RT Book, Section
A1 George, Isaac
A1 Williams, Mathew
A2 Cohn, Lawrence H.
SR Print(0)
ID 55917917
T1 Chapter 24. Myocardial Revascularization after Acute Myocardial Infarction
T2 Cardiac Surgery in the Adult, 4e
YR 2012
FD 2012
PB The McGraw-Hill Companies
PP New York, NY
SN 978-0-07-163310-9
LK accesssurgery.mhmedical.com/content.aspx?aid=55917917
RD 2024/04/19
AB The  ability  of  surgical  interventions  to  minimize  myocardial  loss  after  myocardial  infarction  has  advanced  dramatically  over  the  past  two  decades.  Acute  myocardial  infarction  still  afflicts  approximately  1.5  million  individuals  each  year  in  the  United  States,1  and  30%  of  these  patients  die  before  reaching  the  hospital,  whereas  5%  die  during  hospital  admission.1  Prompt  medical  attention,  including  transport  to  the  hospital,  diagnosis,  and  treatment  of  the  myocardial  infarction,  is  critical  to  patient  survival.  Since  1989,  the  death  rate  from  acute  myocardial  infarctions  has  declined  24%,  while  the  actual  number  of  deaths  declined  only  7%.2  Over  the  last  40  years,  especially  during  the  1980s,  new  pharmacologic  agents,  interventional  cardiology  procedures,  and  coronary  artery  bypass  surgical  techniques  have  advanced  and  have  led  to  a  decrease  in  the  overall  morbidity  and  mortality  associated  with  acute  myocardial  infarction.  Despite  this  overall  improvement,  mechanical  and  electrical  complications  such  as  cardiogenic  shock,  rupture  of  the  ventricular  septum  or  free  wall,  acute  mitral  regurgitation,  pericarditis,  tamponade,  and  arrhythmias  challenge  the  medical  community  caring  for  patients  presenting  with  acute  myocardial  infarction  on  a  daily  basis.3  Of  these  complications,  cardiogenic  shock  complicating  acute  myocardial  infarctions  has  the  most  significant  impact  on  in-hospital  mortality  and  long-term  survival.  The  loss  of  more  than  40%  of  functioning  left  ventricular  mass  and  its  accompanying  systemic  inflammatory  response  are  major  causes  of  cardiogenic  shock  and  are  determined  by  the  degree  of  preinfarction  ventricular  dysfunction,  the  size  of  the  infarcted  vessel,  and  pathologic  level  of  inflammatory  mediators.4,5  Restoration  of  blood  flow  to  the  threatened  myocardium  offers  the  best  chance  of  survival  following  acute  coronary  occlusion,  but  the  means  and  timing  of  revascularization  continue  to  be  a  highly  debated  and  studied  topic.  Thrombolytics,  percutaneous  transluminal  coronary  angioplasty  (PTCA),  intracoronary  stenting,  and  coronary  artery  bypass  (CABG)  surgery  have  decreased  the  mortality  associated  with  acute  myocardial  infarctions.  Advances  in  myocardial  preservation  and  mechanical  support  lead  the  surgical  armamentarium  in  the  treatment  of  acute  myocardial  infarctions.