Abstract
Even though there is a strong evidence suggestive of benefits and safety of dual (aspirin plus clopidogrel) antiplatelet therapy, decreased responsiveness or “resistance” to mono- and/or dual antiplatelet therapy has been described in association with an increased thrombotic risk. Various mechanisms contribute to antiplatelet resistance, with abundant production of inflammatory markers being of particular importance. The current review overviews implications of inflammation in antiplatelet resistance.
Keywords: Aspirin resistance, clopidogrel resistance, inflammation, platelets, aspirin, clopidogrel, megakaryocytes, ribonucleic acid, Thrombopoietin binds, adenosine, diphosphate, thromboxane A2, cyclooxygenase, plasminogen, arachidonic acid, P-selectin, matrix metalloproteinase, serine residue, vitamin K, thienopyridine, ticlodipine, P-glycoprotein, Metoprolol, cytochrome P450, polymorphisms, C-reactive protein, coronary syndrome patients, psoriatic arthritis, ankylosing spondylitis, apolipoprotein B, dyslipidemia, hypercholesterolemia, electrophoresis, mass spectrometry, glutathione-S-transferase, thrombogenesis, vascular endothelial growth factor, cilostazol, Diabetes Mellitus
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