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Klein H.H.,Kohler | Kramer A.,Kardiologische Praxis Siegen | Pieske B.M.,Medizinische Universitatsklinik Graz | Trappe H.-J.,Ruhr University Bochum | De Vries H.,Landgericht Bonn

The general rules governing participation in road traffic in Germany are defined in the driver's license law. Attending physicians are obligated to determine if a patient lacks the ability to drive from the perspective of their medical specialty. This assessment must be documented. In addition to the legal requirements laid down in the driver's license law, the driving ability of patients with cardiovas-cular diseases is covered in the guideline on expert opinions appraising driving capability as specified by the Advisory Board for Traffic Medicine. Since the driver's license law only addresses a few cardiovascular disorders and the guideline on expert opinions no longer reflects the current standard of medical knowledge, a position paper on fitness to drive and cardiovascular diseases was formulated on behalf of the German Cardiac Society. Taking the current level of knowledge into consideration, this position paper describes the conditions when cardiac arrhythmias, syncopes, coronary heart disease, cardiac insufficiency, and arterial hypertension represent grounds for establishing temporary or permanent inability to drive. © Deutsche Gesellschaft für Kardiologie - Herz- und Kreislaufforschung e.V. Source

Ventricular arrhythmias are very common in the general population with a prevalence of 1-75[%], depending on the duration of ECG registration. The prognosis in apparently healthy people is mostly excellent. The diagnosis of a heart disease plays a major role in the estimation of prognosis in patients with frequent premature ventricular complexes (PVCs). In general we distinguish between benign and malignant forms of PVCs. Benign forms are mostly monomorphic and have their origin in the right or left ventricular outflow tract or the fascicle of the his-pukinje system. In spite of the benign character frequent PVCs can lead to a tachycardia induced cardiomyopathy. Rare and asymptomatic benign PVCs need no therapies. In Patients with symptomatic and frequent PVCs an antiarrhythmic therapy with class 1, 2, 3 or 4 can be necessary. Catheter ablation is another excellent therapeutic option. Malignant PVCs are often polymorphic, genetically determined and associated with a high risk of sudden cardiac death. In these patients the implantation of a defi brillator can be considered. Source

Weitgasser R.,Abteilung fur Innere Medizin | Weitgasser R.,Paracelsus Medical University | Abrahamian H.,Internistisches Zentrum | Clodi M.,Interne Abteilung | And 3 more authors.
Wiener Klinische Wochenschrift

Exocrine pancreatic insufficiency (EPI) in diabetic patients is frequent. Studies based on fecal elastase-1 measurement give prevalence rates of 10‒30 % of severe and 22‒56 % of moderate EPI in type 1 and rates of 5‒46 % in type 2 diabetic patients. Nevertheless, not all patients report typical symptoms like diarrhea, steatorrhea and weight loss. For noninvasive testing the determination of fecal elastase-1 has the highest sensitivity and specificity. This test should be performed at least in all symptomatic patients. As differential diagnosis celiac disease (with a prevalence of about 3–5 % of type 1 diabetic patients), autonomic neuropathy, but also diseases like irritable bowel syndrome and gastrointestinal tumors have to be taken into account. Patients with symptoms and a fecal elastase-1 < 100 µg/g should be treated with pancreatic enzymes in adequate daily doses administered at main meals. Treatment improves symptoms significantly, supply with fat soluble vitamins is normalised, risk for osteoporosis is reduced. However, improvement of glucose metabolism has not been demonstrated consistently. A pancreatogenic diabetes, also termed as type 3c diabetes, has not necessarily to be treated with insulin, often—at least initially—treatment with oral antidiabetic drugs is sufficient. © 2016, Springer-Verlag Wien. Source

Auer A.,FH Joanneum University of Applied Sciences | Pail E.,FH Joanneum University of Applied Sciences | Toplak H.,Universitatsklinik For Innere Medizin | Hammer J.,Medical University of Vienna | And 2 more authors.
Journal fur Gastroenterologische und Hepatologische Erkrankungen

