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Abstract
Ischemic stroke has been named one of the leading causes of death worldwide. Whereas numerous biological mechanisms and molecules were found to be associated with stroke, platelets are particularly contributive to its pathogenesis. Recent data indicate considerable variability in platelet phenotype which accounts for differences in platelet surface receptor function, count and reactivity. These features collectively influence both the events leading to a disease and effectiveness of antiplatelet therapies. Consequently, genetic variants predisposing to cerebrovascular diseases can be sequenced using a wide array of techniques and become a useful tool in clinical setting. In this review, we provide an outline of common platelet polymorphisms that impose risk on ischemic stroke development and should be evaluated as targets to improve treatment. As study results are often inconsistent, partly due to differences in demographic characteristics between study populations and the fact that the functional impact of these variants has been relatively small, we conclude that both rare, low-frequency and common variants might account for genetic contribution on abnormal platelet response to antiplatelet drugs.
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Financial & competing interests disclosure
The study was supported financially as part of the research grant from the Polish Ministry of Science and Higher Education “Iuventus Plus” research grant (grant number IP2014 038473).
The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.
No writing assistance was utilized in the production of this manuscript.