing the surface to several 10 L of CO and O(2) at 300 K, STM shows that unreactive features accumulate with each CO and O(2) titration run. HREELS and TDS show formation of increasing amounts of H(2)O, retarded formation of O-cus atoms and incomplete removal of CO-bridge molecules during O(2) dosing, and a changing ratio of single- and double-bonded CO-bridge molecules. It is concluded that H(2)O (presumably from the residual gas) is accumulating at the Ru-cus sites thus blocking them, so that the dissociative adsorption of oxygen is prevented and the CO oxidation reaction is suppressed. Some 10% CO- bridge remains on the surface even during oxygen exposure. Consistent with this interpretation, deactivation of the surface is suppressed at 350 K, at the onset of H(2)O desorption.

Journal Article↗

Excitable CO oxidation on Pt(110) under nonuniform coupling.

A new feedback scheme for guided spatiotemporal pattern formation in reaction-diffusion systems is introduced. In contrast to previously established control methods, we present a coupling protocol that is sensitive to the presence of coherent structures in the medium. Applying this feedback to the catalytic CO oxidation on Pt(110) in both experiments and numerical simulations, we show that temporal evolution and spatial extension of self-organizing objects can be efficiently controlled.

Journal Article↗

[Diagnosis and therapy of chronic heart failure].

Incidence and prevalence of chronic heart failure are continuously increasing. Today, heart failure of different etiologies represents the most frequent cause of death in industrialized countries. Improvements in heart failure diagnosis and treatment have decreased lethality. In this context, a valid diagnosis, causative therapy of treatable heart failure etiologies, and efficient pharmacological as well as non-pharmacological management strategies are of equal importance. The principal goals of therapy are prevention, maintenance or even improvement of quality of life and the decrease of heart-failure-related morbidity and mortality.

Aged↗

Failure of recombinant human growth hormone treatment to improve congestive heart failure in hypopituitarism.

Growth hormone (GH) deficiency decreases left ventricular (LV) contractility, induces LV chamber dilatation and promotes progression to congestive heart failure. It is, however, controversial, whether GH replacement therapy in addition to standard medical heart failure therapy should be considered as routine treatment in GH deficient patients with heart failure. In the present report of a 64-year-old GH deficient patient with heart failure, we demonstrate by using Doppler echocardiography, magnetic resonance imaging and 31P NMR spectroscopy that even a 12 month period of GH replacement therapy had no sustained effect on morphometric or functional parameters of LV performance nor on clinical signs or symptoms of heart failure. It is concluded that GH replacement therapy should currently not be regarded as standard heart failure therapy in patients with GH deficiency and should only be employed under careful monitoring including close follow-up in a standardized way.

Echocardiography, Doppler↗

[The overexpression of NCAM (CD56) in human hearts is specific for ischemic damage].

The main reason for myocardial dysfunction is chronical myocardial ischemia. Recently we could show, that NCAM (CD56), a neural cell adhesion molecule and member of the immunoglobuline superfamily, and the transcription factor AML1 (RUNX1) are overexpressed in chronic ischemic human heart failure compaired to normal hearts. Here we demonstrate, that the overexpression of NCAM (CD56) is specific for ischemic damage as compaired to other heart diseases including congestive cardiomyopathy, hypertrophic obstrutive cardiomyopathy, myocarditis and sarcoidosis. Concerning the transcriptional regulation of NCAM (CD56) by AML1 (RUNX1) we isolated 3 novel isoforms of AML 1 (RUNX1) with different transactivating function, that might be a regulatory element of the NCAM (CD56) overexpression in chronical myocardial ischemia.

Adult↗