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| http://dx.doi.org/10.5811/westjem.2014.1.20043 | DOI Listing |
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Top stories: Cardiac arrest-Patients at risk.
Heart Rhythm
January 2025
Center for Cardiac Arrest Prevention, Department of Cardiology, Smidt Heart Institute, Division of Artificial Intelligence in Medicine, Department of Medicine, Cedars-Sinai Health System, Los Angeles, California. Electronic address:
Atrial Fibrillation-Related Bradycardia and/or Bradycardia-Related Atrial Fibrillation: When and How to Intervene.
Curr Vasc Pharmacol
January 2025
Department of Cardiology, Athens University School of Medicine, Athens, Greece.
Introduction/objective: Atrial fibrillation (AF) could present with slow ventricular-response; bradycardia could facilitate the emergence of AF. The conviction that one "does not succumb" from bradycardia as an escape rhythm will emerge unless one sustains a fatal injury following syncope is in stark difference with ventricular tachyarrhythmia (VA), which may promptly cause cardiac arrest. However, this is not always the case, as a life-threatening situation may emerge during the bradycardic episode, i.
View Article and Find Full Text PDFRisk analysis of cardiovascular toxicity in patients with lymphoma treated with CD19 CAR T cells.
J Transl Med
January 2025
Department of Hematology Oncology, Affiliated Hospital of Guizhou Medical University, No. 4 Bei Jing Road, Yunyan District, Guiyang, 550004, Guizhou, China.
Background: Anti-CD19 chimeric antigen receptor (CAR) T cell therapy is a common, yet highly efficient, cellular immunotherapy for lymphoma. However, many recent studies have reported on its cardiovascular (CV) toxicity. This study analyzes the cardiotoxicity of CD19 CAR T cell therapy in the treatment of lymphoma for providing a more valuable reference for clinicians.
View Article and Find Full Text PDFMechanism of Sirtuin1-Mediated Deacetylation of p65-Mediated Ferroptosis of Hippocampal Neurons in Cerebral Injury after Cardiopulmonary Resuscitation in Rats.
Neurochem Res
January 2025
Department of Radiology, the Second Affiliated Hospital of Kunming Medical University, No.374 Yunnan-Burma Road, Wuhua District, Kunming, Yunnan, 650101, PR China.
Objective: Post-resuscitation brain injury is a common sequela after cardiac arrest (CA). Increasing sirtuin1 (SIRT1) has been involved in neuroprotection in oxygen-glucose deprivation (OGD) neurons, and we investigated its mechanism in post-cardiopulmonary resuscitation (CPR) rat brain injury by mediating p65 deacetylation modification to mediate hippocampal neuronal ferroptosis.
Methods: Sprague-Dawley rat CA/CPR model was established and treated with Ad-SIRT1 and Ad-GFP adenovirus vectors, or Erastin.
Introduction: Out-of-hospital cardiac arrest (OHCA) is a critical condition associated with high mortality rates and neurological impairment among survivors. In comatose OHCA patients who achieve return of spontaneous circulation, early risk stratification is important to inform treatment pathways and potentially improve outcomes. A range of prognostic tools have been developed to predict survival and neurological recovery.
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