TY - JOUR
T1 - Pathophysiology and therapeutic modification of thrombin generation in patients with coronary artery disease
AU - Pothula, Anitha
AU - Serebruany, Victor L.
AU - Gurbel, Paula
AU - McKenzie, Marcus E.
AU - Atar, Dan
N1 - Copyright:
Copyright 2007 Elsevier B.V., All rights reserved.
PY - 2000/8/18
Y1 - 2000/8/18
N2 - Thrombin plays a central role in thrombogenesis: it activates platelets, converts fibrinogen to fibrin, and activates factor XIII, which then crosslinks and stabilizes the fibrin clot. In addition, thrombin amplifies coagulation by activating factors VIII and V, key cofactors in the generation of activated factor X and thrombin, respectively. Even platelet function is influenced by thrombin. Hence, thrombin generation is most important both in the chronic progression of coronary atherosclerotic disease and in its conversion to acute events. To date, various therapeutic approaches capitalize on this knowledge by targeting specific thrombin-related pathways. Among the successful and carefully documented pharmacologic strategies in acute or chronic coronary heart disease are the use of unfractioned heparin, low-molecular-weight heparin, thrombolysis, hirudin, and/or inhibition of thrombin generation by glycoprotein IIb/IIIa antagonists, most often utilized on top of antiplatelet therapy (e.g., with acetylsalicylic acid) and/or vitamin K antagonism. The present review provides insights into the pathophysiology of thrombin generation in coronary atherosclerosis and gives an overview over the above mentioned therapeutic thrombin modifications. (C) 2000 Elsevier Science B.V.
AB - Thrombin plays a central role in thrombogenesis: it activates platelets, converts fibrinogen to fibrin, and activates factor XIII, which then crosslinks and stabilizes the fibrin clot. In addition, thrombin amplifies coagulation by activating factors VIII and V, key cofactors in the generation of activated factor X and thrombin, respectively. Even platelet function is influenced by thrombin. Hence, thrombin generation is most important both in the chronic progression of coronary atherosclerotic disease and in its conversion to acute events. To date, various therapeutic approaches capitalize on this knowledge by targeting specific thrombin-related pathways. Among the successful and carefully documented pharmacologic strategies in acute or chronic coronary heart disease are the use of unfractioned heparin, low-molecular-weight heparin, thrombolysis, hirudin, and/or inhibition of thrombin generation by glycoprotein IIb/IIIa antagonists, most often utilized on top of antiplatelet therapy (e.g., with acetylsalicylic acid) and/or vitamin K antagonism. The present review provides insights into the pathophysiology of thrombin generation in coronary atherosclerosis and gives an overview over the above mentioned therapeutic thrombin modifications. (C) 2000 Elsevier Science B.V.
KW - (Human)
KW - Coagulation
KW - Coronary artery disease
KW - Thrombin
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U2 - 10.1016/S0014-2999(00)00440-4
DO - 10.1016/S0014-2999(00)00440-4
M3 - Review article
C2 - 10940351
AN - SCOPUS:0034683182
SN - 0014-2999
VL - 402
SP - 1
EP - 10
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
IS - 1-2
ER -