Abstract
Cilostazol Decreases Endothelin-1 Level in Patients with an Acute Coronary Syndrome: A Prospective Study
Highlights
Endothelial dysfunction is associated with an imbalance between Nitric Oxide (NO) and Endothelin-1 (ET-1), which has been found to be involved in the pathogenesis of Acute Coronary Syndrome (ACS)
NO concentration was similar in patients receiving cilostazol or aspirin (85.30 ± 30.46 vs. 84.57 ± 29.86 μmol/L, P =0.89)
Cilostazol decreases ET-1concentration in ACS patients compared with aspirin
Summary
Endothelial dysfunction is associated with an imbalance between Nitric Oxide (NO) and Endothelin-1 (ET-1), which has been found to be involved in the pathogenesis of ACS. Cilostazol is a selective inhibitor of phosphodiesterase type III that inhibits platelet aggregation. The superior clinical benefit of cilostazol over aspirin suggests that the drug has non-plateletdirected properties. Animal and in vitro models suggested that the “pleiotropic” properties of cilostazol may be related to its “endothelial protection” effects. Whether cilostazol can influence plasma markers of endothelial dysfunction in real-world patients is still unknown
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