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Thromboembolic complications represent the greatest danger in most neurointerventional (NIR) procedures. The sensitivity of the brain to ischemia is unmatched among organs and is tested as we access smaller intracranial vessels and implant metal constructs. Prophylactic antiplatelet therapy is used to ameliorate these risks. The term ‘resistance’ has been applied to inter-individual variability leading to persistent platelet reactivity during antiplatelet therapy or to thrombosis despite therapy.
Resistance to clopidogrel loading and maintenance dosing occurs in approximately 30–35% of patients. Multiple mechanisms are responsible including genetic polymorphisms, bioavailability, compliance and drug interactions. Recent years have seen tremendous growth in the cardiology literature about antiplatelet resistance; this has led to a Class IIb recommendation for selective genetic and platelet function testing in the current guidelines for the management of unstable angina.1 The debate about antiplatelet testing has also permeated the NIR sphere; several questions need to be sequentially addressed, however, before this practice can be uniformly adopted.
How do we determine antiplatelet resistance?
This issue remains the Achilles’ heel of determining the consequences of inadequate platelet inhibition and, many would argue, poses more questions than answers. Light transmission aggregometry (LTA) is the gold standard to ascertain platelet reactivity, but due to expense and technical logistics is not widely feasible. A variety of bedside alternatives have emerged, the pre-eminent of which is the VerifyNow (VN) assay, a point-of-care platelet function test that uses two different cartridges for aspirin (ASA) and P2Y12 inhibitors. ASA resistance, as measured in aspirin reactivity units, is rare (<5%). For assessing the effect of clopidogrel, LTA and VN-P2Y12 are reasonably correlated (r≈0.8),2 despite a likely sigmoidal rather than direct linear relationship. (By comparison, a weaker correlation exists between activated clotting time and activated partial thromboplastin time; most of us routinely use activated clotting time to dose and monitor procedural anticoagulation effects.) Do we …
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