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Archive for the ‘Echocardiography-hemodynamics’ Category

(This post is about some basics in echocardiography meant for fellows, and echocardiographers. Others can skip please ) 

This is a 27-year-old woman who was referred for routine* cardiac evaluation. What do you see?

What is the diagnosis?

This echo clip is from a woman who is 8 months pregnant. What you are seeing is perfectly physiologically and normal. On lying down there is a mechanical push of the diaphragm altering the LV shape and contraction. In the short axis, the left ventricle is contracting well, but the shape is not spherical in systole implying some desynchrony. Further, the  IVS arena is contracting vigorously, which makes, the other segments appear to be poorly contracting. (Someone could report it as a wall motion defect in antero- lateral segments inviting temporary panic)

It is worthwhile to go through this list of non-ischemic WMA and find the pregnancy at the bottom of the list.

Few more conditions, that can be added to this list

  • Though LBBB is the classical cause for WMA, we have seen even LAFB showing the bumpy motion of IVS and the anterior wall.
  • Some patients with ERS and some patients with Brugada show wall motion defects due to repolarisation heterogeneity. 
  • Regioanl pericarditis
  • Intracardiac scars. Localized fibrosis.
  • Extracardiac tumors 

iFAQ on this topic 

Is this wall motion defect in pregnancy, really an artifact or real? 

They are true artifacts in the sense, the heart is an innocent bystander in this pulsating fight between intra-thoracic vs intrabdominal pressures. A similar situation happens in ascites. 

Any other mechanism other than mechanical push?

WMA due to RV volume overload of pregnancy may also contribute. 

Does this WMA affect cardiac hemodynamics?

Logically it should, but it doesn’t. The normal heart has enormous resilience, it just ignores these subtle pushes from below and keeps working normally. Still, enormous distension of the abdomen especially in twin pregnancies, in small body habitus, can make some women breathless, or orthopenic. I am sure, one of the mechanisms could be this geo-mechanical encroachment.

Final message

Wall motion defects are not synonymous with CAD. There is an important list of non-ischemic conditions that can cause WMA. Cardiology fellows and echo technicians are encouraged to go through the above list one more time. While this knowledge can prevent false alarms, at the same time it is always wise to ask for the ECG before doing echocardiography, and not to miss the omnipotent CAD.

Postamble 

*DIscerned readers might wonder why a routine echo was done in a normal pregnancy. I am surprised to note there is an ongoing fad in this part of the world, to do echocardiographic screening on every pregnant mother to rule out cardiovascular disease. (A luxury even the world’s richest country can’t afford) I am told, this echo is meant to rule out peripartum cardiomyopathy for legal purposes. A spot echo at term can never be going to either predict as an event that is mainly going to happen postpartum. This newfound epidemic of anxiety among obstetricians is unwarranted. 

Reference  

A well-written focused review specifically on this topic 

Yavagal ST, Baliga VB. Non-Ischemic regional wall motion abnormality. J Indian Acad Echocardiogr Cardiovasc Imaging
2019;3:7-11.

 

 

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Doppler E/A ratio reversal is probably the most reported abnormality in clinical echocardiography. We are also pleased to label it as a grade 1 diastolic dysfunction. Making a significant population who come for regular health checks anxious and worried.

Sharing a presentation from the Annual conference ECHO INDIA 2019, I participated in a symposium on Diastolic dysfunction.

Topic : Issues in diagnosing grade 1 diastolic dysfunction: Pearls and Perils

How did we get into this academic trap? Should we continue this practice?

The current ASE guidelines 2016 have a clear message. It has taken off the E/A ratio from the Initial screening for diastolic dysfunction.

Summary & Final message 

Are we ready for the change? By understanding a simple concept, one can reduce the incidence of indiscriminate diagnosis of grade 1 diastolic dysfunction.

