Latest Echo Report-Please help reading it

[Tinu1959]

Got my echo report today. I had one in April 2008. Same technician and same machine. Results are as follows:

August 2008

1. Mitral Valve: EF Slope-110 cm/sec; DE Amplitude-18.7 mm; EPSS-17.6 mm; EPSS is raised.
2. Arotic Valve/LA: Arotic Root Diameter-32.3 mm; Cusp Separation- 18.7 mm; LA size- 38.6 mm; AV sclerosis.
3. LV:  LV size distole=67.6mm; systole= 57.9 mm; Stroke Vol.=56 ml; HR=92 bpm; Cardic Output=5.2   L/min.
4. RV: Normal

Remarks: Dilated LV with varying hypokinesis of all LV walls with anterior/anteroseptal/apex and inferior walls being akinetic. LVEF=30%. Moderate MR+. No LVH seen. No clot seen. RV Fair.

April 2008

1. Mitral Valve: EF Slope-110 cm/sec; DE Amplitude-18.6 mm; EPSS-14.9 mm; EPSS is raised.
2. Arotic Valve/LA: Arotic Root Diameter-29.8 mm; Cusp Separation- 18.1 mm; LA size- 45.2 mm; LA Dilated.
3. LV:  LV size distole=61 mm; systole= 55.4 mm; Stroke Vol.=39 ml; HR=85 bpm; Cardic Output=3.33   L/min.
4. RV: Normal

Remarks: LV is enlarged. Varying degree of hypokinesis of most LV walls seen. The lateral wall is best preserved. No clot seen. LVEF 30%. RV normal.

My LV continues to increase even after one year of MI. Does it mean that measures my doctor has taken so far are not adequate? Need to increase beta-blocker?? Or something else can be done??

In april 2008 the LV stroke volume was 39 ml and Cardic output= 3.33 L/min. Today's report shows these values as 56 ml and 5.2 L/min. Does increase in cardic output imply better heart function?? But EF is 30% in both cases.

This time a remark is added-" AV sclerosis+". The cardiologist who did echo says it is not serious. But this remark was not there earlier. My lipid profile is under control for almost a year. How serious is this?

I know few members on this forum are very knowledgeable on this subject. Please, can you explain??. Thanks in advance.

[Tinu1959]

What I have understood from measurements taken by cardiologists who do echo is they identify perimeter of LV opening area for two positions of LV function and the machine calculates these areas. Ratio of these areas could be the EF. As regard volume measurement, once while doing cath the doctor did measurement of EF which looked like it is volume based. My EF done in January 2008, one by echo gave EF of 30% and by cath 22%. If the cath EF is by volume, than the echo results should be different for volume method and area method?

[kenkeith]

Two methods of assessing pumping ability of the heart:

Ejection fraction. The left ventricle is a chamber which relaxes to fill with blood and then contracts to pump the blood out. Even in a healthy heart, the left ventricle does not pump all of the blood out with each beat. The ejection fraction is defined by the following formula:  LV diastolic volume minus LV systolic volume divided LV diastolic volume.  It is volume sensitive.

The ejection fraction is a useful measure of left ventricular performance. The normal range is 63-77% for males and 55-75% for females (reference: Measurements in Cardiology). If the left ventricle wall is thinned (dilated, overcompensation), a decrease in the ejection fraction is seen.

....The shortening fraction is a slightly different way of measuring left ventricle performance. Instead of measuring and ratio-ing blood volumes, the shortening fraction measures and ratios the change in the diameter of the left ventricle between the contracted and relaxed states: If I remember correctly 26 to 30% is slight impairment and over 30% is normal

[Tinu1959]

Looks like, my explanation was not very clear and therefore confusing.

Let me try again. The cardiologist(in India cardiologist doctors do echo test) who did echo test is different from the cardiologist who is looking after my treatment. The one who did the echo clarified(when I went to him for clarifying CO and EF values) that the measurement of EF is direct and scope of error is less than what can emerge from calculation of CO. Therefore, he adviced me to go by value of EF and ignore the value of CO, since chances of it being inaccurate were more. He certainly did not say that CO is not important parameter, or less important than EF.

