Ejection Fraction and Heart Failure

[TomJohn]

What is a normal increase in ejection fraction with proper medical care?  I had an ejection fraction that over the years had decreased to 20% as the heart failure progressed and in the last six months it quickly returned to 60% being indicated by measurements from both an echo and MUGA testing.  The symptoms of CHF have not changed, so the blood flow per beat has not increased.  I do presently have a BIV-ICD device and my medications are an ACE inhibitor, a beta blocker, and a long-acting nitrate.  Why has the EF increased so greatly and what would that increase indicate?  I have read that typically one could only expect an increase of about 10%, so this jump was not expected.

Tom

[kenkeith]

Correction: If and when there is overcompensation (pathologically oversized heart) the FS is indirectly related to EF.  Contractions (wall movement) is impaired due to the enlarged LV.

[kenkeith]

Generally, there is direct relationship of EF to FS with the difference of the LVED and LVES.  This interaction is true when there is compensation (Frank/starling mechanism) to maintain a balance of blood flow between the left and right side of the heart.  

If and when there is overcompensation (pathologically oversized heart) the FS is indirectly related to FS.  Contractions (wall movement) is impaired due to the enlarged LV.

When there is diastolic noncompliance there can be heart failure with the EF and FS in the normal range and/or there can be LVEF and LVES pathology, or a combination thereof.

There are computerized software algorisms and envolves a  program that calculates the volume and does the calculations.  The algorithm involves cardiac motion in order to detect cardiac wall motion abnormalities, among them: velocity, radial and circumferential strain, local and global Simpson VOLUME,  global and local
ejection fraction (EF) ratio, and segmental volume. Some of these features, including velocity, circumferential strain, and local EF ratio, are based on the inner (endocardial) contour.


Due to the patient examination protocol, only the systole (i.e. contraction phase of the heart) is recorded for some patients. In order for the features to be consistent, the systole is extracted from each patient based on the CAVITY AREA CHANGE. For each frame, the LV cavity area can be estimated accurately based on the inner (endocardial) contour of that frame.

FRACTIONAL SHORTENING: The frame corresponding to the maximal cavity area that is achieved at the end of diastolic phase (expansion phase of the heart) is the frame considered to be the beginning of systole. The frame corresponding to the minimal cavity area (achieved at the end of systolic phase) is the frame assumed to be the end of systole. For the time being, all features are computed based only on the systolic phase. However, the methods used to calculate the features are generally applicable for the diastolic phase as well.

The following is a basic description of some of the features of the algorithm:
• Velocity features: determines how fast any pair of control points change in the x and y coordinate system per frame.
• Circumferential strain features: also called FRACTIONAL SHORTENING, measures how much the contour between any two control points shrinks in the systolic phase. This is measured along the parameter of the contour.

• Radial strain features: also called Thickening, measures how much the contour shrinks for each control point between any two time frames. This is measured along the
radius from a calculated “center” of the LV.
• Local and Global Simpson Volume features: determine the VOLUME as computed by the Simpson rule (with 50 disks) for each frame, and for the systolic phase of the
heart as a whole (this gives the global EF, which captures the whole heart’s contraction abnormalities).

• Segmental VOLUME features: determine the volume per segment per frame, and the segmental EF values (i.e local EFs, which aim to capture the local cardiac contraction
abnormalities).
In general, the global version of certain features (e.g. radial strain, circumferential strain, etc) can be calculated by taking the mean, or standard deviation, of the 6 segment’s respective feature values from any one view. All in all we had 120 local
and global features for each of the 3 views (360 total), all of which were continuous. The limitations of present wall motion analysis programs, e.g. color kinesis and blood pool, is that they only evaluate wall motion and not heart wall thickening, which is the hallmark of ischemia.

[TomJohn]

Kenkeith:
From the earlier correspondences I can see that the fractional shorting (FS) and the ejection fraction (EF) do not correlate very well.  Steve’s EF stayed the same, but the FS went down, and my EF increased and the FS stayed the same.

I consider them both a function of dimensions as FS = ratio function(end of systole and end diastole diameters) and EF = volume function(end of systole and end diastole diameters).  With them both using the same two diameter terms, I do not understand why there is such a difference in the relationship of the two functions.  I would feel that your earlier comment of a shortening fraction values of 9 and 14% correspond to calculated ejection fraction values of 25 and 37% respectively would indicate a relationship.  How is the volume calculated, for I see it using the diameter and done similarly to how one would handle a sphere.  Such a relationship would not explain the trends indicated by the test results furnished by Steve and myself.

With the measurements all taken during the Echo, the FS and EF can change due to the working conditions of the heart at the time of measurement, but will still have a mathematical tie due to the use of common terms.

Since both of these components, the FS and EF, are calculated using measurements from the Echo, what explanation can you furnish to help me understand the relationships of the measurements and resulting calculations?


Tom

[Sirenet]

Thank you for your insight. Your explaining the Frank-Starling Law actually helps me understand why, perhaps the FS has reduced. My LV has reduced somewhat from 6.94 down to 6.34. This, I imagine may be the 'overstretching' that  you mention, affecting the contractability of the heart. Thank you again for taking the time, it is very much appreciated. - Steve

[kenkeith]

Variables that relate to a differential of FS to EF are afterload (i.e. CAD), pathologically enlarged heart (compensatory dilated heart increases contractual strength, Starling mechanism **, but overcompensation reduces contractual strength).

