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Effectiveness of antiplatelet therapy in atherosclerotic disease: comparing the ASA low-response prevalence in CVD,CAD and PAD
Authors:Saskia H Meves  Thomas Hummel  Heinz G Endres  Nora Mayböck  Andreas F C Kaiser  Kay D Schröder  Katja Rüdiger  Ursula Overbeck  Achim Mumme  Andreas Mügge  Horst Neubauer
Institution:1. Department of Neurology, St. Josef-Hospital, Ruhr University Bochum, Gudrunstra?e 56, 44791, Bochum, Germany
2. Department of Vascular Surgery, St. Josef-Hospital, Ruhr University Bochum, 44791, Bochum, Germany
3. Department of Epidemiology, Ruhr University Bochum, 44791, Bochum, Germany
4. Cardiovascular Center, St. Josef-Hospital, Ruhr University Bochum, 44791, Bochum, Germany
Abstract:Although acetylsalicylic acid (ASA, aspirin) reduces the risk of ischemic events in patients with atherosclerosis, a substantial number of incidents continue to occur. As only limited data exist we evaluated the antiplatelet effectiveness of ASA in patients with different manifestations of atherosclerosis as in cerebrovascular, coronary artery and peripheral arterial disease (CVD, CAD, PAD). For the evaluation of the antiplatelet effectiveness of ASA we used whole blood aggregometry (Chrono-log Model 590). The patients in the different subgroups received ASA 100, 200 or 500 mg daily. We analysed 737 consecutive patients: 47.5 % with CVD, 33.6 % with CAD, and 18.9 % with PAD. We identified 28.0 % of the CVD, 18.1 % of the CAD and 21.6 % of the PAD patients to be ASA low-responder (ALR). Comparing subgroups treated with 100 mg ASA, 36.4 % were ALR in the CVD group as were 13.1 % of the CAD and 21.6 % of the PAD patients. Multivariate regression analysis revealed an odds ratio for being ALR of 4.50 (95 % confidence interval (CI) 1.70–11.9) when 100 mg and of 2.97 (95 % CI 1.58–5.60) when 200 mg ASA was taken compared to a dose of 500 mg. Despite the proven benefits of antiplatelet therapy in the secondary prevention of atherosclerotic disease, current antiplatelet management is suboptimal as up to 36 % of patients failed to achieve an adequate platelet inhibitory effect. Our findings may explain, at least in part, the high rates of cardiovascular events observed in the course of atherothrombotic disease and support the need to improve antiplatelet therapy.
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