General mechanisms of coagulation and targets of anticoagulants (Section I). Position Paper of the ESC Working Group on Thrombosis--Task Force on Anticoagulants in Heart Disease

TY - JOUR

T1 - General mechanisms of coagulation and targets of anticoagulants (Section I). Position Paper of the ESC Working Group on Thrombosis--Task Force on Anticoagulants in Heart Disease

AU - De Caterina, Raffaele

AU - Husted, Steen

AU - Wallentin, Lars

AU - Andreotti, Felicita

AU - Arnesen, Harald

AU - Bachmann, Fedor

AU - Baigent, Colin

AU - Huber, Kurt

AU - Jespersen, Jørgen

AU - Kristensen, Steen Dalby

AU - Lip, Gregory Y.H.

AU - Morais, João

AU - Rasmussen, Lars Hvilsted

AU - Siegbahn, Agneta

AU - Verheugt, Freek W A

AU - Weitz, Jeffrey I

AU - European Society of Cardiology Working Group on Thrombosis Task Force on Anticoagulants in Heart Disease

PY - 2013/4

Y1 - 2013/4

N2 - Contrary to previous models based on plasma, coagulation processes are currently believed to be mostly cell surface-based, including three overlapping phases: initiation, when tissue factor-expressing cells and microparticles are exposed to plasma; amplification, whereby small amounts of thrombin induce platelet activation and aggregation, and promote activation of factors (F)V, FVIII and FXI on platelet surfaces; and propagation, in which the Xase (tenase) and prothrombinase complexes are formed, producing a burst of thrombin and the cleavage of fibrinogen to fibrin. Thrombin exerts a number of additional biological actions, including platelet activation, amplification and self-inhibition of coagulation, clot stabilisation and anti-fibrinolysis, in processes occurring in the proximity of vessel injury, tightly regulated by a series of inhibitory mechanisms. "Classical" anticoagulants, including heparin and vitamin K antagonists, typically target multiple coagulation steps. A number of new anticoagulants, already developed or under development, target specific steps in the process, inhibiting a single coagulation factor or mimicking natural coagulation inhibitors.

AB - Contrary to previous models based on plasma, coagulation processes are currently believed to be mostly cell surface-based, including three overlapping phases: initiation, when tissue factor-expressing cells and microparticles are exposed to plasma; amplification, whereby small amounts of thrombin induce platelet activation and aggregation, and promote activation of factors (F)V, FVIII and FXI on platelet surfaces; and propagation, in which the Xase (tenase) and prothrombinase complexes are formed, producing a burst of thrombin and the cleavage of fibrinogen to fibrin. Thrombin exerts a number of additional biological actions, including platelet activation, amplification and self-inhibition of coagulation, clot stabilisation and anti-fibrinolysis, in processes occurring in the proximity of vessel injury, tightly regulated by a series of inhibitory mechanisms. "Classical" anticoagulants, including heparin and vitamin K antagonists, typically target multiple coagulation steps. A number of new anticoagulants, already developed or under development, target specific steps in the process, inhibiting a single coagulation factor or mimicking natural coagulation inhibitors.

KW - Anticoagulants

KW - Blood Coagulation

KW - Blood Coagulation Tests

KW - Guideline Adherence

KW - Heart Diseases

KW - Humans

KW - Physician's Practice Patterns

KW - Treatment Outcome

U2 - 10.1160/TH12-10-0772

DO - 10.1160/TH12-10-0772

M3 - Journal article

C2 - 23447024

SN - 0340-6245

VL - 109

SP - 569

EP - 579

JO - Thrombosis and Haemostasis

JF - Thrombosis and Haemostasis

IS - 4

ER -