title: Hemostatic and fibrinolytic activation is less following cutting balloon angioplasty of the coronary arteries.
abstract: Recent studies have shown that percutaneous coronary intervention (PCI) activates systemic hemostatic activity, reflecting platelet activation and thrombin formation in the coronary arteries. The present study compared systemic levels of hemostatic markers induced by plain old balloon angioplasty (POBA), coronary stenting (STENT), and cutting balloon (CB) angioplasty. Sixty-one patients with stable angina pectoris, who underwent elective PCI or diagnostic coronary angiography (CAG) alone, were investigated. Patients who underwent PCI were divided into the POBA group (n = 11), the STENT group (n = 27), and the CB group (n = 11). Patients who underwent CAG alone were assigned to the CAG group (n = 12). Blood samples were collected before, 24 hours after, and 3 days after PCI or CAG. Plasma concentrations of prothrombin fragment 1+2 (F1+2), fibrinopeptide A (FPA), thrombin-antithrombin III complex (TAT), and plasminogen activator inhibitor-1 (PAI-1) were measured. In the CB group, the F1+2 (1.23 +/- 0.4 nmol/L) level 3 days after PCI was significantly smaller than that of the POBA group (2.37 +/- 0.5 nmol/L) (P < 0.05). The FPA (1.81 +/- 0.9 ng/mL), TAT (3.36 +/- 1.2 ng/mL) and PAI-1 (23.0 +/- 4.1 ng/mL) levels in the CB group 3 days after PCI were significantly smaller than those of the POBA group (P < 0.05, respectively) and STENT group (P < 0.05, respectively), but similar to the CAG group. Systemic hemostasis is activated to a greater extent after POBA and stenting than it is after CB angioplasty of the coronary arteries. This may contribute to the favorable long-term outcome of CB angioplasty.
authors.affiliation: Third Department of Internal Medicine, Toho University School of Medicine, Ohashi Hospital, Tokyo, Japan.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Namiki
authors.forename: Hiroko
authors.initials: H
authors.lastname: Toma
authors.forename: Masato
authors.initials: M
authors.lastname: Nakamura
authors.forename: Ken-Ichi
authors.initials: K
authors.lastname: Matsuda
authors.forename: Hidehiko
authors.initials: H
authors.lastname: Hara
authors.forename: Hisao
authors.initials: H
authors.lastname: Hara
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Asahara
authors.forename: Yasunari
authors.initials: Y
authors.lastname: Soumitsu
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Kobayashi
authors.forename: Tetsu
authors.initials: T
authors.lastname: Yamaguchi
mesh_terms: D000368:Aged; D000789:Angina, Unstable / Q000097:blood / Q000000981:diagnostic imaging / Q000628:therapy*; D000800:Angioplasty, Balloon / Q000379:methods*; D000990:Antithrombin III; D017023:Coronary Angiography; D005260:Female; D005342:Fibrinolysis; D005344:Fibrinopeptide A / Q000032:analysis; D006490:Hemostatics / Q000097:blood*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000097:blood; D010447:Peptide Hydrolases / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011516:Prothrombin; D015607:Stents; D013917:Thrombin / Q000032:analysis
chemical_list: D006490:Hemostatics; D010446:Peptide Fragments; D017395:Plasminogen Activator Inhibitor 1; C046193:antithrombin III-protease complex; C045879:prothrombin fragment 1.2; D005344:Fibrinopeptide A; D000990:Antithrombin III; D011516:Prothrombin; D010447:Peptide Hydrolases; D013917:Thrombin