Introduction: Older individuals and, in particular, individuals at risk of recurrent stroke, may be susceptible to thrombosis when participating in exercise, however, this aspect has not been well investigated.
Methods: Clot microstructure and conventional markers of thrombotic risk were determined in twenty lacunar stroke patients and fifteen healthy age-matched controls before, immediately after and 1 h after a bout of moderate intensity cycling exercise. Data were analyzed using a linear mixed model approach.
Results: At rest, clot microstructure (1.69 ± 0.07 vs. 1.64 ± 0.05, corresponding to a difference of ~ 50% in normalized clot mass; p = 0.009) and thrombocyte count (73%; p < 0.0001) were higher, and activated partial thromboplastin time was lower (18%; p = 0.0001) in stroke patients compared to age-matched controls. Acute exercise increased thrombogenic markers similarly in the two groups: incipient clot microstructure (1.69 ± 0.07 vs. 1.74 ± 0.05; p = 0.0004 and 1.64 ± 0.05 vs. 1.71 ± 0.04; p < 0.0001, for stroke and controls respectively), plasma fibrinogen (12%; p < 0.0001 and 18%; p < 0.0001, for stroke and controls respectively) and the combined coagulation factors II, VII and X (p = 0.0001 and p < 0.0001, for stroke and controls respectively).
Conclusion: The results show that exercise transiently increases the risk of blood clot formation in both stroke patients and controls, however, due to the higher baseline thrombogenicity in stroke patients, the post exercise risk of forming blood clots may be higher in this group.
Trial Registration: Registered at ClinicalTrials.gov (NCT03635177).
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http://dx.doi.org/10.1186/s12959-024-00604-9 | DOI Listing |
Zh Nevrol Psikhiatr Im S S Korsakova
January 2025
Clinical and Diagnostic Center «Medinkom Lab», Yaroslavl, Russia.
Objective: To evaluate the features of primary and recurrent stroke in men aged 18-50 years with atherothrombotic, lacunar, and cardioembolic subtypes.
Material And Methods: A total of 125 men with primary and recurrent stroke were included in the study. The main vascular risk factors and lifestyle-related risk factors were assessed.
Zh Nevrol Psikhiatr Im S S Korsakova
January 2025
Vladimirskii Moscow Regional Research and Clinical Institute, Moscow, Russia.
Objective: To investigate the structural damage in patients with aphasia in the acute phase of ischemic stroke using X-ray computed tomography (CT) scans of the brain.
Material And Methods: We examined 65 right-handed individuals in the acute stage of ischemic stroke in the left middle cerebral artery, including 39 men and 26 women aged 41 to 87 years. The patients were divided into two groups: those with aphasia (group 1, 48) and those without aphasia (group 2, 17).
Eur J Radiol
January 2025
Regional University Hospital Centre of Orléans, Diagnostic Neuroradiology Department, France. Electronic address:
Purpose: Silent brain infarcts, sometimes appearing as incidental lacunes in patients with unknown history of vascular event, are linked to dementia, gait disturbances and depression. We observed that some cavitating lacunes were only visible on b0-diffusion-weighted-imaging (b0-DWI: T2-weighted without diffusion gradients) when T2-weighted-spin-echo (T2-SE) was unavailable. We aimed to evaluate the additional value of b0-DWI in detecting cavitating lacunes.
View Article and Find Full Text PDFAnn Neurol
January 2025
Centre for Clinical Brain Sciences, Edinburgh Imaging, UK Dementia Research Institute, University of Edinburgh, Edinburgh, UK.
Objective: After a recent small subcortical infarct (RSSI), some patients develop perilesional or remote hyperintensities ('caps/tracks') to the index infarct on T2/FLAIR MRI. However, their clinical relevance remains unclear. We investigated the clinicoradiological correlates of 'caps/tracks', and their impact on long-term outcomes following RSSI.
View Article and Find Full Text PDFStroke
January 2025
Stroke Research Group, Department of Clinical Neurosciences, University of Cambridge, United Kingdom. (Z.S., E.L.H., H.S.M.).
Background: Endothelial dysfunction and inflammation have been implicated in the pathophysiology of cerebral small vessel disease (SVD). However, whether they are causal, and if so which components of the pathways represent potential treatment targets, remains uncertain.
Methods: Two-sample Mendelian randomization (MR) was used to test the association between the circulating abundance of 996 proteins involved in endothelial dysfunction and inflammation and SVD.
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