25% ejection Fraction in a marathon runner

[redredrunner]

I need help understanding the medical condition of a running friend of mine.  This man is in his early 50's and is good general health.  However, he has a past history of MI, which he says involved about 30% of his left ventricular wall. This is an old MI, felt to be due to a bout of childhood vasculitis.  He is seen regularly by a cardiologist, and has regular stress echo exams.  His most recent exam showed an ejection fraction of 25%, but no evidence of ischemia.  His cardiologist says he is "cleared for all activities".  This man has no cardiac symptoms that I know of.

The amazing part of this story is that this man is a hard-core runner, who frequently competes in ultramarathon events (30-50 mile trail runs). He can easily outrun other runners with "healthy" hearts.

When I think of someone with an ejection fraction this low, I imagine a "cardiac cripple" who has trouble climbing stairs.  How is it that someone an EF of 25% can compete at such a high level?  This man has a normal heart rate and ventricular volume, so his cardiac output must also be low.

Any comments?

[itdood]

You have to think about how EF is calculated.    It's not a measure of overall heart output from the left ventricle.  That is a seperate measurement, called the Stroke Volume.  Can you find out what his SV is?

It sounds like his heart was damaged at a young age and has had time to adapt.

What a great case study this would make though, someone should study it more to find out how his heart adapted.  Given the LVEF, it doesn't sound like his LV contracts very well.  SOmething has to be making up for it.  Perhaps the LV grew larger?  Other chambers took over?

[kenkeith]

Statistics are been compiled and analyzed and their is conclusion that about 26% of the heart disorder population has an EF below 29% (heart failure range) and don't know they have a heart disorder!

Six years ago I had a silent heart attack with an EF below 29%, and hospitilized with congested heart failure (breathing in dusty environment for several hours probably triggered the CHF) and I was feeling very well prior, but had a dry cough and shortness of breath. I recovered quickly and feel well to this day.

If there has been an MI, by definition there is heart wall damage.  The damage could be related to necrotic (dead heart cells) or stunned heart cells, but those conditions  would result in weak wall contraction and a lower EF.  

There has to be a balance of oxygenated blood to meet the oxygen demand.  Obviously, if the supply is limited by a low cardiac output, there needs to be a reduction of demand...but exercise does not decrease demand...it increases demand.  The athlete must have an outstanding pair of lungs and other compensation.