  • E/A ratio apparently has a no role in diagnosing diastolic dysfunction in the normal population who have normal EF %.
  • Hence, never report E/A ratio in Isolation as grade 1 diastolic dysfunction.
  • However, in patients with HFrEF it does help in triaging diastolic dysfunction.
  • Always look for symptoms and 2D features  (Unexplained dyspnea, LA enlargement, LVH ) before considering diastolic dysfunction.

*For advanced readers and researchers grade 1 diastolic dysfunction does have a deep meaning and always continues to puzzle.

Patient corner

For all those anxious patients who ramble around with a report of grade 1 diastolic dysfunction, I can assure you this. Please realize, 9/10 times, this is just a decorative echocardiography abnormality meant to add some spice to the report  does not have any significance.

*Will post a PPT presentation shortly.

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*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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A 45 year old man came with  recent onset breathlessness.His left ventricle was dilated along with left atrial enlargement.The LV EF was 42% (By current definition mid range preserved systolic function( Circ Heart Fail. 2016 Apr;9(4))

But, he was severely symptomatic because of combined  systolic and  diastolic dysfunction.Diagnosing and grading diastolic dysfunction has been extensively done in last decade.Now , we realise without significant diastolic dysfunction symptoms of pulmonary congestion can never occur in patients with DCM.

We don’t require complex tissue Doppler parameters to diagnose high-grade LV diastolic function.Just have a look at LA dimension,  concentrate the E to A ratio. A tall E that humbles the A by more than 2 to 3 times is clear evidence for  LA mean Pressure exceed  18 to 20 mmhg or so.

This , in combination with dilated LA is a marker of chronic severe diastolic dysfunction.The fact that A is diminutive in no way takes the Importance of Atrial contribution to LV filing at this critically compromised LV status.

Note E:A ratio is 3:1 .This simply means the early (and mid to a certain extent ) diastolic pressure in LA is high and most of the filling takes place before Atrial contraction .There is one more reason for diminutive A . Atrial contractility fails to prevail over E in late diastole as LV end diastolic pressure is significantly high in these patients with diastolic dysfunction.

A dilated left atrium is an Independent marker of significant LV diastolic dysfunction (In the absence of MR) .When does LA begin to enlarge in diastolic dysfunction ? There is uniform rule.Generally LA size more than 4.5cm indicate grade 3 or 4 LV diastolic dysfunction.

LA size and Pulmonary congestion 

It’s a paradox , a roomy  LA dampens the LA pressure curve and A reversal into lungs may not happen.

*AF irony on A reversal

Logic might suggest , loss of atrial contraction might attenuate A reversal and less blood flooding into pulmonary veins.No, It doesn’t happen that way.If  AF is precipitated for any reason its going to be “switch on”  for acute pulmonary edema.

What is the relation between systolic and diastolic dysfunction in DCM ?

We find about 30 % of DCM has documented resting diastolic dysfunction.This is actually a underestimation of true diastolic dysfunction as it can very well manifest only during exertion.

Though generally , there is good correlation of grade of diastolic and systolic dysfunction in terms of severity , some of the patients show severe diastolic dysfunction out of proportion with systolic dysfunction.

Note : In the above patient it’s actually a fairly preserved systolic function but still has advanced diastolic dysfunction.

Grading of diastolic dysfunction .Image courtesy MM Redfield et al: JAMA 289:194, 2003. Note E:A >1.5 is

Final message

Relying on E:A ratio to diagnose diastolic dysfunction  may appear  amateurish for some of us .The rampant reporting of E>A for grade 1 diastolic dysfunction has made this parameter a “Doppler cliché”. But , the fact of the matter is,  it does help us confirm severe (Grade 4) diastolic dysfunction when E stands  tall and towering over an almost dwarfed A.

Clinical Implication

Please realise ,In patients with DCM  when you find an  A that is too diminutive in combination with  a menacingly tall E , it may be prudent to raise diuretic dosage. It’s a sure signal for impending pulmonary edema.

Queued queries 

Can DT and IVRT normalise with progressive diastolic dysfunction ?

(more…)

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