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Available from: Jason M Johanning, Sep 26, 2015
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    ABSTRACT: A group of 100 patients with intermittent claudication (70 male, 30 female), treated with I00 mg ASA per day, were followed over 18 months after elective percutaneous balloon angioplasty. Platelet function was monitored over a period of 12 months by corrected whole blood aggregometry (CWBA). Upon stimulation by arachidonic acid (AA), adenosine diphosphate (ADP) and collagen, CWBA-results were obtained by an electronic acquisition and evaluation system correcting for hematocrit and platelet count of the blood sample. All patients showed a completely inhibited platelet response to AA stimulation. Comparison of the CWBA-results with clinical parameters revealed that reocclusions at the site of angioplasty occurred exclusively in male patients for which CWBA failed to prove an inhibition of aggregation upon both agonists, ADP and collagen, and for these patients the risk of complication is at least 87% higher (p = 0.0093). Only 40% of male patients show the expected effect of ASA on in vitro platelet aggregation at any given point in time and CWBA is capable of predicting those male patients which are at an elevated risk of reocclusion following peripheral angioplasty.
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  • The American journal of medicine 02/2007; 120(1):1-4. DOI:10.1016/j.amjmed.2006.08.023 · 5.00 Impact Factor
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    ABSTRACT: Acute coronary syndromes and other manifestations of atherothrombotic disease are primarily caused by atherosclerotic plaque rupture or fissuring and subsequent occlusive or subocclusive thrombus formation. Platelets play a critical role in the pathophysiology of atherothrombotic disease, and aspirin is the most commonly used antiplatelet agent. Clinical trials have demonstrated the efficacy of aspirin in both primary and secondary prevention of myocardial infarction, stroke, and cardiovascular death. Despite its proven benefit, the absolute risk of recurrent vascular events among patients taking aspirin remains relatively high, an estimated 8% to 18% after two years. Therapeutic resistance to aspirin might explain a portion of this risk. Although formal diagnostic criteria and a validated method of measurement are lacking, aspirin resistance may affect between 5% and 45% of the population. Given the prevalence of cardiovascular disease, the potential impact of aspirin resistance is large. Currently, however, there are many unanswered questions regarding the biological mechanism, diagnosis, population prevalence, clinical relevance, and optimal therapeutic intervention for aspirin resistance.
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