However, when I approached my cardiologist, who looks after my treatment, he said that he was not happy with the current report on two accounts:
1.  The size of LA has decreased w.r.t earlier report whereas LV size is increased. This not  normal.
2. Same what Kenkeith explained, the value of EF does not correlate with stroke volume. He wants to do an echo himself after two months.

Thanks for taking interest and helping me understand my heart condition better. Look forward to continued support.

[maggiemag]

Well I may easily be wrong but I thought the EF was not volume based, but on the left  ventricular dimensions, comparing the end diastolic with the end systolic.  I am  by no means an echocardiographer, but  I have never heard any mention of stroke volume by a cardiologist in reference to an echo.  I said *cath* above but I meant *echo*!  Sorry.

[kenkeith]

I wasn't considering how volume is measured, my reference and I question how two back to back echos (6 months apart) has stroke volume 56 ml and EF is 30% with an Aug. echo... 39 ml stroke volume and EF 30%.  Not cath vs. echo discrepancy...regardless the dynamics are volume based, and the EF is the percent of volume ejected with each stroke.

I agree: " Echoes are good for many diagnostic issues and estimates of many other things, like EF",  EF is based on volume and the timing is 1 heartbeat (stroke) so the question remains how stroke volume can change but EF remains at 30% between the two echocardiograms?

[maggiemag]

I know what you mean about the balance between Bp and fluid.  Sometimes I do feel too weak, and check my BP and it is in the low 80's systolic.  Maybe the day before I had less sodium or fluid than usual and the diuretic is taking off too much.  If my pressure would be low 80's, then I just give myself a *fluid bolus* of about 12 ounces or so and I am ok.  Maybe your diuretic dose needs lowering?

[maggiemag]

I would guess that his doctor meant to ignore stroke volume on ECHO.  It just isn't precise enough to measure, whereas a cath is.  A cardiac cath is the gold standard.  In my years working in ICU's and post of cardiac surgery (peds), only direct catheter measurements were relevant for stuff like that.  Echoes are good for many diagnostic issues and estimates of many other things, like EF, but I personally have never heard a physician discuss stroke volume derived from a cath.  Of course, I may be wrong.

[kenkeith]

Your doctor says ignore stroke volume?? Gosh! Geewhiz!  Stroke volume is the determinate of EF (ejection fraction...means the amount of blood voume pumped out of the left ventricle with each heart stroke.  I gave you the formula!  It is end diastole (filling phase) and that would be the maximum amount of blood volume for a heart beat.  Then subtract end of systole and that would be the blood volume after the heart has contracted (its clear a stronger stroke contractility will sqeeze out more blood and volume in the chamber would be the least at that time).  Now divide by end diastole and that would represent the percentage of blood volume pumped with each stroke and that is EF.

It should be clear that a higher EF depends on left ventricle contractility.  Weak contractility (probably due to heart muscle damage) less sqeezing pressure and less blood is pumped out with each heart beat (stroke volume) and that means a lower EF.  

Then there can be diastole dysfunction and EF can be preserved.  An example of that would be the filling phase (blood volume is reduced as there isn't enough chamber room for an adequate supply) and although the pumping contractility is unimpaired the amount of blood pumped with each stroke is diminished and heasrt failure can ensue.

I'm not sure what you asked the doctor, if you did ask.  Its difficult to believe a doctor would say to ignore stroke voume as meaningless to EF regarding the heart functionality.  Having said all, you should be able to understand that stroke voulme by stronger vs. weaker contractility increases or decreases the amount of blood pumped with each stroke and the measurement is the EF.  

[Tinu1959]

Thanks Maggiemag and Kenkeith for responding to my post. The information you have provided has great value for me. The information gives me confidence that I am on right track and with minor adjustments here and there I may be able keep my condition in control. This also prepares me with right questions to my doctor.

