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Unverdorben M.,Institute For Klinische Forschung | Kleber F.X.,Charite - Medical University of Berlin | Heuer H.,Medizinische Klinik | Figulla H.-R.,Universitatsklinikum Jena | And 9 more authors.
Clinical Research in Cardiology | Year: 2010

Background: Treatment of lesions in small coronary arteries by percutaneous transluminal coronary intervention is limited by a high recurrence rate. We assessed the use of a paclitaxel-coated balloon in this indication. Methods: One-hundred eighteen patients with stenoses in small coronary vessels were treated by a paclitaxel-coated balloon (3 μg/mm2). The main inclusion criteria encompassed diameter stenosis of ≥70% and ≤22 mm in length with a vessel diameter of 2.25-2.8 mm. Follow-up angiography was performed at scheduled 6-month post-intervention or whenever driven by clinical or electrocardiographic signs of ischemia. The primary endpoint was angiographic in-segment late lumen loss. Results: Eighty-two of 118 patients (70%) with a vessel diameter of 2.35 ± 0.19 mm were treated with the drug-coated balloon only, while 32 patients required additional stent deployment. The mean in-segment late lumen loss was 0.28 ± 0.53 mm. In patients treated with the drug-coated balloon only, the in-segment late lumen loss was 0.16 ± 0.38 mm. At 12 months, the rate of major adverse cardiac events was 15% which was primarily due to the need for target lesion revascularization in 14 patients (12%). In those with additional bare metal stent implantation geographical mismatch between coated-balloon dilatation and stent implantation was significantly associated with the occurrence of restenosis. Conclusion: Treatment of coronary stenosis in small coronary vessels with the paclitaxel-coated balloon was well tolerated. It may offer an alternative to the implantation of a drug-eluting stent (ClinicalTrials.gov Identifier: NCT00404144). © 2010 Springer-Verlag.

Werdan K.,Universitatsklinik Und Poliklinik For Innere Medizin Iii | Rub M.,Amper Kliniken AG | Delle-Karth G.,Vienna University Hospital | Geppert A.,Intensive Care Unit | Schondube F.A.,University of Gottingen
Deutsches Arzteblatt International | Year: 2012

Introduction: Infarction-related cardiogenic shock (ICS) is usually due to leftventricular pump failure. With a mortality of 30% to 80%, ICS is the most common cause of death from acute myocardial infarction. The S3 guideline presented here characterizes the current evidence-based treatment of ICS: early revascularization, treatment of shock, and intensive care treatment of multi-organ dysfunction syndrome (MODS) if it arises. The success or failure of treatment for MODS determines the outcome in ICS. Methods: Experts from eight German and Austrian specialty societies analyzed approximately 3600 publications that had been retrieved by a systematic literature search. Three interdisciplinary consensus conferences were held, resulting in the issuing of 111 recommendations and algorithms for this S3 guideline. Results: Early revascularization of the occluded vessel, usually with a percu - taneous coronary intervention (PCI), is of paramount importance. The medical treatment of shock consists of dobutamine as the inotropic agent and norepinephrine as the vasopressor of choice and is guided by a combination of pres - sure and flow values, or by the cardiac power index. Levosimendan can be given in addition to treat catecholamine-resistant shock. For patients with ICS who are treated with PCI, the current S3 guideline differs from the European and American myocardial infarction guidelines with respect to the recommendation for intra-aortic balloon pulsation (IABP): Whereas the former guidelines give a class I recommendation for IABP, this S3 guideline states only that IABP "can" be used in this situation, in view of the poor state of the evidence. Only for patients being treated with systemic fibrinolysis is IABP weakly recommended (IABP "should" be used in such cases). With regard to the optimal intensive- care interventions for the prevention and treatment of MODS, recommendations are given concerning ventilation, nutrition, erythrocyte-concentrate transfusion, prevention of thrombosis and stress ulcers, follow-up care, and rehabilitation. Discussion: The goal of this S3 guideline is to bring together the types of treatment for ICS that lie in the disciplines of cardiology and intensive-care medicine, as patients with ICS die not only of pump failure, but also (and even more frequently) of MODS. This is the first guideline that adequately emphasizes the significance of MODS as a determinant of the outcome of ICS.

