RT Book, Section
A1 Mohler III, Emile R.
A1 Schafer, Andrew I.
A2 Kaushansky, Kenneth
A2 Levi, Marcel
SR Print(0)
ID 1148374027
T1 Atherothrombosis: Disease Initiation, Progression, and Treatment
T2 Williams Hematology Hemostasis and Thrombosis
YR 2017
FD 2017
PB McGraw-Hill Education
PP New York, NY
SN 9781260117080
LK hemonc.mhmedical.com/content.aspx?aid=1148374027
RD 2023/09/21
AB SUMMARYThe  consequences  of  atherosclerotic  vascular  disease  are  the  leading  cause  of  morbidity  and  mortality  in  the  developed  countries  of  the  world  and  are  rapidly  approaching  that  status  in  the  developing  world.  This  chapter  reviews  the  pathologic  mechanisms  of  atherosclerotic  disease  development  and  progression  and  details  the  interaction  of  these  processes  with  the  coagulation  system.  The  earliest  morphologically  visible  lesion  of  arterial  atherosclerosis,  the  fatty  streak,  already  is  an  advanced  metabolic  and  immunologic  locus  that  manifests  as  abnormalities  of  vascular  tone,  inflammation,  cellular  growth,  and  endothelial  cell  dysfunction.  After  years  to  decades,  the  lesions  advance  to  form  plaques  that  grow  and  eventually  either  impinge  on  the  arterial  lumen  or  rupture.  Rupture  of  a  vulnerable  plaque  is  a  catastrophic  event  that,  through  activation  of  both  platelets  and  the  coagulation  cascade,  triggers  thrombosis,  which  leads  to  complete  occlusion,  and  unless  collateral  circulation  has  already  been  established,  results  in  tissue  ischemia.  Based  on  an  increased  understanding  of  the  pathogenesis  and  consequences  of  atheromatous  plaque  development  and  progression,  medical  management  of  atherothrombotic  syndromes  has  improved  and  is  reviewed  for  the  coronary,  cerebrovascular,  and  peripheral  arteries.