title: Increased platelet aggregability in response to shear stress in acute myocardial infarction and its inhibition by combined therapy with aspirin and cilostazol after coronary intervention.
abstract: Although antiplatelet therapy with a specific inhibitor of phosphodiesterase-3 cilostazol improves stent patency compared with use of aspirin (ASA) alone, the specific role of cilostazol on platelet aggregation in patients with acute myocardial infarction (AMI) is less well understood. Thirty-six patients with AMI who were successfully treated with primary angioplasty were randomized to 3 antiplatelet regimens: ASA alone (n = 12), ASA + ticlopidine (n = 12), and ASA + cilostazol (n = 12). We measured shear stress-induced platelet aggregation (SIPA) using a modified cone-plate viscometer on admission and on day 7, and evaluated the inhibitory effects of combination therapy with ASA + cilostazol on SIPA. Compared with cases of stable coronary artery disease, significant increases in SIPA and plasma von Willebrand factor activity were observed in patients with AMI before they received antiplatelet therapy. On day 7 after primary angioplasty, ASA did not inhibit SIPA (65 +/- 15% vs 57 +/- 11%, p = 0.086), whereas both combination therapies of ASA + ticlopidine and ASA + cilostazol significantly inhibited SIPA in patients with AMI (ASA + ticlopidine: 61 +/- 15% vs 45 +/- 13%, p <0. 0001; ASA + cilostazol: 64 +/- 14% vs 43 +/- 9%, p <0.005). There was a significant correlation of SIPA with adenosine diphosphate (ADP)-induced platelet aggregation (r = 0.412, p = 0.003) and with plasma von Willebrand factor activity (r = 0.461, p = 0.0008). These data suggest that patients with AMI have increased platelet aggregability in response to high shear stress. Combined antiplatelet therapy with ASA + cilostazol appears to be as effective as therapy with ASA + ticlopidine for reducing SIPA in patients with AMI who are undergoing primary angioplasty.
authors.affiliation: First Department of Internal Medicine, Mie University School of Medicine, Mie, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Tanigawa
authors.forename: M
authors.initials: M
authors.lastname: Nishikawa
authors.forename: T
authors.initials: T
authors.lastname: Kitai
authors.forename: Y
authors.initials: Y
authors.lastname: Ueda
authors.forename: T
authors.initials: T
authors.lastname: Okinaka
authors.forename: K
authors.initials: K
authors.lastname: Makino
authors.forename: M
authors.initials: M
authors.lastname: Ito
authors.forename: N
authors.initials: N
authors.lastname: Isaka
authors.forename: Y
authors.initials: Y
authors.lastname: Ikeda
authors.forename: H
authors.initials: H
authors.lastname: Shiku
authors.forename: T
authors.initials: T
authors.lastname: Nakano
mesh_terms: D000368:Aged; D001241:Aspirin / Q000627:therapeutic use; D000077407:Cilostazol; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology / Q000628:therapy; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D013777:Tetrazoles / Q000627:therapeutic use*; D013988:Ticlopidine / Q000627:therapeutic use; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D010975:Platelet Aggregation Inhibitors; D013777:Tetrazoles; D014841:von Willebrand Factor; D000077407:Cilostazol; D013988:Ticlopidine; D001241:Aspirin