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Influence of carotid atherosclerotic plaque metabolome on the embolization potential
Project IdNU22-04-00389
Main solverprof. MUDr. David Školoudík, Ph.D., FESO, FEAN
Period5/2022 - 12/2025
ProviderAgentura zdravotnického výzkumu ČR
Statesolved
AnotationLarge vessel atherosclerosis is the most common cause of ischemic stroke and the most frequent cause of death and disability worldwide. The carotid atherosclerotic plaque diagnosis has shifted from pure stenosis quantification to more detailed plaque characterization including plaque composition and microembolization potential, which allows more precise patient risk stratification and management. Development of omics technologies has enabled the metabolomic and lipidomic non-target screening of atherosclerotic plaques as well. Recently published studies revealed disruption in glutathione and purine pathways affecting redox homeostasis in atherosclerotic lesions, moreover, increased levels of lysophospholipids, sphingomyelins and ceramides were observed. Transcranial Doppler (TCD) is able to detect microembolic material (both gaseous and solid) in intracranial arteries non-invasively. Although these microemboli are clinically silent, they may be clinically important by indicating an increased risk of stroke or cognitive decline. We hypothesize that: 1/ plaque and/or plasma metabolomes (including lipidomes) differs significantly between symptomatic and asymptomatic carotid plaques causing stenosis over 50 %; 2/ plaque metabolome (including lipidome) correlates significantly with detected microembolic signals using transcranial Doppler prior to carotid endarterectomy. 3/ metabolome (including lipidome) of thromboemboli differs between patients with cardioembolic and large vessel atherosclerosis etiology of stroke whereas thromboembolus metabolome in patient with symptomatic carotid stenosis will correlate with metabolome (including lipidome) of respective unstable carotid plaque. Preliminary data were obtained, sample size calculations were performed.