RT Book, Section
A1 Romero, Maria E.
A1 Fernandez-Jimenez, Rodrigo
A1 Ladich, Elena
A1 Fuster, Valentin
A1 Ibanez, Borja
A1 Virmani, Renu
A2 Fuster, Valentin
A2 Harrington, Robert A.
A2 Narula, Jagat
A2 Eapen, Zubin J.
SR Print(0)
ID 1191187922
T1 PATHOLOGY OF MYOCARDIAL INFARCTION AND SUDDEN DEATH
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=1191187922
RD 2024/04/19
AB SummaryThis  chapter  discusses  the  pathology  of  myocardial  infarction  (MI)  and  sudden  death.  Severe  loss  of  myocardial  contractility  occurs  within  60  seconds  of  the  onset  of  ischemia;  loss  of  viability  (irreversible  injury)  takes  at  least  20-40  minutes  after  total  occlusion  of  blood  flow.  MI  has  traditionally  been  viewed  as  a  manifestation  of  necrotic  cell  death,  but  other  forms  of  cardiomyocyte  death  have  also  been  observed  in  reperfused  MI;  the  extent  to  which  the  processes  considered  to  comprise  the  spectrum  of  cell  death—necrosis,  apoptosis,  autophagy,  and  necroptosis—each  contribute  to  infarct  size  is  currently  unclear.  Collateral  circulation,  preconditioning,  and  reperfusion  can  influence  infarct  size.  If  ischemic  myocardium  is  reperfused  early,  the  degree  of  myocardial  salvage  greatly  exceeds  the  damage  associated  with  reperfusion  injury.  Myocardium  may  adapt  to  chronic  ischemia  by  decreasing  its  contractility  but  preserving  viability;  this  reversibly,  dysfunctional  tissue  is  commonly  referred  to  as  hibernating  myocardium.  Left  ventricular  remodeling  begins  within  the  first  few  hours  after  an  MI  and  continues  to  progress,  and  the  infarcted  myocardium  undergoes  rapid  turnover  during  the  first  1-2  weeks  after  MI.  MI  also  generates  a  systemic  inflammatory  response.  Histologic  evaluation  (see  accompanying  Hurst’s  Central  Illustration)  has  been  classically  considered  the  gold  standard  for  the  evaluation  of  myocardial  tissue,  but  cardiac  magnetic  resonance  has  become  the  in  vivo  gold  standard  for  quantifying  myocardial  salvage.