PHYSICAL EXERTION INDUCES THROMBIN FORMATION AND FIBRIN DEGRADATION IN PATIENTS WITH PERIPHERAL ATHEROSCLEROSIS

Citation
P. Mustonen et al., PHYSICAL EXERTION INDUCES THROMBIN FORMATION AND FIBRIN DEGRADATION IN PATIENTS WITH PERIPHERAL ATHEROSCLEROSIS, Arteriosclerosis, thrombosis, and vascular biology, 18(2), 1998, pp. 244-249
Citations number
42
Categorie Soggetti
Peripheal Vascular Diseas",Hematology
ISSN journal
10795642
Volume
18
Issue
2
Year of publication
1998
Pages
244 - 249
Database
ISI
SICI code
1079-5642(1998)18:2<244:PEITFA>2.0.ZU;2-J
Abstract
Sudden extreme physical stress is associated with an increased risk of myocardial infarction mainly in people with preexisting atheroscleros is. In this study we compared the effect of submaximal exercise on coa gulation and fibrinolysis in patients with peripheral arterial occlusi ve disease (PAOD) with that in healthy control subjects. Fifteen PAOD patients with intermittent claudication and 15 healthy control subject s, matched for age, sex, medication use, smoking habit, and conditioni ng, were studied. Thrombin-antithrombin III complex (TAT), D-dimer, ti ssue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI)-1 antigens (Ag), t-PA activity, and plasmin-alpha(2)-antiplasmin complex: (PAP), as well as plasma catecholamines, were measured befor e and after a treadmill exercise test. At rest, fibrinogen (3.3+/-0.5 versus sus 2.9+0.5 g/L [mean+/-SD]; P<.05), D-dimer (392+/-128 versus 271+/-113 ng/mL; P<.05), t-PA Ag (9.1+/-5.1 versus 5.5+/-1.2 ng/mL;; P <.02), and PAI-1 Ag (14.9+/-7.1 versus 7.6+/-3.8 ng/mL; P<.002) levels in plasma were markedly higher in the patient group than in the contr ol group. In patients but not in control subjects, exercise of similar intensity elevated circulating concentrations of TAT (from 3.43+1.45 to 4.83+/-2.27 ng/mL; P<.05). Exercise caused a parallel increase in D -dimer, t-PA Ag, t-PA activity, PAP, and catecholamines in both soups, whereas PAI-1 Ag remained stable. Plasma lactic acid was significantl y higher in patients after exercise and was associated with lower-limb ischemia. Compared wit healthy control subjects, patients with PAOD s howed higher t-PA Ag, PAI-I Ag, and D-dimer levels both at rest and af ter exercise. Notably, submaximal exercise on a treadmill enhanced thr ombin formation in patients with PAOD but not in the control subjects. Sudden catecholamine release and local ischemia during exercise may a ccelerate the preexisting prothrombotic potential of the atherosclerot ic vessel wall.