Ryan Shay: What might have caused his death? A discussion of possibilities

Earlier today, we brought you a very abridged summary of today's US Olympic Trials marathon in New York. The race was won by new US running star Ryan Hall, but it was the tragic collapse and death of Ryan Shay (pictured below) that has dominated the headlines.

Sudden death during exercise (and particularly running) has dominated recent news in running, with the collapse of Alberto Salazar earlier this year, followed by the collapse and death of a Spanish football player Antonio Puerta in August, and then most recently, the death of Chad Schieber in the 2007 Chicago Marathon

These events always shock us to the core, because we naturally believe that athletes, especially the elite, are protected against these events. When some of the fittest men in world collapse doing the very activity that is supposed to protect them, it sends a wave of anxiety and doubt through us all. And here at the Science of Sport, we've tried hard to bring you the scientific insights and interpretations of these events.

With the tragic death of Ryan Shay (you can read his profile and bio here), it is of course far too early to diagnose anything. In fact, one of the trickiest and most difficult things about these events is that the cause of death often cannot be established, particularly in the event of some electrical disturbance (arrhythmia). So we must wait on the autopsy result before committing to any analysis, but we did think that perhaps it would be informative and educational to very briefly run through some of the possible medical events and complications that might have contributed to the death of Shay.

Of course, this is very preliminary and is certainly not a diagnosis. Nor is it comprehensive and we acknowledge that we cannot possibly cover everything in this post - it is simply too vast a topic to hit in one go. But we'll do our best to present that information as it becomes available. Until then, our brief look at some of the possibilities...

Introduction to sudden cardiac death - we need a definition

Perhaps surprisingly, there is no universally accepted definition of sudden cardiac death. When we did our post on Alberto Salazar, we drew a response from someone who wanted to point out that heart attacks and cardiac arrests are quite different events. We agree completely and never stated otherwise, and what happened to Salazar was a heart attack, which is defined as a circulation problem. In contrast, sudden cardiac arrest is an electrical problem in the heart.

At this very early stage, taken in isolation, it would appear that Ryan Shay's death falls into the latter category - a cardiac arrest, since most Sudden Cardiac Deaths (SCD) in athletes younger than 35 are caused by these electrical disturbances. In contrast, the heart attack is most often to due Coronary Artery Disease (CAD), something that is usually prevalent in older athletes (over 35). Shay was 28 years old, and so while we again make the disclaimer that we must wait for a proper autopsy result, it would appear to be on the side of cardiac arrest.

The one confounder to this argument is that Shay is reported to have received almost immediate treatment, including defibrillation. Again, I'm not sure that this did happen, or how quickly, but if it was immediate and failed to help, then perhaps we are loooking at a circulation problem? All speculation of course. We covered the circulation possibility in our post on Alberto Salazar a few months ago, so you can read about that there. In this post, we focus on electrical problems.

So the definition for SCD is a "Non traumatic and unexpected sudden cardiac arrest that occurs within 6 hours of a previously normal state of health." That's obviously a vast and all-inclusive definition, but it highlights the reason why these sad events make such an enormous impact on us all - the athlete may have been 100% healthy and normal only hours befor the race, with no known evidence of any abnormality or risk factor for disease.

How often does it happen?

Again, this is a tricky one, because there is no database to track the prevalence of SCD during exercise in young athletes. The largest available studies have estimated that it lies somewhere between 1 per 200 000 and 1 per 1 000 000 athletes per year, which would seem incredibly rare, but it must be borne in mind that this is probably an underestimation, because it's so difficult to diagnose afterwards.

Around 30% of all non-traumatic deaths are due to SCD, with about 30% of the victims being younger than 65 years. Most of the cases (80% or higher) happen either during or immediately after exercise, and it is often the physical activity that may trigger the cardiac arrhythmias. We'll look at this a little later on in this post.

Looking at cause - a very broad overview of the possibilities

Again we must make our disclaimer that we cannot provide an exhaustive list, but hope it's instructive to look at some of the available knowledge on this topic.

To begin with, in most SCD cases, there is a common pattern at the end - you have a combination of exercise and some underlying (and undetected) heart disease which leads to what is called a fatal arrhythmia. Effectively, some underlying condition (structural or electrical) causes the heart to 'degenerate' into a chaotic and abnormal rhythm, and when this happens, the pumping function of the heart is severely compromised.

