RT Book, Section
A1 Gupta, Vedant A.
A1 Moliterno, David J.
A2 Samady, Habib
A2 Fearon, William F.
A2 Yeung, Alan C.
A2 King III, Spencer B.
SR Print(0)
ID 1146596314
T1 Antithrombin Therapies
T2 Interventional Cardiology, 2e
YR 2017
FD 2017
PB McGraw-Hill Education
PP New York, NY
SN 9780071820363
LK accesscardiology.mhmedical.com/content.aspx?aid=1146596314
RD 2023/03/27
AB Acute  coronary  artery  occlusion  is  a  dynamic  process  that  involves  three  essential  processes:  compromise  of  vascular  integrity,  platelet  activation  and  aggregation,  and  acceleration  of  the  coagulation  cascade  with  fibrin  formation.  Although  the  role  of  thrombin  (factor  IIa)  is  well  documented  in  blood  coagulation,  fibrin  formation,  and  thrombus  stabilization,  it  is  also  central  to  interplay  among  these  processes.  Angiographic,  intravascular  ultrasound  (IVUS),  and  pathologic  studies  during  acute  coronary  syndromes  (ACS)  have  helped  delineate  the  pathophysiology  of  coronary  artery  occlusion:  atherosclerotic  plaque  rupture  leads  to  release  of  tissue  factor  (TF),  which  has  broad  impact  to  stimulate  platelets  and  generate  thrombin.  TF  activates  factor  VII,  which  activates  the  common  pathway  via  the  extrinsic  pathway,  and  also  activates  factor  IX,  activating  the  intrinsic  pathway  (Fig.  15-1).1  Subsequent  generation  of  factor  Xa  leads  to  thrombin  activation.