Differential antiplatelet effects of angiotensin converting enzyme inhibitors |
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Authors: | Dr. Dirk Skowasch Achim Viktor Melanie Schneider-Schmitt Prof. Dr. Dr. h.c. Berndt Lüderitz Prof. Dr. Georg Nickenig Prof. Dr. Gerhard Bauriedel |
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Affiliation: | Department of Internal Medicine II, Cardiology, Heart Center University of Bonn, Sigmund-Freud-Str. 25, 53105 Bonn, Germany. Dirk.Skowasch@ukb.uni-bonn.de |
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Abstract: | BACKGROUND: Increasing evidence suggests that angiotensin converting enzyme (ACE) inhibitors exert antithrombotic effects. Based on the assumption of differential effects of various ACE inhibitors on coagulation, the aim of the present study was to evaluate the coagulative activities of cardiovascular (CV) patients treated with either ramipril, captopril, and enalapril, and to compare these with patients treated with established antithrombotics such as aspirin (ASA) and clopidogrel or none of these medication. METHODS: Blood samples of 320 CV patients with coronary artery disease and/or arterial hypertension were analyzed by wholeblood aggregometry. Platelet aggregation was determined by measuring the increase in impedance across paired electrodes in response to the aggregatory agents collagen and adenosine diphosphate (ADP), respectively. These data were correlated with medical treatment. RESULTS: Platelet aggregation was attenuated ex vivo by ramipril and captopril as well as by ASA and clopidogrel. While collagen-induced platelet aggregation was significantly reduced by ramipril (35%; P <0.01) and captopril (27%; P = 0.01), no change was seen with enalapril. After induction with ADP, platelet aggregation was reduced in the presence of captopril therapy by 46% (P <0.05). There was a trend of inhibition with ramipril (32%, P = n.s.), whereas no antithrombotic effect was seen with enalapril. CONCLUSION: Our findings demonstrate that ACE inhibitors decrease platelet aggregation ex vivo. The differential antiaggregatory profile may explain at least in part different effects of ACE inhibitors on cardiovascular endpoints as observed in large clinical trials. |
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