İskemik İnmede Aspirin Direncinin İnme Fenotipi Üzerine Etkisi

Abstract

Antiplatelet resistance is described as the occurrence of clinically significant trombotic events while using antiplatelet agents. Apart from this clinical description, antiplatelet resistance can be defined by the use of laboratory tests. In this study, we sought to idenfity the effect of clinical and laboratory aspirin resistance on stroke phenotype, especially from the perspective of stroke etiology. We therefore assessed in-vitro aspirin resistance using the VerifyNow system within 48 hours after symptom onset analyzed in a consecutive series of patients admitted with a diagnosis of ischemic stroke while using aspirin (n=99). We also collected clinical and demographic data from patients suffering ischemic stroke while not using aspirin (n=314) and additionaly determined aspirin resistance in a subset (n=16) of these. We identified the presence of stroke etiologies that could not be sufficiently overcome by aspirin therapy in the majority of patients admitted with ischemic stroke while using aspirin (43% cardiac embolism, 17% large artery atherosclerosis). Among aspirin users, laboratory evidence for aspirin resistance (17% based on ARU threshold of 550, 31% based on ARU threshold of 510) was not assosicated with with stroke severity, infarct size or stroke etiology. However when patients with aspirin resistance, without aspirin resistance and with no aspirin use are analyzed together, the presence of atrial fibrillation and cardioembolic stroke etiology was approximately 2.5 times more common in patients without aspirin resistance, when compared to aspirin non-users. Our findings highlight that pathopysiologic resistance, signifying the presence of etiologies that can not be efficiently treated with aspirin treatment only, plays a major role in aspirin resistance observed in the setting of ischemic stroke.