D
Dave L. Dixon
Researcher at Virginia Commonwealth University
Publications - 139
Citations - 3173
Dave L. Dixon is an academic researcher from Virginia Commonwealth University. The author has contributed to research in topics: Medicine & Heart failure. The author has an hindex of 23, co-authored 113 publications receiving 1700 citations. Previous affiliations of Dave L. Dixon include Campbell University & MedStar Washington Hospital Center.
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Journal ArticleDOI
Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19.
Aldo Bonaventura,Aldo Bonaventura,Alessandra Vecchié,Lorenzo Dagna,Kimberly Martinod,Dave L. Dixon,Benjamin W. Van Tassell,Francesco Dentali,Fabrizio Montecucco,Steffen Massberg,Marcel Levi,Antonio Abbate +11 more
TL;DR: In this paper, the authors proposed that SARS-CoV-2 infection induces a process known as immunothrombosis, in which activated neutrophils and monocytes interact with platelets and the coagulation cascade, leading to intravascular clot formation in small and larger vessels.
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The CardioMetabolic Health Alliance Working Toward a New Care Model for the Metabolic Syndrome
Laurence S. Sperling,Jeffrey I. Mechanick,Ian J. Neeland,Cynthia J. Herrick,Jean-Pierre Després,Chiadi E Ndumele,Krishnaswami Vijayaraghavan,Yehuda Handelsman,Gary A. Puckrein,Maria Rosario G. Araneta,Quie K. Blum,Karen K. Collins,Stephen Cook,Nikhil V. Dhurandhar,Dave L. Dixon,Brent M. Egan,Daphne P. Ferdinand,Lawrence Herman,Scott E. Hessen,Terry A. Jacobson,Russell R. Pate,Robert E. Ratner,Eliot A. Brinton,Alan D. Forker,Laura L. Ritzenthaler,Scott M. Grundy +25 more
TL;DR: The Cardiometabolic Think Tank consensus was that the metabolic syndrome (MetS) is a complex pathophysiological state comprised of a cluster of clinically measured and typically unmeasured risk factors, is progressive in its course, and is associated with serious and extensive comorbidity as mentioned in this paper.
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Interleukin-1 Blockade in Recently Decompensated Systolic Heart Failure: Results From REDHART (Recently Decompensated Heart Failure Anakinra Response Trial)
Benjamin W. Van Tassell,Justin M. Canada,Salvatore Carbone,Cory R. Trankle,Leo F. Buckley,Claudia Oddi Erdle,Nayef Abouzaki,Dave L. Dixon,Dinesh Kadariya,Sanah Christopher,Aaron Schatz,Jessica A. Regan,Michele Viscusi,Marco Giuseppe Del Buono,Ryan Melchior,Pranav Mankad,Juan Lu,Robin Sculthorpe,Giuseppe Biondi-Zoccai,Edward J. Lesnefsky,Ross Arena,Antonio Abbate +21 more
TL;DR: In this paper, the IL-1 (interleukin-1) receptor antagonist (anakinra) could inhibit the inflammatory response and improve peak aerobic exercise capacity in patients with recently decompensated systolic heart failure.
Journal ArticleDOI
Collaborative Drug Therapy Management and Comprehensive Medication Management―2015
Sarah McBane,Anna Legreid Dopp,Andrew M. Abe,Sandra Benavides,Elizabeth A. Chester,Dave L. Dixon,Michaelia Dunn,Melissa D. Johnson,Sarah J. Nigro,Tracie Rothrock-Christian,Amy H. Schwartz,Kim Thrasher,Scot Walker +12 more
TL;DR: The clinical pharmacy discipline must continue to establish and expand its use of CDTM agreements and other collaborative privileging mechanisms to provide CMM, and continued growth in the provision of CMM by appropriately qualified clinical pharmacists in collaborative practice settings will enhance recognition of their positive impact on medication‐related outcomes.
Journal ArticleDOI
Interleukin-1 Blockade Inhibits the Acute Inflammatory Response in Patients With ST-Segment-Elevation Myocardial Infarction.
Antonio Abbate,Cory R. Trankle,Leo F. Buckley,Michael J. Lipinski,Darryn L. Appleton,Dinesh Kadariya,Justin M. Canada,Salvatore Carbone,Charlotte S. Roberts,Nayef Abouzaki,Ryan Melchior,Sanah Christopher,Jeremy Turlington,George Mueller,James P. Garnett,Christopher S. Thomas,Roshanak Markley,George F. Wohlford,Laura Puckett,Horacio Medina de Chazal,Juan Guido Chiabrando,Edoardo Bressi,Marco Giuseppe Del Buono,Aaron Schatz,Chau Vo,Dave L. Dixon,Giuseppe Biondi-Zoccai,Michael C. Kontos,Benjamin W. Van Tassell +28 more
TL;DR: In patients presenting with ST‐segment–elevation myocardial infarction, interleukin‐1 blockade with anakinra significantly reduces the systemic inflammatory response compared with placebo.