TY  - CHAP
M1  - Book, Section
TI  - Mechanical Complications of Myocardial Infarction
A1  - Davies, Ryan R.
A1  - Robich, Michael P.
A1  - Coady, Michael A.
A2  - Yuh, David D.
A2  - Vricella, Luca A.
A2  - Yang, Stephen C.
A2  - Doty, John R.
Y1  - 2014
N1  - 
T2  - Johns Hopkins Textbook of Cardiothoracic Surgery
AB  - EpidemiologySix  to  ten  percent  of  patients  develop  cardiogenic  shock  after  myocardial  infarction.Mitral  regurgitation  (MR)  occurs  in  8  to  50  percent  of  patients  after  myocardial  infarction.Post-infarct  ventricular  septal  defects  (VSD)  occurs  in  <0.5  percent  of  myocardial  infarction  (MI)  patients.Only  24  percent  of  medically  treated  patients  with  post-infarct  VSD  survive  30  days.In  autopsy  series,  30  percent  of  myocardial  infarction  (MI)  is  accompanied  by  ventricular  free  wall  rupture  (VFWR).The  incidence  of  left  ventricular  aneurysms  depends  on  exact  definition;  10  to  35  percent  of  patients  will  develop  region  of  systolic  akinesia  or  dyskinesia  after  transmural  myocardial  infarction  (MI).PathophysiologyIn  cardiogenic  shock  associated  with  MI,  worsening  ventricular  function  leads  to  decreased  coronary  perfusion,  worsening  ischemia,  and  an  enlarging  infarct  zone.Three  primary  pathologic  mechanisms  exist  for  post-infarct  MR:Papillary  muscle  ruptureAcute  ischemic  MRChronic  ischemic  MR.Post-infarct  VSD  follows  large  transmural  infarction  with  weakening  of  the  septal  wall.Post-infarct  VSD  results  in  left-to-right  shunt  of  variable  magnitude  with  diversion  of  blood  flow  from  systemic  to  pulmonary  circulation  and  low-cardiac-output  state,  ultimately  into  cardiogenic  shock.VFWR  occurs  after  large,  transmural  MI  in  myocardium  without  collaterals.Traditionally  ventricular  aneurysm  is  defined  as  region  of  myocardium  exhibiting  abnormal  diastolic  contour  with  systolic  dyskinesia  and  paradoxic  bulging.Ventricular  remodeling  after  large  transmural  infarct  leads  to  infract  expansion  and  aneurysm  formation.Clinical  featuresSymptoms  of  systemic  and  coronary  hypoperfusion,  including  cold,  clammy  extremities,  cyanosis,  oliguria,  and  altered  sensorium.Cardiogenic  shock  associated  with  MI  leads  to  pulmonary  edema,  chest  pain,  and  shortness  of  breath.New  holosystolic  murmur  best  heard  at  the  apex  is  noted  in  MR  associated  with  MI.Post-infarct  VSD  typically  occurs  5  to  6  days  after  MIEighty  percent  of  VFWR  occur  within  7  days  after  infarct.Subacute  VFWR  results  in  a  worsening  pericardial  effusion  and  hypotension  without  pulseless  electrical  activity  and  cardiac  arrest.Pseudoaneurysm  formation  from  VFWR  occurs  approximately  3  months  after  MI  with  variable  symptomatology.Commonly  presents  with  congestive  heart  failureLV  aneurysm  commonly  presents  with  congestive  heart  failure,  angina,  and/or  dyspnea.Mural  thrombus  present  in  50  percent  of  ventricular  aneurysm  patients  at  surgery.DiagnosticsInvasive  hemodynamic  monitoring  important  in  optimizing  both  coronary  and  systemic  perfusion.Electrocardiography  (ECG)  confirms  cardiac  ischemia;  chest  X-ray  rules  out  pneumothorax.Emergent  echocardiography  (ECHO)  to  rule  out  other  mechanical  causes  of  shock,  including  papillary  muscle  or  ventricular  rupture.Echocardiography  (ECHO)  allows  evaluation  of  left  ventricular  (LV)  function  and  mitral  apparatus;  can  accurately  diagnose  pulmonary  muscle  (PM)  rupture  as  well  as  exclude  other  mechanical  causes  of  cardiovascular  collapse.Location  of  infarct  of  echocardiography  (ECHO)  correlates  with  location  of  post-infarct  VSD.ECHO  is  important  to  differentiate  post-infarct  VSD  from  acute,  severe  mitral  regurgitation  (sensitivity  and  specificity  ~100  percent).Angiography  allows  delineation  of  coronary  anatomy,  estimation  of  ventricular  aneurysm  size,  and  guided  placement  of  intra-aortic  balloon  pump  (IABP).Rapid  pericardiocentesis  is  both  diagnostic  and  therapeutic  for  VFWR.Echocardiography  (ECHO)  identifies  effusion  with  pericardial  clots  for  VFWR;  Doppler  evaluation  may  identify  rupture  site.MRI  may  be  useful  in  evaluating  pseudoaneurysms.TreatmentMedicalNo  pharmacologic  agent  has  been  demonstrated  to  improve  survival  for  cardiogenic  shock  associated  with  acute  MI;  inotropes/vasodilators/vasopressors  should  be  used  to  stabilize  the  patient  in  preparation  for  definitive  therapy.Thrombolysis  is  of  unproven  benefit  for  patients  in  cardiogenic  shock.Medical  therapy  for  acute  MR  and  papillary  muscle  rupture  is  supportive  only.Intra-aortic  balloon  ...
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/24
UR  - accesssurgery.mhmedical.com/content.aspx?aid=1104589461
ER  -