Heart and Soul

My absolute most pleasurable moment in triathlon came at 6:25:02 PM on November 20, 2011. It was at that moment I crossed the finish line of Ironman Arizona, just after sunset. I raised my arms and face to sky and howled in pleasure and release. I had just won my age group for the second time in Tempe (my fifth Ironman win), after running down and staying ahead of someone two years my junior, who actually ran a faster marathon than I did. All this 14 months after nearly killing myself (and almost becoming paralyzed) against the back end of a pick-up truck at Ft. Lewis, Washington.

I had no right to be there, to be racing, much less to win, but somehow, it all happened and put me floating on top of the world. My bubble was very short lived, though. About two hours later, after showering, dressing, and walking to a local pub to meet with my coach and teammates, I got the word that, hours earlier a continent away, another of our teammates, running towards a similar joyous finish line in the Philadephia Marathon, had collapsed and died, leaving behind his wife and young children, and a lot of friends across the world in the online endurance communities.

Another guy I know, more of an average Joe type of athlete, stopped all serious exercising last summer/fall when he was diagnosed with “Hypertrophic Cardiomyopathy” – presumably the same diagnosis which fell Chris G.

What’s going on here? We know that 1-2/100,000 citizen marathoners die during a race, usually near the finish, from cardiac events. And triathlon more frequently encounters deaths during the first segment of a race, the swim. Maybe 2-4/100,000 participants don’t make it out of the water. Just three days ago, another man was lost during the iconic Escape From Alcatraz Tri in San Francisco Bay. Renowned triathlon pioneer Dan Empfield has written recently about this phenomenom.

Now, I’m not a cardiologist, or even much of a scientist. But I do speak the language a bit. In the midst of all this attention being paid to sudden cardiac events in endurance races, I found myself doing a little bit of research. I’ve learned that some runners, as they age, have more of a problem with atrial fibrillation (heart flutter), which, coupled with  other aspects of the athlete’s heart (slow rate, big stroke pumps) may be a source of dysfunction as well as health. But the most recent theory goes something like this, drawing on a number of threads which have appeared in the past 10-15 years. First of all, we know that many runners show signs of cardiac muscle damage after a marathon. Enzymes which appear after cardiac muscle damage are elevated. Second, we know that the right ventricle, the part of the heart which sends blood to the lungs, can show signs of abnormal function immediately after a race. In some triathletes, more so among those  who are older, with a longer time in the sport, and who have a higher maximum VO2 (oxygen uptake and use capacity, a sign of superior fitness), that dysfunction does not disappear, and may even be associated with signs of fibrosis in the septum, the wall between the ventricles through which runs the major conduction chain controlling heart beats.

So my pet theory is: the right ventricle gets overworked, leading to muscle damage there in the septum.  In the process of repairing the damage, muscle bundles are reduced to fibrous tissue, which neither contracts nor carries the electric impulses required for the heart to beat in a coordinated fashion. When increased stress is put on the heart, such as at the start of a swim, jumping into cold water with no warm-up surrounded by 100s or 1000s of intense hyperactive racers, or at the end of a marathon, when there is a sudden uptick in effort to “finish strong”, the right ventricle can’t do its thing properly. Whether that’s beat strongly enough, or carry the conduction impulse properly, it doesn’t matter. The heart stops working properly, even though the body, and indeed the heart itself, has proven to be strong during months and years of training and racing. Result – sudden cardiac death.

I went to my primary care doctor with this theory, and we agreed I would get an EKG and an Echocardiogram to at least start looking into this. I shared with my MD an article from Australia and Belgium (European Heart Journal, Dec 6, 2011, by La Gerche, Burns, Mooney, et al.) It’s specific to long-course triathletes, studied pre and post [immediate and 1 week later] races that showed an increased risk [relative to other IMers] for evidence of cardiac fibrosis who met the following criteria: competing for longer (20 yrs vs 8 years), had greater predicted VO2 max for age, and were older (50+). So that’s me!

What did I hope to find? The EKG might show if I had any hidden conduction abnormalities. The Echocardiogram (an ultrasound of the heart) was because those with evidence of fibrosis (determined by delayed gadolinium enhancement, whatever that is) had a LOWER right ventricular ejection fraction (like I said, I’m not a cardiologist, so you’ll just have to accept that as a measure of cardiac function) than those without. So the Echo + and EKG (never had one before) seemed like good initial non-invasive screening tests to get which might actually produce some valuable information as far as my risk stratification. The article suggests the gold standard for determining if there is right ventricular injury is a cardiac MRI, which doubt I’m gonna get unless I hoot and holler a lot.

The results came back (as filtered by my MD):

1. Sinus bradycardia. [Duh! My resting HR is 38-40, which is considered abnormal.]
2. Normal left ventricular size with mild septal hypertrophy and normal
systolic function with EF of 60%, with grade 1 diastolic dysfunction.
3. Minimal left atrial enlargement.
4. Normal cardiac valves.
5. Possible PFO. [Patent Foramen Ovale, a non-significant finding in 30% or so of adults]
6. Normal pulmonary artery pressure.

The EKG is a little more problematic but I expect the changes are most likely related to the bradycardia due to your level of fitness. I’ll check with cardiology and see if they’d like to see you.”

Notice nothing at all is said about RIGHT ventricular function, which is what I wanted to find out about. Although the “normal pulmonary artery pressure” may give a clue as to right ventricular function. So that’s where I leave the story for now, with further updates “as they become available”. For now, I continue to live my life as I always have, pushing just a little bit against the fabric of my limitations to see just what is possible, without killing myself in the process.