Background: Low-FODMAP diet is based on the concept of reducing fermentable, short-chain carbohydrates in order to alleviate unspecific gastrointestinal symptoms, primarily concerning the irritable bowel syndrome (IBS). Methods: Unsystematic literature research and a pilot study were conducted. Over the period June 2014 to October 2014 ten patients with gastrointestinal symptoms (ROME III criteria) were included in the study. The treatment consisted of a low- FODMAP diet over a period of two weeks while patients were hospitalized, and a continuation of this diet for two months on a self-reliant basis. Validated questionnaires (IBS-SSS) were used. Results: In 10 patients the severity of abdominal pain and the severity of flatulence was reduced by 85 % (p = .01) and 75 % (p = .004), respectively. Satisfaction with stool habits was improved by 43 % (p = .004). These results are significant and clinically relevant (measured on the VAS-scale). Improvement of the negative impacts of IBS on life in general did not reach statistical significance (p = .053). After two additional months of performing this diet on their own, all of the interviewed patients (n = 5) still followed the low-FODMAP diet on a daily basis. Summary: The results are comparable to the current state of relevant studies; however, there is yet a lack of randomised controlled studies. In uncontrolled studies few patients are necessary to show significant effects due to large effect sizes. The content of FODMAP is not yet known for many food items, which is why exposure limits for a low- FODMAP diet are based on experience. It seems advisable to establish the diet gradually. Conclusion: A low-FODMAP diet can reduce IBS symptoms. Source

Fischer T.H.,University of Gottingen | Eiringhaus J.,University of Gottingen | Dybkova N.,University of Gottingen | Forster A.,University of Gottingen | And 12 more authors.
European Journal of Heart Failure

Methods and results Western blots showed a significantly increased expression (by 54 ± 9%) and autophosphorylation at Thr286 (by 129 ± 29%, P < 0.05 each) of CaMKII in HF compared with healthy myocardium. However, no significant difference could be detected in ICM compared with DCM as to the expression and autophosphorylation of CaMKII nor the phosphorylation of the target sites ryanodine receptor 2 (RyR2)-S2809, RyR2-S2815, and phospholamban-Thr17. Isolated human cardiomyocytes (CMs) of patients with DCM and ICM showed a similar frequency of diastolic Ca2+ sparks (confocal microscopy) as well as of major arrhythmic events (Ca2+ waves, spontaneous Ca2+ transients). Despite a slightly smaller size of Ca2+ sparks in DCM (P < 0.01), the calculated SR Ca2+ leak [Ca2+ spark frequecy (CaSpF) × amplitude × width × duration] did not differ between CMs of ICM vs. DCM. Importantly, CaMKII inhibition by autocamide-2-related inhibitory peptide (AIP, 1 μmol/L) reduced the SR Ca2+ leak by 80% in both aetiologies (P < 0.05 each) and effectively decreased the ratio of arrhythmic cells (P < 0.05). Conclusion Functional and molecular measures of the SR Ca2+ leak are comparable in human ICM and DCM. CaMKII is equally responsible for the induction of the 'RyR2 leakiness' in both pathologies. Thus, CaMKII inhibition as a therapeutic measure may not be restricted to patients suffering from DCM but rather may be beneficial for the majority of HF patients.Aims The sarcoplasmic reticulum (SR) Ca2+ leak is an important pathomechanism in heart failure (HF). It has been suggested that Ca2+/calmodulin-dependent protein kinase II (CaMKII) is only relevant for the induction of the SR Ca2+ leak in non-ischaemic but not in ischaemic HF. Therefore, we investigated CaMKII and its targets as well as the functional effects of CaMKII inhibition in human ischaemic cardiomyopathy (ICM, n = 37) and dilated cardiomyopathy (DCM, n = 40). © 2014 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology. Source

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