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This a story from a middle aged IT professional who had recently suffered from a cardiac event. His concern is, he has an ejection fraction (EF) of 45%, finds difficult to walk to the nearby mall ,while his neighbour, also a heart patient, has only 32% EF , but goes for cycling and hiking ! He finds this very odd and totally unacceptable. .He desperately needed an answer from his cardiologist.


How is this possible, doctor? I am sort of depressed for two reasons. You are saying, I had only a mild heart attack and recovered well with no significant blocks in the angiogram, but, I still find it difficult to do routine activities. The latest EF is recorded as 45%. I am taking all your medications sincerely.

“Doctor, I feel awkward, but I can’t stop asking this question to you. More than my heart condition, it is my neighbour’s one that is bothering me. He was critically ill sometime back. Has undergone a bypass, after two early stent failures, I am seeing him daily now. So active he is, able to hike even the hill in our county. He told me his EF is just 32%. It sounds atrocious. What is the use of having more EF than him, doctor ? Do you think I need to be referred to any specialized cardiac centre ?”

“My dear patient, relax. If you want a straight-forward answer, “you are suffering from EF neurosis” Exercise capacity and overall well-being of an individual have little to do with the Ejection Fraction (EF) of the heart. Forget that number”.

“Sorry doctor, I am not clear , do you mean to say I have a mental health issue? ”

Ok , let me go little more deeper for the sake of your understanding. Hope you don’t mind. EF% can be sort of the daily weather report. It can change even beat to beat depending upon the loading conditions of the heart. We, the cardiologists are partly responsible for creating this anxiety at your level with this number .The prevailing literature and the confused google , has misled you guys, to believe that EF% is akin to “bank balance” of available heart function. Let me apologize on behalf of all of us.

There are many cardiac and non-cardiac parameters that determine one’s exercise capacity. Lung function is vital. Systemic factors like quality of your Hb%, renal function, lastly, the most important factor, the status of your skeletal muscle structure and function. If I can go technical, the degree of LV size, associated MR, the stress of LV filling, pulmonary vein compliance, the way your lung vasculature reacts, RV function, degree of PH, all that matters.

In your case, each of these parameters is good. So, I can reiterate that your heart is in fairly good condition. It is most likely that your skeletal muscles are hibernating and taking too much rest, and their mitochondria are suffering from disuse. Further, your thinking pattern also makes you easily fatigued. You must also understand dyspnoea is a cortical sensory perception defect. It depends upon the behaviour of your cerebral centres that are localized in the amygdala nuclei.

“Please doctor, I expected a practical solution from you”

“Ok, let me tell you a positive proposal which will definitely help. Trust your heart and believe in my words and the drugs you take. Ignore this EF stuff. Send a friend’s request immediately to your neighbour and join him on his daily hiking. If he can do it, you can also do it. I expect ,both the issues that is causing you depression will vanish soon. One caution, don’t overexert. Stop 10 to 20% short of your maximum possible capacity.”

Thank you doctor , I think you’re right I am not taking enough efforts and lack confidence .Will meet you again with good news “

Final message

Unless, it is extremely low contractile function, EF% has no linear correlation with functional capacity. This is the message to all those heart failure patients. Don’t feel bad if you are labelled as LV dysfunction or ‘Heart failure’. You can steal a success story from with the help of skeletal muscle training and dyspnea sensitization program (This is not a great new discovery, it’s all there in the ancient Indian medicine, it was called pranayama, a controlled regular breathing exercise)

Reference

1.Lv J, Li Y, Shi S, Xu X, Wu H, Zhang B, Song Q. Skeletal muscle mitochondrial remodeling in heart failure: An update on mechanisms and therapeutic opportunities. Biomed Pharmacother. 2022 Nov;155:113833. doi: 10.1016/j.biopha.2022.113833. Epub 2022 Oct 7. PMID: 36271583.

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What   are the factors other than EF %  that determine  functional capacity in cardiac failure ?

