title: Prethrombotic state due to hypercoagulability in patients with permanent transvenous pacemakers.
abstract: Venous thrombosis is a relatively usual but serious complication of permanent transvenous pacing. However, the pathogenesis has not been defined. To clarify underlying abnormalities in the coagulation-fibrinolysis system in patients with permanent transvenous pacemakers, we measured serum levels of fibrinopeptide A (FPA), thrombin-antithrombin III complexes (TATs), plasmin-alpha 2 plasmin inhibitor complexes (PICs), D-dimer (D-D), beta-thromboglobulin (beta-TG), and platelet factor 4 (PF4) in 53 patients with permanent transvenous pacemakers and 10 control subjects. The patients were divided into two groups, as follows, according to the presence of mural thrombus documented along the pacing lead(s) by digital subtraction angiography and transesophageal echocardiography: Group Th (-), patients without venous route thrombus; and Group Th (+), patients with venous route thrombus. FPA and TAT levels increased significantly even in Group Th (-), and further increased in Group Th (+) compared with control subjects (FPA: 7.5 +/- 4.9, 15.3 +/- 8.8 vs 3.0 +/- 1.4 ng/mL, respectively, P < 0.05; TAT: 2.9 +/- 1.3, 4.8 +/- 2.3 vs 1.7 +/- 0.6 ng/mL, respectively, P < 0.05). There were no differences in levels of D-D, PIG, beta-TG, and PF4 among control subjects, Group Th (-), and Group Th (+). These findings suggest that the hypercoagulable state appears in patients with permanent transvenous pacemakers, even without apparent venous thrombosis. The patients with permanent transvenous pacemakers are thought to be in the prethrombotic state even if they have no venous route thrombosis.
authors.affiliation: Division of Cardiology, Osaka Rosai Hospital, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Ito
authors.forename: J
authors.initials: J
authors.lastname: Tanouchi
authors.forename: J
authors.initials: J
authors.lastname: Kato
authors.forename: M
authors.initials: M
authors.lastname: Nishino
authors.forename: K
authors.initials: K
authors.lastname: Iwai
authors.forename: H
authors.initials: H
authors.lastname: Tanahashi
authors.forename: M
authors.initials: M
authors.lastname: Hori
authors.forename: Y
authors.initials: Y
authors.lastname: Yamada
authors.forename: T
authors.initials: T
authors.lastname: Kamada
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015901:Angiography, Digital Subtraction; D000933:Antifibrinolytic Agents / Q000097:blood; D000990:Antithrombin III / Q000032:analysis; D001777:Blood Coagulation / Q000502:physiology*; D002304:Cardiac Pacing, Artificial / Q000009:adverse effects; D017548:Echocardiography, Transesophageal; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005341:Fibrinolysin / Q000032:analysis; D005342:Fibrinolysis / Q000502:physiology; D005343:Fibrinolytic Agents / Q000097:blood; D005344:Fibrinopeptide A / Q000032:analysis; D006331:Heart Diseases / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010138:Pacemaker, Artificial / Q000009:adverse effects*; D010447:Peptide Hydrolases / Q000032:analysis; D010978:Platelet Factor 4 / Q000032:analysis; D015842:Serine Proteinase Inhibitors / Q000097:blood; D013924:Thrombophlebitis / Q000097:blood / Q000209:etiology; D013927:Thrombosis / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology*; D000979:alpha-2-Antiplasmin / Q000032:analysis; D001620:beta-Thromboglobulin / Q000032:analysis
chemical_list: D000933:Antifibrinolytic Agents; D005338:Fibrin Fibrinogen Degradation Products; D005343:Fibrinolytic Agents; D015842:Serine Proteinase Inhibitors; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; D001620:beta-Thromboglobulin; C036309:fibrin fragment D; D005344:Fibrinopeptide A; D010978:Platelet Factor 4; D000990:Antithrombin III; D010447:Peptide Hydrolases; D005341:Fibrinolysin