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排序方式: 共有2076条查询结果,搜索用时 15 毫秒
51.
Ovidiu Chioncel John Parissis Alexandre Mebazaa Holger Thiele Steffen Desch Johann Bauersachs Veli‐Pekka Harjola Elena‐Laura Antohi Mattia Arrigo Tuvia B. Gal Jelena Celutkiene Sean P. Collins Daniel DeBacker Vlad A. Iliescu Ewa Jankowska Tiny Jaarsma Kalliopi Keramida Mitja Lainscak Lars H Lund Alexander R. Lyon Josep Masip Marco Metra Oscar Miro Andrea Mortara Christian Mueller Wilfried Mullens Maria Nikolaou Massimo Piepoli Susana Price Giuseppe Rosano Antoine Vieillard‐Baron Jean M. Weinstein Stefan D. Anker Gerasimos Filippatos Frank Ruschitzka Andrew J.S. Coats Petar Seferovic 《European journal of heart failure》2020,22(8):1315-1341
Cardiogenic shock (CS) is a complex multifactorial clinical syndrome with extremely high mortality, developing as a continuum, and progressing from the initial insult (underlying cause) to the subsequent occurrence of organ failure and death. There is a large spectrum of CS presentations resulting from the interaction between an acute cardiac insult and a patient's underlying cardiac and overall medical condition. Phenotyping patients with CS may have clinical impact on management because classification would support initiation of appropriate therapies. CS management should consider appropriate organization of the health care services, and therapies must be given to the appropriately selected patients, in a timely manner, whilst avoiding iatrogenic harm. Although several consensus‐driven algorithms have been proposed, CS management remains challenging and substantial investments in research and development have not yielded proof of efficacy and safety for most of the therapies tested, and outcome in this condition remains poor. Future studies should consider the identification of the new pathophysiological targets, and high‐quality translational research should facilitate incorporation of more targeted interventions in clinical research protocols, aimed to improve individual patient outcomes. Designing outcome clinical trials in CS remains particularly challenging in this critical and very costly scenario in cardiology, but information from these trials is imperiously needed to better inform the guidelines and clinical practice. The goal of this review is to summarize the current knowledge concerning the definition, epidemiology, underlying causes, pathophysiology and management of CS based on important lessons from clinical trials and registries, with a focus on improving in‐hospital management. 相似文献
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Nils Bomer Niels Grote Beverborg Martijn F. Hoes Koen W. Streng Mathilde Vermeer Martin M. Dokter Jan IJmker Stefan D. Anker John G.F. Cleland Hans L. Hillege Chim C. Lang Leong L. Ng Nilesh J. Samani Jasper Tromp Dirk J. van Veldhuisen Daan J. Touw Adriaan A. Voors Peter van der Meer 《European journal of heart failure》2020,22(8):1415-1423
54.
A Mocroft B Neesgard R Zangerle A Rieger A Castagna V Spagnuolo A Antinori FC Lampe M Youle JJ Vehreschild C Mussini V Borghi J Begovac C Duvivier HF Gunthard A Rauch J Tiraboschi N Chkhartishvili N Bolokadze F Wit JC Wasmuth S De Wit C Necsoi C Pradier V Svedhem C Stephan K Petoumenos H Garges F Rogatto L Peters L Ryom 《HIV medicine》2020,21(9):599-606
55.
Renhai Cao Hong Ji Ninghan Feng Yin Zhang Xiaojuan Yang Patrik Andersson Yuping Sun Katerina Tritsaris Anker Jon Hansen Steen Dissing Yihai Cao 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(39):15894-15899
Interplay between various lymphangiogenic factors in promoting lymphangiogenesis and lymphatic metastasis remains poorly understood. Here we show that FGF-2 and VEGF-C, two lymphangiogenic factors, collaboratively promote angiogenesis and lymphangiogenesis in the tumor microenvironment, leading to widespread pulmonary and lymph-node metastases. Coimplantation of dual factors in the mouse cornea resulted in additive angiogenesis and lymphangiogenesis. At the molecular level, we showed that FGFR-1 expressed in lymphatic endothelial cells is a crucial receptor that mediates the FGF-2–induced lymphangiogenesis. Intriguingly, the VEGFR-3–mediated signaling was required for the lymphatic tip cell formation in both FGF-2– and VEGF-C–induced lymphangiogenesis. Consequently, a VEGFR-3–specific neutralizing antibody markedly inhibited FGF-2–induced lymphangiogenesis. Thus, the VEGFR-3–induced lymphatic endothelial cell tip cell formation is a prerequisite for FGF-2–stimulated lymphangiogenesis. In the tumor microenvironment, the reciprocal interplay between FGF-2 and VEGF-C collaboratively stimulated tumor growth, angiogenesis, intratumoral lymphangiogenesis, and metastasis. Thus, intervention and targeting of the FGF-2– and VEGF-C–induced angiogenic and lymphangiogenic synergism could be potentially important approaches for cancer therapy and prevention of metastasis. 相似文献
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58.
Stephan von Haehling Joerg C. Schefold Ewa A. Jankowska Jochen Springer Ali Vazir Paul R. Kalra Anja Sandek Günter Fauler Tatjana Stojakovic Michael Trauner Piotr Ponikowski Hans-Dieter Volk Wolfram Doehner Andrew J.S. Coats Philip A. Poole-Wilson Stefan D. Anker 《Journal of the American College of Cardiology》2012
59.
Vincent JJ Odekerken Teus van Laar Michiel J Staal Arne Mosch Carel FE Hoffmann Peter CG Nijssen Guus N Beute Jeroen PP van Vugt Mathieu WPM Lenders M Fiorella Contarino Marieke SJ Mink Lo J Bour Pepijn van den Munckhof Ben A Schmand Rob J de Haan P Richard Schuurman Rob MA de Bie 《Lancet neurology》2013,12(1):37-44
60.
PS Spencer K Vandemaele M Richer VS Palmer S Chungong M Anker Y Ayana ML Opoka BN Klaucke A Quarello JK Tumwine 《African health sciences》2013,13(2):183-204