As a Colorado native and fanatic Denver Broncos fan,
I have been going to NFL games since I was old enough to wear a jersey.
However, there was one preseason Broncos game that I will never forget. I remember in 2005 when the Broncos were
playing the San Francisco 49ers at home. While the game was not particularly
remarkable, what happened after certainly was. The starting offensive guard for
the 49ers, a relatively young player named Thomas Herrion, passed away in the
locker room after the game. It was later determined that Herrion died as a
result of a condition called hypertrophic cardiomyopathy (HCD). HCD is a
condition in which the muscles in the bottom half of the heart become
significantly larger than normal. As a result of the muscles getting so large,
the chamber of the heart that hold oxygen rich blood becomes much smaller and
much less capable of pumping blood to the rest of the body. The current theory
is that this condition is caused by some sort of genetic mutation. As a result
of the large number of high profile athletes that have either died or been
forced to retire as a result of this condition, a lot of research has been done
in an attempt to identify the genetic cause. Recent studies have demonstrated
that a mutation in the genes that are responsible for making cardiac Troponin C
(cTNC) are somehow involved (Parvatiyar et al., 2012). Troponin C is an
important protein involved in muscle movement. When cTNC binds to calcium
floating around the muscle, it changes shape and allows other proteins to
function and the muscle to contract. This action is kind of like a hand deactivating
an emergency brake in a car allowing the accelerator to move the car. Recent
studies have found that a mutation in region of the protein that actually binds
to calcium can lead to HCD. This mutation causes the protein to be extra sensitive
to calcium levels which in turn makes the heart muscles extremely excitable.
This increase in activity leads to a buildup of muscle over time, especially in
the regions of the heart related to HCD. Though this mutation is not the only
cause of HCD, it is a new and exciting discovery that could lead to a better
understanding of how the disease progresses.
References:
Parvatiyar, M.S., Landstrom A.P., Figueiredo-Freitas, C., Potter, J.D.,
Ackerman, M.J., Piimto, J.R.. (2012). A
mutation in TNNC1-encoded cardiac troponin C, TNNC1-A31S, predisposes to. Journal
of Biologic Chemistry, 1-24.
I found it interesting that part of the reason HCD is so hard to diagnose is that it is very hard to distinguish from “athlete’s heart.” It is very common for professional athletes to have a benign increase in cardiac mass as a result from their systematic training. This makes it much harder to try and discern whether the increase in cardiac mass is due to systematic training or because of a mutation. At some point, one has to wonder whether changes need to be made to the typical sport physical to try and cut down on these tragic and unexpected deaths.
ReplyDeleteMaron, B., & Pelliccia, A. (2006). Ciculation. The Heart of trained athletes, 114, 1633-1644.
I have heard of this before and when I was reading about it I found this procedure they do called alcohol septal ablation. This is basically shooting straight absolute alcohol into the arteries of the heart where the heart is thickened this has immediate improvement of the decreasing the thickness of the heart and can do this permanently. But there are complications associated with this procedure, like an AV block. Sometimes the patients need pace makers to control their heart after this procedure. But it is favored in older patients who have other diseases that make it difficult for placing a pace maker. I agree with Tim that changes might need to be made to the typical sports physicals to detect this problem.
ReplyDeletehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780820/