RT Book, Section
A1 Vilahur, Gemma
A1 Fuster, Valentín
A1 Ibanez, Borja
A2 Fuster, Valentin
A2 Narula, Jagat
A2 Vaishnava, Prashant
A2 Leon, Martin B.
A2 Callans, David J.
A2 Rumsfeld, John S.
A2 Poppas, Athena
SR Print(0)
ID 1202443605
T1 Pathogenesis of Coronary Thrombosis and Myocardial Infarction
T2 Fuster and Hurst's The Heart, 15e
YR 2022
FD 2022
PB McGraw-Hill Education
PP New York, NY
SN 9781264257560
LK accesscardiology.mhmedical.com/content.aspx?aid=1202443605
RD 2024/04/25
AB Chapter  SummaryThis  chapter  discusses  the  most  recent  advances  in  the  understanding  of  the  pathophysiology  of  vulnerable  plaque  formation  and  provides  new  insights  into  the  molecular  mechanisms  and  sequence  of  events  that  drive  thrombus  formation  at  the  culprit  site  (see  Fuster  and  Hurst’s  Central  Illustration).  High-risk  atherosclerotic  plaques  are  characterized  by  a  high  inflammatory  burden  tightly  intertwined  with  the  formation  of  leaky  neovessels  that  penetrate  from  the  adventitia,  favoring  intra-plaque  hemorrhage.  Atherosclerotic  plaque  disruption  (either  fibrous  cap  rupture  or  superficial  erosion)  exposes  thrombogenic  surfaces  that  trigger  a  complex  and  coordinated  activation  of  platelets  and  the  coagulation  system,  leading  to  thrombus  formation  and  the  perpetuation  of  the  inflammatory  response.  Recent  large-scale  clinical  trials  have  verified  the  benefits  of  anti-inflammatory  therapies  in  the  reduction  of  cardiovascular  events.  Other  factors  are  also  known  to  affect  or  modulate  thrombus  growth  either  locally  (eg,  degree  of  stenosis  and  lesion  injury,  and  fluid  dynamics)  or  systemically  (traditional  and  newly  identified  cardiovascular  risk  factors  and  extracellular  vesicles).  Further  progress  toward  better  characterization  of  rupture-prone  atherosclerotic  plaques  and  the  higher  susceptibility  to  thrombosis  (the  so-called  vulnerable  patient)  will  reduce  the  risk  of  atherothrombotic  events,  the  leading  cause  of  morbidity  and  mortality  worldwide.