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1.
F1000Res ; 12: 806, 2023.
Article de Anglais | MEDLINE | ID: mdl-38966192

RÉSUMÉ

Background: Gastrointestinal bleeds (GIB) are associated with high morbidity and mortality, with upper GIB accounting for 20,000 deaths annually in the United States of America. Accurate risk stratification is essential in determining and differentiating high-risk versus low-risk patients, as low-risk patients have an overall better prognosis. Patients taking antithrombotics to reduce the risk of thromboembolic events have a 4% chance of developing a GIB. This then places physicians in a difficult position as they must perform a risk-and-benefit analysis of whether to reinstate antithrombotics after a major GIB. This systematic review aims to assess the general trends in time for resuming anticoagulation in the setting of upper GI bleed. Methods: A literary search of three different databases was performed by three independent reviewers. The research databases included PubMed, ScienceDirect, and ProQuest. Specific keywords were used to narrow the search and articles were screened based on inclusion and exclusion criteria. Results: Our initial search generated 11,769 potential articles and 22 articles were ultimately used for this review using specific inclusion and exclusion criteria. There is an increase in thrombotic events following a GIB if anticoagulants are not resumed. We also found that the best time to resume therapy was 15-30 days post-GIB. Conclusions: Therefore, the decision to resume anticoagulation therapy should consider the patients' medical history and should fall within 15-30 days post-GIB.


Sujet(s)
Anticoagulants , Hémorragie gastro-intestinale , Antiagrégants plaquettaires , Humains , Anticoagulants/usage thérapeutique , Anticoagulants/effets indésirables , Hémorragie gastro-intestinale/traitement médicamenteux , Hémorragie gastro-intestinale/induit chimiquement , Antiagrégants plaquettaires/usage thérapeutique , Antiagrégants plaquettaires/effets indésirables
2.
J Aging Res ; 2022: 9780067, 2022.
Article de Anglais | MEDLINE | ID: mdl-36245899

RÉSUMÉ

Vascular dementia (VD) is a neurocognitive disorder whose precise definition is still up for debate. VD generally refers to dementia that is primarily caused by cerebrovascular disease or impaired cerebral blood flow. It is a subset of vascular cognitive impairment, a class of diseases that relate any cerebrovascular injury as a causal or correlating factor for cognitive decline, most commonly seen in the elderly. Patients who present with both cognitive impairment and clinical or radiologic indications of cerebrovascular pathology should have vascular risk factors, particularly hypertension, examined and treated. While these strategies may be more effective at avoiding dementia than at ameliorating it, there is a compelling case for intensive secondary stroke prevention in these patients. Repeated stroke is related to an increased chance of cognitive decline, and poststroke dementia is connected with an increased risk of death. In general, most physicians follow recommendations for secondary stroke prevention in patients with VD, which can be accomplished by the use of antithrombotic medicines such as antiplatelets (aspirin, clopidogrel, ticlopidine, cilostazol, etc.). In individuals with a high risk of atherosclerosis and those with documented symptomatic cerebrovascular illness, antiplatelets treatment lowers the risk of stroke. While this therapy strategy of prevention and rigorous risk management has a compelling justification, there is only limited and indirect data to support it. The following systematic review examines the role of antiplatelets in the management of vascular dementia in published clinical trials and studies and comments on the current evidence available to support their use and highlights the need for further study.

3.
Thromb Res ; 212: 58-71, 2022 Apr.
Article de Anglais | MEDLINE | ID: mdl-35219933

RÉSUMÉ

Extracorporeal membrane oxygenation (ECMO) is a form of prolonged mechanical cardiopulmonary supportive therapy implemented for the survival of patients with refractory cardiac and respiratory dysfunction. Venovenous (VV) and venoarterial (VA) ECMO are both used to buy time in severe respiratory failure while VA ECMO also provides hemodynamic support. Unfortunately, the risk of developing circuit or cannula associated and systemic thrombosis in patients supported by ECMO and post circuit decannulation is a devastating complication, although the relationship between venous thromboembolism (VTE) and ECMO use has not been fully established. Due to the lack of knowledge and literature centered on this topic area, currently there are no official guidelines for prompt diagnosis by screening or to optimize prevention and treatment of VTE in this specific population. This review analyzes the relationship between ECMO and subsequent VTE. We also discuss pertinent prophylactic and therapeutic anticoagulation treatments in patients diagnosed with VTE while on ECMO along with the obstacles associated with them.


Sujet(s)
Oxygénation extracorporelle sur oxygénateur à membrane , Insuffisance respiratoire , Thromboembolisme veineux , Thrombose veineuse , Adulte , Oxygénation extracorporelle sur oxygénateur à membrane/effets indésirables , Hémodynamique , Humains , Insuffisance respiratoire/étiologie , Thromboembolisme veineux/étiologie , Thrombose veineuse/étiologie
4.
F1000Res ; 11: 466, 2022.
Article de Anglais | MEDLINE | ID: mdl-36249997

RÉSUMÉ

Background: Rheumatoid arthritis (RA) is a highly prevalent, chronic inflammatory condition of the synovial joints that affects approximately 1% of the global population. The pathogenesis of RA is predominantly inflammatory in nature, thereby accelerating the co-occurrence of other immunoinflammatory conditions such as atherosclerosis. Apart from traditional cardiovascular risk factors, RA patients possess a multitude of other factors that predispose them to early atherosclerotic disease. The aim of this systematic review is to assess the prevalence of premature atherosclerosis in RA patients and elucidate the role that proinflammatory cytokines, RA-related autoantibodies, and endothelial dysfunction play in the pathophysiology of RA-mediated atherosclerosis. We also discussed novel biomarkers that can be used to predict early atherosclerosis in RA and current guidelines used to treat RA. Methods: This review followed the PRISMA guidelines to select and analyze relevant articles. A literature search for articles was performed on February 25, 2022, through three research databases including PubMed, ProQuest, and ScienceDirect. The query used to identify relevant publications was "Rheumatoid arthritis and atherosclerosis" and the search duration was set from 2012-2022. Relevant articles were selected based on the inclusion and exclusion criteria. Results: Our initial search generated 21,235 articles. We narrowed our search according to the inclusion and exclusion criteria. After assessing eligibility based on the full content of the articles, 73 articles were ultimately chosen for this review. Conclusion: There is an increased prevalence of accelerated atherosclerosis among RA patients. We found evidence to explain the role of proinflammatory cytokines, RA-related autoantibodies, and endothelial dysfunction in the pathophysiology RA-mediated atherosclerosis. Therapies targeting either the inflammatory load or traditional CV risk-factors seem to improve vascular outcomes in RA patients. Novel markers of atherosclerosis in RA may be useful in predicting premature atherosclerosis and serve as new targets for therapeutic intervention.


Sujet(s)
Polyarthrite rhumatoïde , Athérosclérose , Humains , Athérosclérose/complications , Athérosclérose/épidémiologie , Polyarthrite rhumatoïde/complications , Facteurs de risque , Cytokines , Autoanticorps
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