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  • Title: [Decreased platelet aggregation during angiotensin-converting enzyme inhibitor therapy. Results of a pilot study].
    Author: Skowasch D, Lentini S, Andrié R, Jabs A, Bauriedel G.
    Journal: Dtsch Med Wochenschr; 2001 Jun 15; 126(24):707-11. PubMed ID: 11446026.
    Abstract:
    BACKGROUND AND OBJECTIVE: Plaque rupture and subsequent thrombosis are key events in the complication and progression of atherosclerotic disease. Recently, the HOPE study showed a significant decrease in cardiovascular complications with the angiotensin converting enzyme (ACE) inhibitor (ramipril). To assess the therapeutic potential of this drug class, the present study evaluates the coagulative activity in cardiovascular patients with ACE inhibitors and compares these data with those of untreated patients and with those of patients taking aspirin, resp. METHODS: Blood samples from 204 patients with coronary heart disease and/or arterial hypertension were analyzed by whole-blood lumi-aggregometry. Platelet aggregation was determined by the increase in impedance across paired electrodes in response to the stimulatory agents collagen and ADP, respectively. The data were correlated with the presence or absence of ACE inhibitor and/or aspirin medication. Analogously, the coagulative potential of beta-blockers, calcium antagonists, CSE-inhibitors and nitrates were studied. RESULTS: As the central finding, study participants treated with ACE inhibitors showed a decreased platelet aggregation compared to untreated control patients, indicated by a significantly reduced increase in impedance. Platelet aggregation induced by collagen decreased by 18% (p = 0.025), that induced by ADP by 39% (p = 0.039). With aspirin medication, the collagen-induced decrease amounted to 20% (p = 0.020); no significant effect was seen by ADP stimulation. With combined intake of ACE inhibitors and aspirin, collagen-induced platelet aggregation was found markedly reduced. Platelet aggregation decreased by 26% (p = 0.003). Beta-blockers, calcium antagonists, CSE inhibitors and nitrates did not reveal a significant influence on platelet aggregation. CONCLUSIONS: ACE inhibition decreases platelet aggregation, as detected and quantified by ex vivo whole-blood aggregometry. Beyond known effects of this drug class, in particular on endothelium and fibrinolysis, antithrombotic effects may explain the positive influence on major clinical cardiovascular events.
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