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ABSTRACT: Die Hyperkaliämie ist eine potenziell lebensbedrohliche Elektrolytabnormalität, die eine sofortige Therapie erfordert. Diese
Übersichtsarbeit soll einen Überblick über die Genese, die pathophysiologischen Zusammenhänge, die klinischen Manifestationen
und die Therapieoptionen der Hyperkaliämie geben. Therapeutisch ist v.a. zwischen der Akuttherapie der Kaliumwirkungen an
erregbaren Geweben, insbesondere am Myokard, und kaliumsenkenden Therapiemaßnahmen zu unterscheiden.
Hyperkalemia is a potentially lethal electrolyte abnormality that requires immediate initiation of therapy. This review offers
a survey of the genesis, pathophysiological aspects, clinical manifestations, and current therapeutic options in severe hyperkalemia.
Therapeutically, it has to be differentiated between acute therapy reducing the impact of potassium on excitable tissues,
especially in the myocardium, and potassium-lowering therapies.
SchlüsselwörterHyperkaliämie-Elektrolytabnormalität-Herzrhythmusstörungen-Senkung des Kaliumspiegels-Dialyse
KeywordsHyperkalemia-Electrolyte balance-Cardiac arrhythmias-Potassium-Dialysis
Intensivmedizin + Notfallmedizin 04/2012; 47(7):488-493.
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ABSTRACT: Pharmacological modulation of the glucagon-like peptide-1 (GLP-1) system has emerged as a new therapeutic option for treatment of diabetes mellitus. In addition to the glucose lowering potential GLP-1 was found to have a variety of cardioprotective effects. GLP-1 reduced the size of myocardial infarction during acute ischemia by activation of prosurvival pathways including PI3-kinase, Akt und ERK1/2. In addition, GLP-1 prevented atherosclerotic lesion formation in experimental models and improved endothelial function while acting anti-inflammatory. Furthermore GLP-1 was found to improve chronic heart failure by increasing insulin independent cellular glucose transport. Consequently GLP-1 based therapies might reduce cardiovascular events in diabetic patients which is currently evaluated in clinical endpoint studies.
Herz 03/2012; 37(3):287-93. · 0.92 Impact Factor
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ABSTRACT: Patients with type 2 diabetes have an increased risk for developing symptoms of heart failure. These can be accompanied by a reduction of left ventricular ejection fraction (HFREF, systolic heart failure) or by a preserved function (HFPEF, diastolic heart failure). The pathophysiology of both entities is distinct and involves impairment of myocardial metabolism and coronary circulation alike. Although diabetes and heart failure often coincide, the management of these patients particularly with respect to the specific benefits or possible hazards of antidiabetic treatment is vague. Therefore, from a pathophysiological as well as clinical viewpoint, 1) diabetic patients with symptoms of heart failure have to be differentiated regarding systolic as well as diastolic left ventricular function by echocardiography and tissue doppler imaging. 2) Heart failure in diabetic patients needs similar attention due to a prognosis and interactions. 3) Optimized blood glucose lowering in combination with improvement of other cardiovascular risk factors is evident for HFREF and is assumed to be beneficial for HFPEF. 4) Antidiabetic medication has to be specifically adapted for both entities. As prospective, controlled studies are scarce, future interventional studies should specifically focus on clinical outcome in diabetic patients with different entities of heart failure.
DMW - Deutsche Medizinische Wochenschrift 03/2012; 137(9):437-41. · 0.53 Impact Factor
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ABSTRACT: Cardiac biomarkers in intensive care medicine are an excellent complement to existing clinical and diagnostic information in specific diseases. Due to their lack of specificity, the diagnostic properties of common cardiac biomarkers, such as natriuretic peptides and cardiac troponins, remain ambiguous, while their prognostic value has already been proven. In addition, there are several promising new biomarkers that might contribute to a "multimarker strategy" in the critically ill patient in the future, but further evaluation is still required.
Medizinische Klinik, Intensivmedizin und Notfallmedizin. 02/2012; 107(1):17-23.
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Seppo Ylä-Herttuala,
Jacob Fog Bentzon,
Mat Daemen,
Erling Falk,
Hector M Garcia-Garcia,
Joerg Herrmann,
Imo Hoefer,
J Wouter Jukema,
Rob Krams,
Brenda R Kwak, Nikolaus Marx,
Marek Naruszewicz,
Andrew Newby,
Gerard Pasterkamp,
Patrick W J C Serruys,
Johannes Waltenberger,
Christian Weber,
Lale Tokgözoglu
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ABSTRACT: Plaque rupture and subsequent thrombotic occlusion of the coronary artery account for as many as three quarters of myocardial infarctions. The concept of plaque stabilisation emerged about 20 years ago to explain the discrepancy between the reduction of cardiovascular events in patients receiving lipid lowering therapy and the small decrease seen in angiographic evaluation of atherosclerosis. Since then, the concept of a vulnerable plaque has received a lot of attention in basic and clinical research leading to a better understanding of the pathophysiology of the vulnerable plaque and acute coronary syndromes. From pathological and clinical observations, plaques that have recently ruptured have thin fibrous caps, large lipid cores, exhibit outward remodelling and invasion by vasa vasorum. Ruptured plaques are also focally inflamed and this may be a common denominator of the other pathological features. Plaques with similar characteristics, but which have not yet ruptured, are believed to be vulnerable to rupture. Experimental studies strongly support the validity of anti-inflammatory approaches to promote plaque stability. Unfortunately, reliable non-invasive methods for imaging and detection of such plaques are not yet readily available. There is a strong biological basis and supportive clinical evidence that low-density lipoprotein lowering with statins is useful for the stabilisation of vulnerable plaques. There is also some clinical evidence for the usefulness of antiplatelet agents, beta blockers and renin-angiotensin-aldosterone system inhibitors for plaque stabilisation. Determining the causes of plaque rupture and designing diagnostics and interventions to prevent them are urgent priorities for current basic and clinical research in cardiovascular area.
Thrombosis and Haemostasis 06/2011; 106(1):1-19. · 5.04 Impact Factor