Shortening fraction values of 9 and 14% correspond to calculated ejection fraction values of 25 and 37% respectively. The results indicate that the shortening fraction is altered not only by changes in cardiac contractility but also by the Starling mechanism.

** The Frank-Starling law of the heart (also known as Starling's law or the Frank-Starling mechanism) states that the greater the volume of blood entering the heart during diastole (end-diastolic volume), the greater the volume of blood ejected during systolic contraction (stroke volume)... As an anology a hand spring when manually stretched will recoil with greater force and over stretched will lose its recoil properties and become flaccid.

The significance for FS is the degree of the heart muscle mass, enlargement, that is associated with the EF if any.

[Sirenet]

I hope you don't mind my jumping in here... You talk of FS, few I have seen do. My last echo's FS has me concerned. Met with my cardios PA yesterday to go over results of my recent echo. My EF has not changed from last. 1/208 showed 24% and recent said 20-25%. However my FS on recent echo is 1/2 from the one from 1/2/08. It went down from 13 to 6.2. Of course PA told me not to worry about it, but it has me very concerned. Particularly since I started coreg (& other) meds, with no  help in EF.  My recent echo shows 3 areas of the heart which are akinetic.( too much heart damage, I am advised to increase EF)
  I was wondering how significant you consider the FS #? I don't see my cardio for another 2 months. Thanks, Steve

[kenkeith]

There is a correlation between ejection fraction (EF) and fractional shortening (FS).  EF is measured by volume is not exactly the same as measurement of functionality by dimensions of LV at end of systole and end diastole.

Your dimensions at both test dates have an identical FS.  FS=LVED-LVES divided by LVED.  Greater than 30% is normal and 26-30% mild decrease in EF.  Using your LVED's and LVES's (5.9 - 4.1 divided by 5.9 = 30%), etc..

[TomJohn]

Kenkeith:
I do agree with you that I am seeing diastolic dysfunction.  One of the items that does not fit is that the Echoes showed on 09/04/2007 a diastolic diameter of 5.9 cm and a systolic diameter of 4.1 cm.  Then on 05/16/2008 the diastolic was 5.2 cm and systolic was 3.6 cm.  The diastolic reduction was 12% and the systolic was also 12%.  That was a large ejection fraction change for how small and in the same direction the diameters trended.  Since a MUGA test was then done on 05/29/2008 and also indicated an EF of 59% others must also have questioned it.

I have had a severe enough heart problem, which goes back to 06/2002 when the first pace maker was installed.  Since then, I am now on my third upgrade being a BIV-ICD device.  Over the six years, I have seen things change, but not so quickly.  I also have not heard of one switching from years of systolic dysfunction to diastolic dysfunction.  If it does exist, what does it indicate on the way of future changes?

Tom

[brittn]

I had 2 blockages in the same week in 02.  While I was in cardio ICU and unconscious I sufferd a 100% blockage due to a clot.  My telematry was malfunctioning and they dont know how long i was out for!  When I was realeased I had a ton of problems.  I kept getting hospitalized do to severe breating issues.  Finally they did a stress test and i was <13%.  They finally Diagnosed CHF and started me on correg.  Soon I could sleep again(it was almost a year without sleep due to no breath and panic attacks!  The correg was a miracle.  Each year my Ef had risen and my last test(a week ago) showed 42%
After 8 stress tests they used andenosine this time.  I thiught I would die!  AFter 30 seconds I had a real flush and couldnt breathe a bict.  It was 14 min before I cot it back.  I really swear I saw the white liite and pray death will be easier.  I refuse that med ever ahain!
britt

[brittn]

?

[kenkeith]

EF is increased with stronger contractions resulting from mediation and/or left ventricle dilatation (within limits).  These two factors increase the volume (each heartbeat), and cardiac output is stroke volume times heart rate. The formula for EF: Diastolic volume (filling phase) per stroke is blood volume measured at end of diastolic (maximum filling capacity...relaxed state) minus the volume at the end of systole (minimum amount of blood left in the chamber).  Divide end diastolic volume into the difference between end systole and end diastole is the fraction (%) pumped with each stroke.  

CHF by definition is an EF below 29% (left side non-compliance) indicating there may be an insufficient blood/oxygen supply meeting system demand.  Relating to the formula for EF, you can see the EF will increase if the volume entering the LV is reduced,  but the contractility for EF remains the same or increases.  

QUOTE: "The symptoms of CHF have not changed, so the blood flow per beat has not increased."   Blood flow will not increase with diastolic dysfunction but EF can be preserved with DD.  Also, a probability there are pulmonary/respiratory issues and lack of oxygen within the blood supply going to the LV causing heart failure symptoms..

[Momto3]

Hi TomJohn,

My Dad had a similar thing occur.  He had an EF of 24%, and the doctor implanted a  BIV-ICD in November 2007.  About 6 months later, his EF was 42%.  The doctor said that was a pretty significant jump, and he would not commit to that number until my Dad has his next follow up appointment (this Fall).  

He takes a number of medications including an ACE and beta blocker.  I'm not sure of his classification, but he is able to manage on a daily basis.  He does take breaks during any physical activity (including walking), but does well overall.  Are you able to manage your normal daily routine?