Hofmann U.,University of Wurzburg | Frantz S.,Universitatsklinik Und Poliklinik For Innere Medizin Iii
Circulation Research | Year: 2015

A large body of evidence produced during decades of research indicates that myocardial injury activates innate immunity. On the one hand, innate immunity both aggravates ischemic injury and impedes remodeling after myocardial infarction (MI). On the other hand, innate immunity activation contributes to myocardial healing, as exemplified by monocytes' central role in the formation of a stable scar and protection against intraventricular thrombi after acute infarction. Although innate leukocytes can recognize a wide array of self-antigens via pattern recognition receptors, adaptive immunity activation requires highly specific cooperation between antigen-presenting cells and distinct antigen-specific receptors on lymphocytes. We have only recently begun to examine lymphocyte activation's relationship to adaptive immunity and significance in the context of ischemic myocardial injury. There is some experimental evidence that CD4+ T-cells contribute to ischemia-reperfusion injury. Several studies have shown that CD4+ T-cells, especially CD4+ T-regulatory cells, improve wound healing after MI, whereas depleting B-cells is beneficial post MI. That T-cell activation after MI is induced by T-cell receptor signaling implicates autoantigens that have not yet been identified in this context. Also, the significance of lymphocytes in humans post MI remains unclear, primarily as a result of methodology. This review summarizes current experimental evidence of lymphocytes' activation, functional role, and crosstalk with innate leukocytes in myocardial ischemia-reperfusion injury, wound healing, and remodeling after myocardial infarction. © 2014 American Heart Association, Inc.

Vogel B.,Universitatsklinikum Wurzburg | Frantz S.,Universitatsklinik Und Poliklinik For Innere Medizin Iii
Analytical biochemistry | Year: 2015

The long known toxicity of free chromatin mediated by histones regained attention after discovery of neutrophil extracellular traps (NETs). Free histones from necrotic cells or NETs can damage prokaryotic and eukaryotic cells and are responsible for the aggravation of a growing list of diseases. DNases degrade the toxic chromatin polymer to nucleosomes and efficiently reduce local high histone concentrations. Therefore, DNase activity as a biomarker is of growing interest in basic and clinical research. Here a detailed one-step protocol is presented that allows rapid and sensitive detection of DNases down to 400 fg/μl per reaction based on the detection of fluorescent ethidium bromide/DNA complexes in a 96-well plate reader. The flexible protocol uses an internal standard for background correction and allows convenient and reliable data analysis using common laboratory equipment and chemicals without elaborate preparations. The DNase activity of a sample is clearly defined by substrate amount, incubation time, and (if appropriate) a DNase standard for absolute quantification in Kunitz units per milligram sample protein. Quantitative kinetic determination is possible within less than 1h down to 5 pg DNases/μl per reaction. Copyright © 2014 Elsevier Inc. All rights reserved.

Shinagawa H.,Kitasato University | Shinagawa H.,University of Wurzburg | Frantz S.,University of Wurzburg | Frantz S.,Universitatsklinik Und Poliklinik For Innere Medizin Iii
Current Heart Failure Reports | Year: 2015

Today, innate immunity is recognized as an important pathophysiologic factor and therapeutic target for cardiac remodeling after myocardial infarction (MI). The innate immune system exerts its function via soluble and cellular components. Recently, function and kinetics of immune cells after MI have been clarified using new innovative technology. Therefore, herein, we will discuss the function of neutrophils, monocytes, and macrophages in the pathophysiology of cardiac remodeling after MI in basic as well as clinical science. © 2015, Springer Science+Business Media New York.

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