RT Book, Section
A1 Narula, Jagat
A1 Virmani, Renu
A1 Narula, Navneet
A1 Ibanez, Borja
A1 Fuster, Valentin
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 1202443540
T1 Pathological Basis of Atherosclerotic Coronary Artery Disease
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=1202443540
RD 2024/04/18
AB Chapter  SummaryThis  chapter  describes  plaque  characteristics  contributing  to  coronary  thrombosis,  provides  mechanistic  insights  into  lesion  progression,  and  summarizes  diagnostic  imaging.  At  least  half  of  both  physiologically  and  anatomically  significant  lesions  do  not  fair  worse  with  modern  medical  therapy  than  with  revascularization,  and  it  is  likely  that  the  plaques  of  event-free  patients  are  stable  or  have  low  wall  shear  stress.  Recognition  of  high-risk  plaques  is  prudent,  and  it  is  thus  important  for  clinicians  to  understand  the  pathology  of  atherosclerotic  disease  of  coronary  arteries  (see  Fuster  and  Hurst’s  Central  Illustration).  Plaque  rupture  is  thought  to  be  responsible  for  at  least  two-thirds  of  cases  of  coronary  thrombosis  and  subsequent  acute  coronary  events,  including  sudden  death;  plaque  erosion  accounts  for  most  of  the  remaining  cases  of  thrombosis,  and  calcified  nodules  contribute  to  less  than  5%  of  adverse  outcomes.  The  importance  of  progressively  increasing  necrotic  core  burden  covered  by  thin  and  inflamed  fibrous  caps  is  highlighted.  The  rapid  enlargement  of  plaques  is  attributed  to  repeated  subclinical  plaque  rupture–thrombosis–healing  cycles.  On  the  other  hand,  fibroatheromatous,  fibrous  or  fibrocalcific  plaques  in  the  absence  of  overlying  thrombosis,  and  the  presence  of  significant  luminal  obstruction  form  the  basis  of  stable  chest  pain  syndromes.  Native  coronary  atherosclerosis  develops  over  decades  to  result  in  clinical  events  and  differs  from  clinical  events  associated  with  accelerated  vein  graft  atherosclerosis  or  in-stent  neoatherosclerosis.