Journal of the American College of Cardiology

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ISSN / EISSN : 07351097 / 15583597
Current Publisher: Elsevier BV (10.1016)
Total articles ≅ 79,970
Google Scholar h5-index: 180
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Latest articles in this journal

Josephine Warren, Bronwyn A. Kingwell, Stephen J. Duffy
Journal of the American College of Cardiology, Volume 74, pp 2012-2013; doi:10.1016/j.jacc.2019.08.013

Mukul Sharma
Journal of the American College of Cardiology, Volume 74, pp 1924-1925; doi:10.1016/j.jacc.2019.08.1013

The publisher has not yet granted permission to display this abstract.
Journal of the American College of Cardiology, Volume 74; doi:10.1016/s0735-1097(19)37549-7

Marta Cortes-Canteli, Anna Kruyer, Irene Fernandez-Nueda, Ana Marcos-Diaz, Carlos Ceron, Allison T. Richards, Odella C. Jno-Charles, Ignacio Rodriguez, Sergio Callejas, Erin H. Norris, et al.
Journal of the American College of Cardiology, Volume 74, pp 1910-1923; doi:10.1016/j.jacc.2019.07.081

Abstract:Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder with important vascular and hemostatic alterations that should be taken into account during diagnosis and treatment. This study evaluates whether anticoagulation with dabigatran, a clinically approved oral direct thrombin inhibitor with a low risk of intracerebral hemorrhage, ameliorates AD pathogenesis in a transgenic mouse model of AD. TgCRND8 AD mice and their wild-type littermates were treated for 1 year with dabigatran etexilate or placebo. Cognition was evaluated using the Barnes maze, and cerebral perfusion was examined by arterial spin labeling. At the molecular level, Western blot and histochemical analyses were performed to analyze fibrin content, amyloid burden, neuroinflammatory activity, and blood–brain barrier (BBB) integrity. Anticoagulation with dabigatran prevented memory decline, cerebral hypoperfusion, and toxic fibrin deposition in the AD mouse brain. In addition, long-term dabigatran treatment significantly reduced the extent of amyloid plaques, oligomers, phagocytic microglia, and infiltrated T cells by 23.7%, 51.8%, 31.3%, and 32.2%, respectively. Dabigatran anticoagulation also prevented AD-related astrogliosis and pericyte alterations, and maintained expression of the water channel aquaporin-4 at astrocytic perivascular endfeet of the BBB. Long-term anticoagulation with dabigatran inhibited thrombin and the formation of occlusive thrombi in AD; preserved cognition, cerebral perfusion, and BBB function; and ameliorated neuroinflammation and amyloid deposition in AD mice. Our results open a field for future investigation on whether the use of direct oral anticoagulants might be of therapeutic value in AD.
Juerg Schwitter
Journal of the American College of Cardiology, Volume 74, pp 1756-1759; doi:10.1016/j.jacc.2019.07.075

The publisher has not yet granted permission to display this abstract.
Rina Ariga, Stefan Neubauer, Hugh Watkins
Journal of the American College of Cardiology, Volume 74; doi:10.1016/j.jacc.2019.08.005

Journal of the American College of Cardiology, Volume 74; doi:10.1016/s0735-1097(19)37475-3

Carlos Collet, Jeroen Sonck, Bert Vandeloo, Takuya Mizukami, Bram Roosens, Stijn Lochy, Jean-Francois Argacha, Danny Schoors, Iginio Colaiori, Giuseppe Di Gioia, et al.
Journal of the American College of Cardiology, Volume 74, pp 1772-1784; doi:10.1016/j.jacc.2019.07.072

The publisher has not yet granted permission to display this abstract.
Garima Sharma, Amy A. Sarma, Mary Norine Walsh, Sharonne N. Hayes, Sheila Sahni, Sherry-Ann Brown, Toniya Singh, Robert A. Harrington, Pamela S. Douglas, Claire S. Duvernoy
Journal of the American College of Cardiology, Volume 74, pp 1839-1842; doi:10.1016/j.jacc.2019.08.016

Mark J. Sarnak, Kerstin Amann, Sripal Bangalore, João L. Cavalcante, David M. Charytan, Jonathan C. Craig, John S. Gill, Mark A. Hlatky, Alan G. Jardine, Ulf Landmesser, et al.
Journal of the American College of Cardiology, Volume 74, pp 1823-1838; doi:10.1016/j.jacc.2019.08.1017

Abstract:Chronic kidney disease (CKD) is a major risk factor for coronary artery disease (CAD). As well as their high prevalence of traditional CAD risk factors, such as diabetes and hypertension, persons with CKD are also exposed to other nontraditional, uremia-related cardiovascular disease risk factors, including inflammation, oxidative stress, and abnormal calcium-phosphorus metabolism. CKD and end-stage kidney disease not only increase the risk of CAD, but they also modify its clinical presentation and cardinal symptoms. Management of CAD is complicated in CKD patients, due to their likelihood of comorbid conditions and potential for side effects during interventions. This summary of the Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference on CAD and CKD (including end-stage kidney disease and transplant recipients) seeks to improve understanding of the epidemiology, pathophysiology, diagnosis, and treatment of CAD in CKD and to identify knowledge gaps, areas of controversy, and priorities for research.