My present coreg dose is 18.75x2 daily(target is 25 mgx2). ACEI(ramipril) is 6.25 mgx2 daily(target is 10 mgx2, I am not sure?). I have fluid retention problem when BP is low. I need to increase my fluid intake(from 1.5 lit/day to higher) when BP is low. If I do not increase fluid intake it sometimes leads to feeling of weakness. I am gradually learning to keep a balance between BP and fluid intake. This is on my doctor's advise. Maggiemag, I am trying my best to reach target dose of coreg. Initially I was able to tolrate only 12.5 x2 daily. When I increased the dose to 18.75x2 I had many problems. Gradually I got used to it. With some time gap I will further increase it.

Kenkeith, I did ask my doctor about EF(30%) remaining same in both echos. He clarified that measurement of EF is more accurate than stroke volume and I should ignore stroke volume.

[kenkeith]

Does what the doctor stated make sense?  I believe that is consistant to what I said.

CO is a product of blood volume per heart stroke and heart rate. The higher/better the stroke volume (weak, strong, stronger contractions) the fewer heart beats (more for weak, less for strong, least for stronger) are required to meet demand (held constant for illustration) for blood oxygen.  A well-condition individual requires fewer heartbeats due to strong contractions.  It is the stroke that determines EF...not the CO, as CO can vary by an increase or decrease of HR.  Good contractions requires healthy heart cells unimpaired from previous damaging events.

Metrics are somewhat subjective, and a fast heart rate interfers with the visibility to focus accurately the borders of heart walls, and there probably is a margin of error of 10% or more.

None pathological heart condition can be a dilated left ventricle (no LVH on your report indicates it is not considered abnormal).  The LV dilates normally (compensatory) to increase contractions (stroke volume with each heart beat) to maintain a blood flow equalibrium between the left and right side of the heart.... The 56 ml stroke volume on AUG is a result of stronger contractions relative to April and CO will increase with HR held constant ( remember CO is the product of heart rate and stroke volume...that is what is relevant...not heart rate.

You should have asked your doctor why EF is 30% on AUG and April tests when the stroke/volume has increased??? That's my question?

[maggiemag]

Ok, lots of questions and information!  Here's my take:  I bet your blood pressure is under better control with this echo, hence the heart is working less hard and has less pressure to pump against, hence the higher cardiac output.  I do not ever remember, however, a cardiac output reported on any echo I have had and I have had a ton of them!  I would say that the CO derived from an echo would be considered not too accurate, and I personally would not give it another thought.  The ONLY CO I would pay attention to would be from the thermodilution method on cardiac cath.
As for the av sclerosis, I have that reported on all my echoes and no one cares.  This is very common with age.
I would also not care too much about the numbers for aortic root diameter.  Mine has varied pretty wildly on echo over the years, and as long as it isn't too far above the normal, I wouldn't worry.  (I know this is easier said than done, and I DO tend to be a minimizer, but it works for me!)
As far as the LV dimension goes, mine got larger after treatment as well.  I have not had an MI though, I have non-ischemic dilated CM.  I had great difficulty reaching higher doses of my ACEI.  It was only after I was able to get to 10 mg./day of the Lisinipril, that my LV got smaller.  I have normally very low BP so was able tolerate only 2.5 mg./day for 4 years or so, and the target dose of that drug is 20 mg./day, which I will never hit.  So see what ACEI you are on and what the target dose is.  Maybe your doctor could bump up your dose a tad.
I would say the same thing about your Coreg dose.  The target dose is 25 mg. twice a day.  If your BP can tolerate it, maybe they could bump that dose up as well.  Some people never hit it,like me! :-)  The highest I ever got was 12.5 mg. twice a day.  My BP runs about 94 systolic average and frequently down in the higher 80's, if that gives you any idea.  They want your BP as low as you can tolerate it without passing out.
Some lightheadedness when you stand up is normal and many tolerate that ok so have to be on a higher dose of their cardiac drugs.
Remember, Tinu, that the most important thing is how you feel.  So if you feel better and your EF is unchanged, that is good!  Give yourself a big pat on the back for doing your best!  You seek knowledge about your condition and are doing everything  you can to get better!  Hope this helps.
Margaret

