Hypertriglyceridaemia as predictor of platelet response to aspirin in patients presenting with first ischaemic stroke
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Aspirin (ASA) may exert antiplatelet properties beyond the cyclooxygenase (COX-1) pathway. Some stroke survivors exhibit a reduced or even an absent antiplatelet response after ASA, this phenomenon being known as “aspirin resistance”, that involves insufficient control of thromboxane A2 through platelet COX-1-related mechanisms and nonplatelet/COX-1 unrelated mechanisms. COX-1-independent mechanisms may be particularly relevant in dyslipidaemic patients. This study prospectively enrolled 96 consecutive ASA users after first-ever ischaemic stroke in order to evaluate their blood lipid profile depending on their antiplatelet response to ASA determined by means of a platelet function analyzer. The poststroke duration was 3-26 months and the allowed daily ASA doses ranged from 75 to 325 mg, with a mean of 158 mg. Among the patient population, 37 were identified as low ASA responders and 59 as adequate responders. The blood lipid profile was similar between both groups excepting triglycerides, which were significantly increased in low ASA responders compared to adequate responders. The fact that hypertriglyceridaemia was associated with decreased platelet response to ASA might be related to a diminished platelet membrane fluidity associated with an inability of ASA to down-regulate such strongly protected platelets.
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