RT Book, Section
A1 Gould, K. Lance
A1 Gewirtz, Henry
A1 Narula, Jagat
A2 Fuster, Valentin
A2 Harrington, Robert A.
A2 Narula, Jagat
A2 Eapen, Zubin J.
SR Print(0)
ID 1191187602
T1 CORONARY BLOOD FLOW AND MYOCARDIAL ISCHEMIA
T2 Hurst's The Heart, 14e
YR 2017
FD 2017
PB McGraw-Hill Education
PP New York, NY
SN 9780071843249
LK accesscardiology.mhmedical.com/content.aspx?aid=1191187602
RD 2024/04/19
AB SummaryThis  chapter  discusses  the  pathophysiology  of  coronary  thrombus  formation  (see  accompanying  Hurst’s  Central  Illustration),  which  constitutes  the  basis  of  acute  coronary  events.  The  luminal  thrombus  in  up  to  three  fourths  of  cases  may  be  secondary  to  plaque  rupture,  and  in  the  remaining  cases  it  may  result  from  plaque  erosion;  very  infrequently  calcific  nodules  may  induce  luminal  thrombosis.  Upon  plaque  rupture,  components  of  deeper  layers  of  the  plaque  are  exposed  to  the  circulating  blood,  which  leads  to  marked  platelet  aggregation.  The  nature  of  the  substrate  exposed  after  plaque  rupture  likely  determines  whether  a  nonocclusive  mural  thrombus  persists  or  whether  the  thrombus  progresses  to  become  occlusive.  Indeed,  the  atheromatous  core  of  a  plaque  is  substantially  more  active  than  other  substrates  at  triggering  thrombosis  and,  therefore,  ruptured  plaques  with  large  atheromatous  core  are  at  high  risk  of  leading  to  acute  coronary  syndromes.  The  local  geometry  at  the  site  of  damage  (degree  of  stenosis)  and  local  hemodynamic  conditions,  as  well  as  the  presence  of  circulating  systemic  factors,  also  influence  the  mechanisms  of  thrombus  formation.