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Archive for the ‘Echocardiography – LV dysfunction’ Category

*The post is not meant for those who understood GLS (Global longitudinal  strain) in a proper perspective. I am writing this, after a surprising answer from many students of Echocardiography, when I asked them what is GLS?  Most answered, GLS currently is the best global LV functional index available. What a misunderstanding? The fact is, EF % will always be the best global parameter*, while GLS remains a regional function index.(*The limitation of EF% is in the methods of measuring it and not in EF itself.)

                                   We are trying hard to ditch LV EF%  by Teichholz’s / even 2D Simpson method, as they are considered a crude way to measure global LV function. Unfortunately, we are doing this without a credible alternative. GLS is being promoted as the next best. The normal GLS is around(-20 ± 2) . Nothing is perfect. Best global LV function probably can be achieved by 3D Voxel Echo/MRI)

Normal GLS with various machines

Please note, the bullseye 17 segment model though brings an illusion of a radial perspective of cardiac contraction, its purely longitudinal stain represented in short axis format.

The much popular GLS (Global longitudinal stain ) is a poor surrogate for global function. The word global is apparently misguiding and conveys a false message. When we refer to GLS, it is an adjective for longitudinal function and nothing to do with overall global LV function. (Though we have many studies to show it has good correlation with global LV function).

The longitudinal function is presumed to contribute 60 % of LV function.  This means GLS is at best 60 % accurate in determining global LV function. Mind you, the heart doesn’t work in a longitudinal plane alone. The muscle fibers of heart are arranged in three distinct fashion (LOC) subendocardial- longitudinal,  Mid-oblique, & Sub epicardial -concentric (Remember LOC ) Each fiber either lengthens or shortens.

The left ventricle not only shortens longitudinally, It also contracts radially, shrinks circumferentially, rotates clockwise at the base (5-10º) , counter rotates at apex (Up to 60º) twist,  & un-twists.  It’s worth reminding ourselves, we are ignoring all these components and happy to fall for GLS.

What can be done to improve the accuracy of true global strain?

The simplest way is, to look LV in  short-axis by 2D and confirm everything is okay with radial contractile forces and deformation. Mind you, the most accurate tool to measure stain is the good old M mode with undisputed temporal (time) resolution ad frame rate the M mode thickening best deformation parameter to measure radial stain ( at a particular plane though).

Is the measurement of true global strain possible?  (GLS+ GRS)

Probably yes. What about GLS plus GRS (Global radial strain)  GLS measured by speckle + RS (Radial thickening by 2D/aided by M Mode)  We are working on a project where the radial strain component is added to GLS. Roughly, it should pull the negative GLS  beyond + 20  (If we assume GRS is + 30 to 60 ) This should be correlated with 3D voxel Echo  /MRI .

Final message

Beware,The “G in GLS” is a perfect miscommunicator. * GLS  can never reflect global LV function. If EF% by M-mode was criticized, for measuring only one aspect of cardiac function ie radial, the same would apply for GLS, in that it measures only longitudinal function. Never discard M mode/2D. It still, pours unadulterated ultrasonic data from myocardial contractile units in the highest resolution. We should continue to use it. In the name of modernity, we make it look outdated.

Reference

M S Amzulescu, M De Craene, H Langet, A Pasquet, D Vancraeynest, A C Pouleur, J L Vanoverschelde, B L Gerber, Myocardial strain imaging: review of general principles, validation, and sources of discrepancies, European Heart Journal – Cardiovascular Imaging, Volume 20, Issue 6, June 2019, Pages 605–619, https://doi.org/10.1093/ehjci/jez041

*

 

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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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