Filippo Crea
doi : 10.1093/eurheartj/ehac233
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1777–1781
Yaling Han
doi : 10.1093/eurheartj/ehac002
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1782–1783
Krzysztof Dyrbus, Mariusz Gasior, Peter E Penson, Maciej Banach
doi : 10.1093/eurheartj/ehab771
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1784–1786
Domenico Corrado, Alessandro Zorzi, Cristina Basso, Gaetano Thiene
doi : 10.1093/eurheartj/ehac043
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1787–1791
Leonarda Galiuto, Massimo Massetti
doi : 10.1093/eurheartj/ehac132
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1792–1793
Ricardo Ladeiras-Lopes, Rafael Vidal-Perez, Diogo Santos-Ferreira, Michael Alexander, Lavinia Baciu, Sarah Clarke, Filippo Crea, Thomas Felix Lüscher
doi : 10.1093/eurheartj/ehac150
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1794–1798
The association between the dissemination of scientific articles on Twitter and online visibility (as assessed by the Altmetric Score) is still controversial, and the impact on citation rates has never been rigorously addressed for cardiovascular medicine journals using a randomized design. The ESC Journals Study randomized 695 papers published in the ESC Journal Family (March 2018–May 2019) for promotion on Twitter or to a control arm (with no active tweeting from ESC channels) and aimed to assess whether Twitter promotion was associated with an increase in citation rates (primary endpoint) and of the Altmetric Score. This is the final analysis including 694 articles (one paper excluded due to retraction). After a median follow-up of 994 days (interquartile range: 936–1063 days), Twitter promotion of articles was associated with a 1.12 (95% confidence interval: 1.08–1.15) higher rate of citations, and this effect was independent of the type of article. Altmetric Attention Score and number of users tweeting were positive predictors for the number of citations. A social media strategy of Twitter promotion for cardiovascular medicine papers seems to be associated with increased online visibility and higher numbers of citations.
Marios K Georgakis, Jürgen Bernhagen, Laura H Heitman, Christian Weber, Martin Dichgans
doi : 10.1093/eurheartj/ehac094
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1799–1808
Decades of research have established atherosclerosis as an inflammatory disease. Only recently though, clinical trials provided proof-of-concept evidence for the efficacy of anti-inflammatory strategies with respect to cardiovascular events, thus offering a new paradigm for lowering residual vascular risk. Efforts to target the inflammasome–interleukin-1ك–interleukin-6 pathway have been highly successful, but inter-individual variations in drug response, a lack of reduction in all-cause mortality, and a higher rate of infections also highlight the need for a second generation of anti-inflammatory agents targeting atherosclerosis-specific immune mechanisms while minimizing systemic side effects. CC-motif chemokine ligand 2/monocyte-chemoattractant protein-1 (CCL2/MCP-1) orchestrates inflammatory monocyte trafficking between the bone marrow, circulation, and atherosclerotic plaques by binding to its cognate receptor CCR2. Adding to a strong body of data from experimental atherosclerosis models, a coherent series of recent large-scale genetic and observational epidemiological studies along with data from human atherosclerotic plaques highlight the relevance and therapeutic potential of the CCL2–CCR2 axis in human atherosclerosis. Here, we summarize experimental and human data pinpointing the CCL2–CCR2 pathway as an emerging drug target in cardiovascular disease. Furthermore, we contextualize previous efforts to interfere with this pathway, scrutinize approaches of ligand targeting vs. receptor targeting, and discuss possible pathway-intrinsic opportunities and challenges related to pharmacological targeting of the CCL2–CCR2 axis in human atherosclerotic disease.