The list below shows some of the more common causes or underlying conditions that account for SCD in younger (<35>

• Hypertrophic Cardiomyopathy (36%)
• Congenital coronary anomalies (17-19%) (WE WILL LOOK AT THESE TWO IN MORE DETAIL)
• Idiopathic left ventricular hypertrophy (ILVH) (9% -10%)
• Aortic rupture
• Arrhythmogenic right ventricular dysplasia
• Aortic valve stenosis
• Prolonged QT syndrome
• Mitral valve prolapse (MVP)
• Commotio cordis
• Wolff-Parkinson-White (WPW) syndrome
• Atherosclerotic coronary artery disease

We won't look at all these---it would be a thesis to do so---so instead, we'll look at one or two in the interests of discussing some of the more likely explanations. Again, this does not suggest that Shay's death could not be caused by any of the others, or indeed possibilities not on the list.

Hypertrophic Cardiomyopathy (HCM)

This is the most common cause of SCD in younger athletes who die during competition. The condition is characterized by a thickening of the heart muscle (myocardium), which means the demand for blood flow is increased. When the blood flow is restricted, the myocardium becomes unstable and the fatal arrhytmia can occur.

The frightening thing about HCM is that it goes undetected an incredibly high percentage of the time. It is estimated that the condition occurs in about 1 in 500 people, yet the diagnosis is only made in about 1 in 30,000 cases! That is an extra-ordinarily low diagnosis rate. A really difficult issue is that athletes will naturally have larger hearts as a result of training. So when an extremely fit young athlete dies (as was the case with Ryan Shay), the diagnosis is made a little more complex by the fact that the heart muscle is enlarged anyway.

HCM is usually a genetically transmitted condition, but it expresses in varying degrees. The problem, apart from the very low detection rates, is it may not manifest itself until adolescence or even early adulthood, and for that reason, many young athletes may have nothing wrong until the condition manifests itself. The first clinical manifestation (that is, the occasion on which the condition presents itself) is death.

However, research has also found that about 21% of the athletes who die from this condition (which can be diagnosed after the event) did complain about symptoms, which can include chest pain, exertional shortage of breath (dyspnoea), light-headedness, and fainting.

Coronary artery abnormalities

These are the second most common cause of death, and there are a few possible abnormalities in the category. Again, the problem is that these are very rarely diagnosed during life. The coronary circulation, incidentally, is the part of the circulation that provides blood to the heart muscle (as opposed to the pulmonary to the lungs and systemic to the body). So when there are abnormalities in the coronary circulation, the blood flow to the muscle can again be compromised---much in the same way that HCM can cause the same thing.

So what happens here is that there are structural problems, where the connections between the arteries in this coronary 'network' are abnormal. This can cause arteries to become compressed, and again fail to provide sufficient blood to the heart muscle, leading to the development of potentially fatal arrythmias.

As is the case for HCM, the majority of cases are only diagnosed after death, if at all. In 31% of the cases, symptoms were discovered retrospectively - these again include fainting and angina (characteristic chest pain).

Therefore, as with HCM, it is another condition where some symptoms may be noticed, but never acted upon. As an elite athelte, shortages of breath, and over-exertion which may cause severe discomfort and often almost cause the athlete to faint are nothing new. Also, elite athletes tend to be 'wired' or conditioned to ignore these symptoms and push on past the pain and discomfort. For this reason, it is possible that athletes such as Ryan Shay felt some symptoms, regardless of their condition, but sadly ignored them, perhaps attributing them to normal "training pains," with tragic results.

Another possibility - myocarditis

One final possibility that we must mention is a condition known as myocarditis. This is, as the name suggests (the -itis part suggests it) an inflammatory condition of the myocardium (the heart tissue). It is most often associated with a viral infection, which can then affect the heart muscle.

The problem here is that the elite athlete, who may well have a good deal riding on the event (financial, prestige, etc) will often choose not to rest when they have a viral infection. For this result, they are perhaps vulnerable to this kind of condition. If one looks at an athlete like Ryan Shay, who may aspire to a place in the Olympic Games, who has perhaps dedicated a full year of training to this one race, to sit out for a slight infection would not perhaps seem feasible. Whether or not this happened to Ryan Shay is unknown, although perhaps in the coming days it will be revealed. The important point for everyone to learn is that when you feel that you have a viral infection, it's better to err on the side of caution and avoid competition. Also, as illustrated by the HCM and Coronary Artery abnormality cases, the presence of symptoms should be taken very, very seriously.

Conclusion

These are two of the most common conditions that cause SCD in young athletes, as well as a third possibility which is often in play in the elite athlete. There are of course many others, including mitral valve prolapse, a condition diagnosed in Chad Schieber, who died in the Chicago Marathon.

Over the coming days, the autopsy results and further insights may be revealed. If that is the case, then we'll do our very best to interpret and explain them. Until then, we mourn the death of a young athlete and look with new perspective on upcoming sports events.

Ross

Read more on sudden cardiac death, heart attacks and marathon medicine at these posts.

