Archive for the ‘Echocardiography – LV dysfunction’ Category

Wall motion defect , in patients after CABG is fairly common.These  defects are difficult  to interpret  as the mechanisms can be multiple.Though the commonest wall motion defect appears to  involve the interventricular septum. it can occur anywhere in antero-lateral zone.

The mechanism attributed is  the effect of pericardiotomy , which surgeons as we understand leave it open after grafting  .This can cause lack of localised ventricular interdependence and results in a a brisk septal movement (bounce )It is an indirect effect .

post cabg wall motion defect

Note the, wall motion defects are confined to the exposed areas of the heart during cardiac surgery .In short axis echocardiography it correlates anywhere between 9 to 3 O clock position. Though interventricular septum is not covered by pericardium in the true sense , there is a indirect bounce effect over IVS due to interference with anterior ventricular interdependence .

More commonly a direct wall motion defect in the 12 to 3 O clock position in short axis is seen .This can closely mimic true wall motion defect as pericardial adhesions can tether these segments. Careful observation is warranted.Myocardial thickening is the key differentiating feature.

What is the physiological impact of these wall motion defects ?

It is generally considered benign (It is !) .Though in echo it looks awkward and suggest desynchrony. The real issue is , it can  mislead the echocardiographer to errors in calculation of that universally  sacred parameter called EF %

Importance of  knowing pre existing wall motion defect.

This has to be reviewed with old reports as it can wrongly create a new wall motion defect de-crediting the surgeons.

New pathological wall motion defect.

Of course it can happen due to peri-operative ischemic insult or infarct . However , It need to emphasised transient wall motion defects are common post CABG due to apparent hypoxia.This seems to be more pronounced with on pump surgeries than off pump .(Expected though) In my opinion, 2-4 weeks cooling off period is required before  a meaningful assessment of  wall motion post CABG.

Late pericardial reactions and localised constrictive features has been reported.

Disappearance of wall motion defect : How  common ?

Any disappearance of WMA is welcome . It happens rarely though . Some of the post ACS population (Both STEMI and UA/NSTEMI) can experience this ,  as they could harbor  zones of myocardial segments afflicted by  ischemic stunning rather than true  necrosis , that might  disappear.


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The diastolic mitral filling pattern has been  named and  graded  umpteen times in the last  decade. We believe it has  reached some semblance of clarity.I beg to differ.

pseudo abnormal relaxation grade 1 003

Image template taken  from  http://www.learntheheart.com

There need to be one more  grade between Grade 1 and grade 2 .Grade 1  is defined as A velocity > E velocity . This is the  commonest abnormal pattern and is often  man made.We can’t help it . We have to report it  anyway. Significant number of elderly show this pattern  without any pathology. It simply represents augmented atrial contribution  at times of apparent ventricular stress .

I wish a good chunk  of  grade 1  pattern ,  especially  in elderly or during tachycardia should be labelled  as physiological  grade 1 pattern  (or simply as  normal variant ) . However I would prefer it to be named as  pseudo abnormal pattern* !

* In my experience , currently medicine is taught in a complex manner .Facts that are told  in simple terms are rejected  straightaway . It would seem,too much clarity is not good for  science So,let us get confused one more  time  for the sake of our patients !

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LV ejection fraction (EF) is the most commonly used  LV systolic functional index.Since , it is an  easily acquired parameter,  it’s popularity has zoomed among both learned and novice cardiology professionals .(Not withstanding the serious shortcomings!)

In one of the evening rounds  in my CCU , a young cardiology fellow told me about a  patient  with acute  anterior MI with ST elevation V1 to V5.

The patient  was lying supine with trunk up . HR was 110 . BP was  100 /70 There were few basal crackles .The patient was undergoing  lysis with streptokinase.

It was  suggested  to me by the  fellow  that  the patient is  going in for “Impending  cardiogenic shock since his EF is just 30%”

That prompted me to ask this question

How good is the EF  a measure  of size of MI during STEMI ?

EF during  STEMI  is highly variable parameter.The following are important con-founders in LV EF measurement during STEMI.


  • Acute ischemia induced LV dysfunction .(Ischemic stunning from  the watershed zone  significantly over estimate LV dysfunction)
  • Mitral regurgitation  if present will underestimate it
  • Effect of tachycardia and bradycardia can be significant
  • The posture of the patient and  measurement errors (A good Simpson score is rarely  possible in a sick patient )
  • Associated  hemo -dynamic drugs like NTG/Dopamine etc which alter  pre and after load   and changes the frank starling forces.

* Please recall  , LV EF is never included as a criteria to diagnose cardiogenic  shock, confirming the  flimsy  nature of this parameter during acute phase of STEMI !

Final message

The purpose of echocardiography during STEMI is to rapidly identify any mechanical complication , not to waste time in calculating EF.

EF is not a good indicator  to  quantify the extent of STEMI  or it’s prognosis. LVEF cannot be used  to risk stratify STEMI in the first  48 hours .One can expect  the true LV function  to prevail only  at discharge.

Ideally ,LV  function should be reevaluated by 2 weeks to get a fair idea of true myocardial function .By this time all  confounders will resolve.

Clinical implication

Since many of us are suffering from an academic obsession and blindly follow the scientific guidelines, a hurriedly diagnosed  “severe”  LV dysfunction post STEMI may land our  patients to  inappropriate intervention !


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