In our experience we have found the following factors  contribute immensely to the functional capacity of cardiac failure patients

  1. LV  filling  defects  (30 % of DCM have significant LV relaxation defects )*
  2. Integrity of  RV  function
  3. Mitral valve  competence(Even a mild MR can be important .It lowers the threshold for pulmonary congestion  )
  4. Severity of Pulmonary hypertension
  5. Lung Function *(Restrictive PFT common , gross cardiomegaly can reduce lung space )
  6. Basal exercise capacity .
  7. Skeletal muscle  function (Mitochondrial training )*
  8. High body weight
  9. Will power and self esteem *
  10. Spouse support and motivation

* May  have  major Impact on functional capacity

Final message

Physicians and even cardiologists are   obsessed  with EF %  to a large extent . My guess is , it   is not likely to end in the near future . The irony is ,  we have passed it  to our  colleagues  (Like anesthetists !)  and patients as well .(  for various reasons )

                        Please remember  , there are at-least 10 factors  that are  important  in the genesis of  symptoms of heart failure  . The list can extend  further  if we include  like associated renal  dysfunction , hemoglobin concentration  , etc .

Even though LV pump primarily determines  the ultimate outcome in cardiac failure ,  it is unwise  to  blame the EF %  for all the suffering  . If only  we realise this fact , one  can take  appropriate  measures .

**   Paradoxically modalities aimed to improve LVEF by positive inotropics has never been shown to improve the outcome .In-fact , there is more evidence for the contrary !

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Can the LV  ejection fraction change with every  heart beat  ?

EF % is one of  the  glamorous  cardiac functional indices that has  caught  the  imagination of both patients and physicians. How accurate it is ? How reproducible it is ? How many methods are available  to arrive at EF % ?

Picture courtesey http://rachel.worldpossible.org/ocw.tufts.edu Munther Homoud, M.D

 How many of us  realise  it can  potentially   change  with  every  heart beat ? *

Apart from the heart rate dependency ,  the echocardiographic error can be amplified  by

  • Difficulty in identifying  the  leading and trialling edges  of endocardium
  • Patient posture errors
  • Edge detection errors in 2D
  • Pap muscle shadowing .
  • Angle errors
  • Sub optimal echo windows  when EF is measured  in the  bed side  in critical care units
  • Mental status of performing sonographer/cardiologist  (One who chops  2D shells hurriedly and obliquely !  )

All these make this index a highly  variable parameter(  next only   to your  city temperature ! ) This happens whether you measure EF  with M Mode, 2D Simpson , 3D volumetric etc .

* The term  “beat to beat” changes may be  a little exaggerated  statement .It is used   to convey the point of   ” huge  variability” of this parameter.  It  means there can be variations of EF %  with varying heat rate.

The heart is not an Independent organ rather, it is a slave to preload and afterload !

How to overcome the limitation  of EF ?

To overcome this  error a new  parameter called myocardial performance index (MPI) which accounts for heart rate came into vogue . (Did it come really ? Ihaven’t seen a single cardiologist  do this in his clinic ) . 3D volumetrics,  velocity vector imaging , and many other innovations has been added.  Nothing  was  able to replace the EF % . Because of complexities in the newer  modalities  most cardiologists (including  the author  )  continue to romance  the  much flawed EF %  .

Simplicity  shall   reign supreme   .  .  . in spite of  inaccuracies ,  in any walk of life  !

 How does  EF  change  beat to beat ?

The answer is simple . The contractility of heart is dependent   upon the previous  diastole ,  during which heart fills. Heart is primarily an elastic organ. Whenever the  filling is  is more   ventricle is stretched  more ( diastolic filling is the stretch ) and the subsequent force of contraction is more . This is the basis of famous frank starling law.

LV filling is dependent on RV filling which in turn depend on venous return ..Venous return is a function of  vascular tone and the persons physical activity .

Apart from this  adrenergic drive make the heart contract vigorously . This is the reason ,  many patients  with  severely compromised  LV function  in ICU  , supported  with  inotropic agents  show vigorous contraction of heart .(Basis of doubutamine  stress test )

** Every one of us is aware about the huge influence  the preload  has ,  on LV contractility .  Surprisingly,  it   can also  swing  with changing  after load . This fact is often  under recognised .This is called Anrep effect .

