Chicago is still reeling from the aftermath of the Chicago Marathon as they struggle to ascertain why Chad Schieber, an otherwise healthy 35 year old police officer, could die during the event. Certainly, everyone’s heart goes out to the grieving family, and at times like this, we all search for “the cause” – why should an otherwise fit individual die?
The coroner’s report that described “mitral valve prolapse” as the cause. But for those of us in the cardiac field, we wonder, how the heck can the presence of mitral valve prolapse cause death?
Mitral valve prolapse is caused by a redundancy of the mitral valve that causes the mitral valve (which separates the left atrium from the main pumping chamber of the heart, the left ventricle) to bow, or prolapse, into the left atrium. The leaflets are prevented from bowing too far back into the left atrium during systole by strong strands of tissue (called chordae) that act to tether the leaflets to the left ventricular chamber (think of the lines attached to a parachute that serve to hold air inside the parachute). Some patients have some leakage of the valve from the left ventricle backward into the left atrium caused by the bowing leaflets. Tons of folks live just fine with a minor leakage. But if the leakage gets too severe, or if one of the chordae ruptures, the flow of blood backward into the lungs can be so severe that the lungs fill abruptly with fluid, and respiratory collapse and perhaps death, occurs.
We are given limited information in the coroner’s report if a chordal rupture occurred in Mr. Stokes, only that he had “mitral valve prolapse.” So if he did NOT have chordal rupture, then we are left to wonder, would the mitral valve prolapse in and of itself, have killed him? Likely not. So if not, what other causes might explain his untimely demise?
First, let me say, I doubt we will ever know. But much more common in marathoners running on a hot day is the presence of heat stroke and electrolyte abnormalities. Given the hype about the need for water and the experience of this runner, it’s hard to imagine that heat stroke would be the most likely cause here, but it can’t be excluded. Electrolyte abnormalities, on the other hand, may have played a significant role.
There are two main “electrolytes of life,” as I like to call them: sodium and potassium. Sodium is the major electrolyte outside of cells, and potassium is the main electrolyte inside of cells. Sweat is important cooling mechanism for the body, since evaporative heat loss is a very effective way to lose heat. But with sweat goes sodium and a small amount of potassium, too. And so the marathoner drinks water – lots of water – but often, does not replace any of the sodium lost with sweating.
And the results for the heart can be catastrophic. An important study was recently reported in the New England Journal of Medicine regarding hyponatremia (low sodium levels) in marathon runners in the Boston Marathon. This weekend, I had a chance to see this first-hand on Sunday when a marathon runner presented to our ER with hyperventilation, confusion and muscle fasciculations (diffuse fine twitching) and positive cardiac markers. Here were his lab studies:
Sodium 125 (ref: 133-145 meq/L)
Potassium 3.4 (ref: 3.5-5.3meq/L)
Chloride: 90 (ref:98-108 meq/L)
CO2 17 (ref: 23-32 meq/L)
Myoglobin: 1453 (ref: 21-98)
CK-MB 62.5 (ref:0.6-6.3)
Troponin-I 0.31 (ref: 0.0-0.06)
His EKG was normal.
What was striking were his confusion and muscle fasciculations. If effect, his sodium was so low that it was affecting all of the excitable tissues: his neurons and muscles. Fortunately for this individual, he did not have any skipped heart beats.
But throw a few extra heart beats into a heart exposed to that low sodium (which certainly could happen in the setting of mitral valve prolapse) and fatal cardiac arrhythmias can occur abruptly and irreversibly, resulting in sudden death.
So could this have been the real cause of death for this young man? Perhaps. Perhaps not. But blaming it all on mitral valve prolapse sends the wrong message to the thousands of patients living with this common heart valve anomaly.