RT Book, Section
A1 Falk, Erling
A1 Fuster, Valentin
A2 Fuster, Valentin
A2 Harrington, Robert A.
A2 Narula, Jagat
A2 Eapen, Zubin J.
SR Print(0)
ID 1191187295
T1 ATHEROTHROMBOSIS: DISEASE BURDEN, ACTIVITY, AND VULNERABILITY
T2 Hurst's The Heart, 14e
YR 2017
FD 2017
PB McGraw-Hill Education
PP New York, NY
SN 9780071843249
LK accessmedicine.mhmedical.com/content.aspx?aid=1191187295
RD 2024/04/19
AB SummaryThis  chapter  discusses  the  pathophysiological  development  of  atherothrombosis.  Atherothrombosis  is  the  chronic,  lipid-driven,  multifocal  inflammatory  process  of  atherosclerotic  plaque  development  (see  accompanying  Hurst’s  Central  Illustration)  and  subsequent  thrombosis.  Individual  susceptibility  to  well-known  risk  factors  for  atherothrombosis  varies  considerable,  and  better  detection  of  at-risk  individuals  may  be  achieved  by  visualizing  the  arterial  wall.  Plaques  are  very  heterogeneous  in  size  and  composition.  Many  plaques  remain  asymptomatic,  some  become  obstructive,  and  a  few,  if  any,  become  vulnerable  to  plaque  rupture  or  erosion.  The  major  determinants  of  plaque  vulnerability  seem  to  be  the  size  of  the  necrotic  core  and  the  thickness  of  the  fibrous  cap.  However,  because  of  the  complexity  of  the  processes  leading  to  plaque  vulnerability  and  susceptibility  to  thrombosis,  trying  to  predict  the  fate  and  clinical  impact  of  a  particular  plaque  may  be  futile.  Combining  knowledge  of  risk  factors  and  detection  of  overall  disease  burden,  and  treating  patients  who  are  at  highest  risk,  may  be  the  best  strategy  for  this  systemic  disease.  Inflammatory  activity  is  present  in  most,  or  all,  atherosclerotic  lesions  within  the  body  and  might  therefore  be  a  useful  marker  of  systemic  disease  activity.  Additionally,  focal  calcifications  are  very  common  in  atherosclerotic  plaques,  and  the  total  amount  of  coronary  artery  calcium  correlates  strongly  with  plaque  burden  and  is  a  strong  predictor  of  coronary  events.