[Tinu1959]

Thanks for the valuable information. After your mail I met the cardiologist who conducted echo. He explained that the increased cardic output could be due to the fact that the formulae used for calculating CO is such that even a 1 mm difference in measurement of diameter results in multiplied value. That could be the reason for higher difference with respect to earlier CO value. Whereas in case of EF, the LV areas are directly measured and even if some error is there it does not get multiplied. Therefore calculation of EF is more reliable than CO. Does it make sense??

The echo report also shows that while LA size is reduced the LV size is increased. In my understanding as a layman, both should either increase or decrease together. This was also explained that the angle of measurement sometimes can make such difference.

Form above it looks like echo is not very reliable test. It is difficult to use the values as absolute or as trend. What could be a better alternative to this test?? Any suggestions??

[kenkeith]

The faster the heart beats the less is the reliability of the estimates to be accurate.  This because the movement of the walls are less delineated and it is difficult for manual held transducer to exactly outline the maximum dimensions at end of systole (filling capacity) and end of systole's contraction. The faster the heartbeat the fuzzier the borders (explained to me by the doctor at time of my first echo).  Your Aug. report indicates a HR of 92 bpm...April 85 bpm.

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QUOTE:
In april 2008 the LV stroke volume was 39 ml and Cardic output= 3.33 L/min. Today's report shows these values as 56 ml and 5.2 L/min. Does increase in cardic output imply better heart function?? But EF is 30% in both cases.
__________________________________________________________________

ans. Cardiac output (CO) is stroke volume times HR/min.  (4/08...39 ml X 85 + 3.33 l/min) (8/08...56 X 92 + 5.2).  Not relevant, but what is relevant is stroke volume.  The dilated LV for August is producing stronger contractions as it should do.  But if and when the LV dilates (over compensates) there will be weaker contractions and that cause a drop of stroke volume and the heart rate will have to increase (probably above 100 at rest) to meet the same demand experienced with the 92 HR.

I'm not sure why EF remains at 30%.  It seems to me an increase in stroke volume would increase EF? The formula is blood volume in the LV at end of diastole minus volume at end of systole divided by LV end diastole.  As your record indicates there is an increase of stroke volume!

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QUOTE:
This time a remark is added-" AV sclerosis+". The cardiologist who did echo says it is not serious. But this remark was not there earlier. My lipid profile is under control for almost a year. How serious is this?
______________________________________________________________________

ans. AV sclerosis can cause the LV ventricle to dilate and when serious impedes CO causing the heart to work harder.
_________________________________________________________________
QUOTE:
My LV continues to increase even after one year of MI. Does it mean that measures my doctor has taken so far are not adequate? Need to increase beta-blocker?? Or something else can be done??
___________________________________________________________________

ans.  The goal of medication for heart failure should be to reduce the heart's workload by dilating vessels.  Blood pressure should be as low as possible without any serious side effects.  Heart rate should be as low as possible, also, but with mitral valve regurgitation a slow beating heart may be contraindicated, etc.  If contractions are weak, there are meds to increase contractions.  

I believe I answered all questions?!  Pulse rate and heartbeat would be the same.  There may be a very slight delay (msec) with reading the pulse.

[Tinu1959]

Can pulse rate and heart rate be different?? Generally my resting pulse is 70-75 bpm. Today in my echo report I found that the heart rate recorded is 92 although before the test I measured my pulse manually, it was 75-80. I take beta-blockers and I was under the impression that my pulse rate is now under control being 70-75 in resting and walking 100. Now if the pulse rate is high I need to increase beta-blocker. I already take Coreg 18.75 mg in morning and 15.625 mg in evening. Any suggestions??