Thrombinogenesis and its pharmacological modulation in atherosclerosis.
Appearance of thrombin in circulating blood can be monitored in the clinical setting by measuring specific thrombin markers, such as fibrinopeptide A, thrombin-antithrombin III or prothrombin fragment 1 + 2. In myocardial infarction monitoring of thrombin activity is of growing clinical interest. High levels of thrombin markers indicate an increased risk to a patient with myocardial infarction. Persistent, high thrombin marker levels, despite heparin anticoagulation, point to ongoing thrombin generation that may necessitate more anticoagulation, increased antiplatelet treatment, angioplasty or, in the future, use of new antithrombotic drugs. Recently, new sensitive methods have been developed to study the reaction of thrombin generation in clotting blood. These methods permitted to demonstrate that, aspirin, contrary to several other antiplatelet drugs, delay the process of thrombin formation. Continuous dampening of thrombin formation by aspirin might be one of the mechanisms responsible for its prophylactic and therapeutic efficacy. Hypercholesterolemic subjects might profit less than others from this type of treatment, since aspirin dampening effects are not so evident in hypercholesterolemia.
Szczeklik
A
A
Jagiellonian University School of Medicine, Department of Medicine, Cracow, Poland.
Musiał
J
J
Dropiński
J
J
Krzanowski
M
M
Królikowski
W
W
Undas
A
A
Swadźba
J
J
Duplaga
M
M
Bodzoń
W
W
D000818:Animals; D001161:Arteriosclerosis / Q000188:drug therapy / Q000378:metabolism*; D003864:Depression, Chemical; D006801:Humans; D009203:Myocardial Infarction / Q000378:metabolism; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D013917:Thrombin / Q000096:biosynthesis*
D010975:Platelet Aggregation Inhibitors; D013917:Thrombin