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Tenecteplase Thrombolysis for Stroke up to 24 Hours After Onset With Perfusion Imaging Selection: The CHABLIS-T II Randomized Clinical Trial.
Stroke
January 2025
Department of Neurology, National Center for Neurological Disorders, National Clinical Research Centre for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China (X.C., L.H., Y.L., Yiran Zhang, X.L., S.L., L.Y., Q.D.).
Background: Whether it is effective and safe to extend the time window of intravenous thrombolysis up to 24 hours after the last known well is unknown. We aimed to determine the efficacy and safety of tenecteplase in Chinese patients with acute ischemic stroke due to large/medium vessel occlusion within an extended time window.
Methods: Patients with ischemic stroke presenting 4.
Inhibition of nitric oxide synthase transforms carotid occlusion-mediated benign oligemia into large cerebral infarction.
Theranostics
January 2025
Department of neurology, Dongguk University Ilsan Hospital, Goyang 10326, Republic of Korea.
It remains unclear why unilateral proximal carotid artery occlusion (UCAO) causes benign oligemia in mice, yet leads to various outcomes (asymptomatic-to-death) in humans. We hypothesized that inhibition of nitric oxide synthase (NOS) both transforms UCAO-mediated oligemia into full infarction and expands pre-existing infarction. Using 900 mice, we i) investigated stroke-related effects of UCAO with/without intraperitoneal administration of the NOS inhibitor (NOSi) N-nitro-L-arginine methyl ester (L-NAME, 400 mg/kg); ii) examined the rescue effect of the NO-donor, molsidomine (200 mg/kg at 30 minutes); and iii) tested the impact of antiplatelet medications.
View Article and Find Full Text PDFTranscoronary cooling and dilution for cardioprotection during revascularisation for ST-segment elevation myocardial infarction: design and rationale of the STEMI-Cool study.
Am Heart J
December 2024
Department of cardiology, Guy's and St Thomas' NHS Foundation Trust, Harefield Hospital, London, UK; King's College London, London, UK.
Background: ST-segment elevation myocardial infarction (STEMI) is treated with immediate primary percutaneous coronary intervention (pPCI) to restore coronary blood flow in the acutely ischaemic territory, but is associated with reperfusion injury limiting the benefit of the therapy. No treatment has proven effective in reducing reperfusion injury. Transcoronary hypothermia has been tested in clinical studies and is well tolerated, but is generally established after crossing the occlusion with a guidewire therefore after initial reperfusion, which might have contributed to the neutral outcomes.
View Article and Find Full Text PDFSpontaneous Coronary Dissection Review: A Complex Picture.
Rev Cardiovasc Med
December 2024
Cardiologia, Ospedale Maggiore, 26900 Lodi, Italy.
Spontaneous coronary artery dissection (SCAD) represents a quite rare event but with potentially serious prognostic implications. Meanwhile, SCAD typically presents as an acute coronary syndrome (ACS). Despite the majority of SCAD presentation being characterized by typical ACS signs and symptoms, young age at presentation with an atypical atherosclerotic risk factor profile is responsible for late medical contact and misdiagnosis.
View Article and Find Full Text PDF-mediated clonal hematopoiesis modestly improves neurological deficits and is associated with inflammation resolution in the subacute phase of experimental stroke.
Front Cell Neurosci
December 2024
Hematovascular Biology Center, Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, Charlottesville, VA, United States.
Introduction: Recent work has revealed that clonal hematopoiesis (CH) is associated with a higher risk of numerous age-related diseases, including ischemic stroke, however little is known about whether it influences stroke outcome independent of its widespread effects on cardiovascular disease. Studies suggest that leukocytes carrying CH driver mutations have an enhanced inflammatory profile, which could conceivably exacerbate brain injury after a stroke.
Methods: Using a competitive bone marrow transplant model of -mediated CH, we tested the hypothesis that CH would lead to a poorer outcome after ischemic stroke by augmenting brain inflammation.
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