So , imagine the scenerio . . .the heart is simply  a “squeezing- slave”  of   pre load and  after load  !  . . . And still we are happy with assessing the cardiac function ,  in isolation without giving any respect to the loading conditions.

Final message

EF ,  would rank  first among all  medical  investigations ,  that is  significantly  flawed , still  continue  to  enjoy huge popularity  ! It has little value as a  screening   test for assessing  LV function in  general  population . But ,  it  has an  important role to assess  the damage following   MI and in  the  follow up of patients with   significantly  compromised LV function.

Cardiologist are aware of this fact ,  but most non cardiologists , especially  Anesthetists  and Surgeons  revere  the  EF% with    sanctity  . This is definitely un-called for . It is the duty of the cardiologists to pass on  this  message to their colleagues in other fields.

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The LV ejection fraction ,  is  the most revered medical parameter for both physicians and cardiologists.There are anesthetists and surgeons , who  do not  operate  a  cardiac patient  without knowing it.There are  physicians  who  do monthly assessment of EF in their patients  with dilated  cardiomyopathy.

Now ,every one is interested to know what is their EF ?  Thanks to the global  information highway .We witness ,   patients who are extremely delighted when their  EF increases from 45% to 48% . Similarly , they get depressed when it falls by 2% .

Why this hoopla around the LV EF ?

Every one knows EF is nothing but a LV contractile force at a particular  beat of the heart . It is possibly a crudest possible way to screen for   LV function.( Of course it can still be useful  in patients  with established myocardial disease to follow up  LV dysfunction)

The  most important caveat in  EF is it’s dependence on the loading conditions  of heart .It is   also  heavily influenced by the  heart rate.We now, even a severely dysfunctional LV can contract vigorously with inotropic stimulation  like dobutamine  or whenever local catecholamines.

Our obsession with EF is complete and it is not expected to get cured in the near future.

There are many hundreds of articles in cardiology literature  which  ridicules the EF as sole parameter for assessing LV function. Still ,  it is the number one parameter to asses LV function  in real world as well as in  vast number of land mark clinical  trials .  Are all those trial  results to be doomed ?

Even as  the  LV EF is   being labeled as  futile index  ,   we  also  realise we have not traveled  far from our great clinical   ancestors . Thousands of  years ago   the Chinese  yellow  emperor  of medicine  found  the cardiac contractility  by pulse volume  and predicted death accurately  ,  probably  better  than the live 3d echocardiography   derived EF   guided by LV volume rendering algorithm !

The purpose of this article is to tell the current generation physicians  there are some simple and probably  accurate  clinical tips  to rule out significant LV dysfunction.

One can confidentially tell  the LV  EF  would  be > 50%  in 99% of population if they have the following !

  • A brisk upstroke of carotid pulse.*
  • A well palpated tapping apical impulse**
  • A Loud  first heart sound(S1)
  • A  totally normal ECG (Even a normal QRS complex  is suffice !) ***
  • Normal CT ratio in Xray chest
  • A  comfortable brisk walk of  at 6 km/hour for 10 m .

* A brisk central arterial pulse is nothing but the reflection of LV DP/DT a sophisticated echo parameter assessed  with much hype ! A good thumb with an   alert brain can accurately tell a given patients dp/dt is within normal range.

** A loud S1 and tapping apical impulse indicate the velocity of closure of  anterior mitral leaflet.Which is in turn reflect the force of contraction of the antero lateral  papillary muscle of LV .So what you hear a loud s1 is nothing but the contractile function of the most important  part of LV namely the pap muscle of LV.

*** A normal ECG ,  generally tells us  all is  well with LV myocardium . Finally,  it makes  immense sense to correlate the functional capacity to EF. (90% correlation)

Final message

Mind you ,  all the above modalities come either  free of cost or a fraction of  echocardiography  . It is estimated up to 90% echocardiography scans to R/O LV dysfunction can be avoided . The global health care costs can be saved and be utilised for some better purpose like protecting our atmospheric shell  from the  hazardous   gases

Note of caution

While ,one can rule out signficant LV dysfunction by above mode  ,  it can miss  other forms of LV dysfunction like relaxation defect etc . (ofcourse the EF also misses it !) .Judicious use of functional  imaging modalities are adviced in those who require it.

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