Ana Devesa, Manuel Lobo-Gonzلlez, Juan Martيnez-Milla, Belén Oliva, Inés Garcيa-Lunar, Annalaura Mastrangelo, Samuel Espaٌa, Javier Sanz, José M Mendiguren, Hector Bueno, Jose J Fuster, Vicente Andrés, Antonio Fernلndez-Ortiz, David Sancho, Leticia Fernلndez-Friera, Javier Sanchez-Gonzalez, Xavier Rossello, Borja Ibanez, Valentin Fuster
doi : 10.1093/eurheartj/ehac102
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1809–1828
Experimental studies suggest that increased bone marrow (BM) activity is involved in the association between cardiovascular risk factors and inflammation in atherosclerosis. However, human data to support this association are sparse. The purpose was to study the association between cardiovascular risk factors, BM activation, and subclinical atherosclerosis.
Peter Libby, Matthias Nahrendorf, Filip K Swirski
doi : 10.1093/eurheartj/ehac149
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1829–1831
Angela K Lucas-Herald, Augusto C Montezano, Rheure Alves-Lopes, Laura Haddow, Malika Alimussina, Stuart O’Toole, Martyn Flett, Boma Lee, S Basith Amjad, Mairi Steven, Katriona Brooksbank, Linsay McCallum, Christian Delles, Sandosh Padmanabhan, S Faisal Ahmed, Rhian M Touyz
doi : 10.1093/eurheartj/ehac112
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1832–1845
Hypogonadism is associated with cardiovascular disease. However, the cardiovascular impact of hypogonadism during development is unknown. Using hypospadias as a surrogate of hypogonadism, we investigated whether hypospadias is associated with vascular dysfunction and is a risk factor for cardiovascular disease.
Nicolle KrÙ†nkel
doi : 10.1093/eurheartj/ehac152
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1846–1848
Simon Kraler, Florian A Wenzl, Georgios Georgiopoulos, Slayman Obeid, Luca Liberale, Arnold von Eckardstein, Olivier Muller, François Mach, Lorenz Rنber, Sylvain Losdat, Martin O Schmiady, Konstantinos Stellos, Kimon Stamatelopoulos, Giovanni G Camici, Annie Srdic, Francesco Paneni, Alexander Akhmedov, Thomas F Lüscher
doi : 10.1093/eurheartj/ehac143
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1849–1860
Andrei C Sposito
doi : 10.1093/eurheartj/ehac173
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1861–1863
Andreas Edsfeldt, Maarten Swart, Pratibha Singh, Lea Dib, Jiangming Sun, Jennifer E. Cole, Inhye Park, Dania Al-Sharify, Ana Persson, Mihaela Nitulescu,Patricia Das Neves Borges, Christina Kassiteridi, Michael E. Goddard, Regent Lee, Petr Volkov, Marju Orho-Melander, Lars Maegdefessel, Jan Nilsson, Irina Udalova, Isabel Goncalves, Claudia Monaco
doi : 10.1093/eurheartj/ehab920
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1864–1877
Inflammation is a key factor in atherosclerosis. The transcription factor interferon regulatory factor-5 (IRF5) drives macrophages towards a pro-inflammatory state. We investigated the role of IRF5 in human atherosclerosis and plaque stability.
Alexandra A C Newman, Yannick Cyr, Kathryn J Moore
doi : 10.1093/eurheartj/ehac060
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1878–1880
Lars Müller, Erika Mendoza, Markus Stücker
doi : 10.1093/eurheartj/ehac162
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Page 1881
Christian-Alexander Behrendt, Raphael Twerenbold, Stefan Blankenberg
doi : 10.1093/eurheartj/ehac164
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Pages 1882–1883
Luca Oechslin, Roberto Corti, Patric Biaggi, Oliver Gaemperli
doi : 10.1093/eurheartj/ehac082
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Page 1884
Jiangyou Wang, Han Chen, Longyan Zhang
doi : 10.1093/eurheartj/ehac107
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Page 1885
doi : 10.1093/eurheartj/ehac022
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Page 1798
doi : 10.1093/eurheartj/ehac077
European Heart Journal, Volume 43, Issue 19, 14 May 2022, Page 1848
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