Ejection fraction question

[Davsey27]

Hello guys and gals,

I recently found out that my ejection fraction is 50 percent 50-70 percent reference range.Some say that 55 percent to 70 is good.Having Cfs and
exercise being a limitation curious if this number is a problem and how any of you have been able to raise yours.

I also have mitral valve prolapse and test revealed thickening mitral valve

All others markers in echo were normal

Anyways this CFS I think may be due
To one of the 5 past herpes viruses including cmv and/or coxkyaackie b

Thank you I appreciate it

 

[Sushi]

I also have mitral valve prolapse and test revealed thickening mitral valve

Do you have regurgitation, and if so what level? This could affect your ejection fraction if you have significant regurgitation.

 

[Davsey27]

Do you have regurgitation, and if so what level? This could affect your ejection fraction if you have significant regurgitation.

Hello sushi,

I was told by my doctor that their is some leakage but is minor

I first learned mitral valve prolapse as a teenager and would get palpations

Few years back before CFS when I was
able to play ping pong the mitral valve
palpations went away

Post CFS at 33 seems that it is back
and I find it hard to condition oneself
with CFS and multiple herpes viruses/
Cockysaxkie B

Report says thickened mitral valve
and trace regurgitation

The doctor said it is your anxiety causing this and that exercise is good for CFS

Thank you mr sushi
I appreciate it

 

[valentinelynx]

Interestingly, MR usually increases EF (the heart is pumping out more blood because it's going out the aorta and mitral valve. In severe cases of regurgitation, the extra work of pumping through 2 valves will eventually cause the heart to poop out, at which time EF will begin to decline. However in @Davsey27 's case, the regurgitation is insignificant ("trace") so it's unlikely to cause any changes in ejection fraction or cardiac function. But, no, I don't believe anxiety is causing it. That's absurd! As is the statement that exercise is good for CFS.

CFS is associated with low circulating blood volume which means reduced preload to the heart. Preload is the amount of blood that fills the heart prior to the heart contracting and pushing the blood out into the aorta and circulation. This is a potential explanation for a mild decrease in EF. However, this interesting study of cardiac function in CFS patients (it is reduced) did not find a difference in EF between patients and controls. Nor has a number of other studies.

On the other hand, 50% is not necessarily abnormal. If you had previously had an echo and your EF was 70% and now it's 50% then I might be concerned, but not for a single measure of 50%, especially if the echo didn't find anything to explain it like left ventricular hypertrophy or dilation, any ventricular wall motion abnormalities (indicating prior infarction) or abnormal heart rhythms.

I'd be more concerned about getting a better doctor!

 

[HTester]

CFS is associated with low circulating blood volume which means reduced preload to the heart. Preload is the amount of blood that fills the heart prior to the heart contracting and pushing the blood out into the aorta and circulation. This is a potential explanation for a mild decrease in EF. However, this interesting study of cardiac function in CFS patients (it is reduced) did not find a difference in EF between patients and controls. Nor has a number of other studies.

This is good reasoning, but it seems pretty clear that the cause of decreased heart function (cardiac output) in the Hollingsworth study is the decreased end-diastolic volume (EDV). Indeed, a heart must be working very well to manage no decrease (or only a small decrease) in EF despite a 30% decrease in EDV. Assuming the right heart is doing as well as the left heart, it's not at all obvious that we're facing a heart problem.

One hypothesis would be that the apparent decrease in cardiac function is completely secondary to the general decrease in blood volume in CFS. I'm new to PR discussions outside the IDO metabolic trap. Can someone list the current ideas that are proposed to explain the dramatically decreased blood volume that David Bell first reported as a cardinal feature of CFS? I've read that David Systrom is working on this at Harvard, but I don't know what hypothesis they are testing.

 

[Moof]

@HTester, I haven't followed it very closely (I don't get POTS symptoms, so it's not high on my reading list), but I think this is one of the theories underlying low blood volume:

https://www.ahajournals.org/doi/full/10.1161/01.cir.0000160356.97313.5d

 

[voner]

@HTester,

here is the description of Dr. Systroms Mestinon trial...

Detailed Description:
The hypothesis of the investigators' study is that small fiber polyneuropathy is a cause of low biventricular filling pressures/preload failure of the heart and poor oxygen extraction in the muscle bed, leading to symptoms of exertional intolerance and post-exertional malaise. The objective of this study is to examine the exercise response to pharmacologic cholinergic stimulation in patients already undergoing a clinically indicated level 3 cardiopulmonary exercise test (CPET). This will be achieved by inhibiting acetylcholinesterase with pyridostigmine, thus increasing acetylcholine levels, downstream levels of norepinephrine, and enhanced vascular regulation.
To test our hypothesis, the investigators propose the following specific aims:

1. Define the gas exchange responses, such as oxygen uptake, end-tidal carbon dioxide (CO2), and ventilatory efficiency to pyridostigmine
2. Define the hemodynamic responses, such as right atrial pressures, pulmonary capillary wedge pressures and cardiac output to pyridostigmine
3. Evaluate skeletal muscle oxygen extraction to pyridostigmine

These determinations will occur during a clinically indicated level 3 CPET, which includes exercising on a stationary bicycle with a right heart catheter (RHC) and a radial arterial line in place. To stimulate the cholinergic response, a single dose of an oral acetylcholinesterase inhibitor, pyridostigmine, versus placebo will be given after the level 3 CPET. Recovery cycling will be performed after a rest period of 50 minutes. This will be administered in a double-blind, randomized control trial.

https://clinicaltrials.gov/ct2/show/NCT03674541?cond=ME/CFS

 

[Davsey27]

Yes this is what I’m interested about if there is a connection to PEM,the heart and herpes family viruses

I have moved from high emf Atlanta down to laccombe Louisiana and haven’t yet noticed much of a change in ability to do physical labor.

I have been volunteering at someone’s house through workaway and it hasn’t.been easy being away from the parents but

Do feel better around the beach and at times I wonder if Cytalomeglavirus/Ebv/Zoster or Cockysaxkie B is causing the PEM

At times it feels like there is some unexplained weakness that causes nuerodegeneration type symptoms I wonder if it’s herpes going into the brain.

Thank you lady’s and gents

 

[valentinelynx]

but it seems pretty clear that the cause of decreased heart function (cardiac output) in the Hollingsworth study is the decreased end-diastolic volume (EDV).

Yes, that's the same as low preload. Preload, or filling pressure, is another term for EDV.