• Heart attack in Alberto Salazar - Coronary Artery disease?
• Sudden cardiac death in sport - a call to action from FIFA and soccer
• Chad Schieber death in the 2007 Chicago Marathon - Autopsy results and discussion
• Chicago Marathon death - no evidence of dehydration
  
  
  
  

Ryan Shay: 1979 - 2007

The USA today decided on its three-man marathon team they will send to Beijing in 2008, but the tragic news from the Olympic trials in New York City today is that of the sudden death Ryan Shay. Initial reports state that the 28 year-old 2001 NCAA Champion (10,000 m) collapsed around the five-mile mark and was taken to Lenox Hill Hospital. He was pronounced dead at 8:46 AM.

Shay was building on an already impressive running career. His list of plamares include:

• 2001 NCAA Champion (10,000 m)
• 2003-04 USA Half-Marathon Champion
• 2003 USA Marathon Champion
• 2004 USA 20 km Champion
• 2005 USA 15 km Champion

Personal Best times included:

• 3000 m : 7:58.5
• 5000 m: 13:35:08
• 10000 m: 28:26.91
• Marathon: 2:14:08

Shay was also a nine-time NCAA All-American runner, and clearly a true champion. Although his marathon times would not have won him a big city marathon, he proved again and again that he had what it took to win races when it counted, as evidenced by his repeat title as the US Half-marathon Champion in 2003-04, and also by his numerous conference titles in the Big East.
The elite American men are a relatively small bunch, and his peers expressed their sadness after the trials today. Eventual winner Ryan Hall, shown on the line to the right of Shay, said, "You never expect to hear anything like that and for it to be my good friend's spouse, it cut me through the heart. He had such great heart.'' In an eerie and strange event from early in the race, the ambulance that carried Shay to the hospital passed the leaders at around 10 miles. One wonders how it could have shaken the competitors to know that their fellow runner was in trouble. Hall has dedicated his Olympic training to Shay's memory.

Currently the cause of Shay's death is unknown, and an autopsy is scheduled for later Saturday. Although his coach, Joe Vigil, said he was unaware of any health problems, sudden death is a risk during exercise and does occur even in apparently healthy and young atheltes, albeit very rarely. The cause of sudden death during exercise is almost always cardiac-related, and reports so far are that Shay received CPR on the way to the hospital.

We are stunned by this tragic loss, and here at The Science of Sport we send our deepest condolences to Shay's wife Alicia, and his parents and seven siblings.

Update: For a preliminary discussion of Sudden Cardiac Death, and some of the more common causes for sudden death in young athletes, read our latest post

No Cinderella Story at the USA Men's Olympic Marathon Trials:

Saturday morning in New York City, mostly in Central Park 131 qualifiers lined up to battle for the right to represent the USA in Beijing next year. In short it was not a Cinderella story as the favorites established their dominance, although not from early in the race. There was one notable change to the format this year---runners were accepted on a number of different qualifying times from 5000 m up the marathon distance. This added quite a bit of depth although there were many runners making their debut or making only their second attempt at this distance.

Noel takes a back seat

Tropical depression Noel was threatening to put a real damper on the weather, but in the end the runners had to face only a bit of wind and nothing too hectic. Temps were in the low 40's at the start as Michael Wardian from Virginia became the first "TV Runner" and took an early 100+ m lead. In Wardian's defense, though, the pace was pretty pedestrian at the start as the pack was on pace for only about a 2:20 finish. Most of the runners were likely elated at the early pace as it gave them a chance to stay with the favorites. However after approximately nine miles things started to change.

The first move - What was Sell thinking?

Around nine miles someone surged, and suddenly Abdi Abdiraham, Meb Keflezighi, Ryan Hall, Fasil Bizuneh, and Dathan Ritzenheim had a gap. Brian Sell of Team Hanson, who lead for 20 miles in the pre-Athens trials, did not respond. This was surprising as it was not a massive acceleration, and instead the five seemed to float away slowly. Nevertheless, Sell and the others let them go while many pundits and fans must have been thinking what a bad tactic that was. Dan Brown responded late and bridged the gap after a few minutes. He was followed by two counter-attacks, first by Josh Cox and then by Khalid Khannouchi, both of which failed.

In the end Sell's patience payed off as he took third eventually (2:11:40) behind Ritzenheim (2:11:07) and Ryan Hall. Hall's 2:09:09 was a US Olympic Trials record although was not surprising as he ran 2:08:24 in his debut in London this year. Hall also has a 59:43 half-marathon best, also an American record.

The final results looked like this:

1) Ryan Hall (2:09:02) (Trials record)
2) Dathan Ritzenheim (2:11:07)
3) Brian Sell (2:11:40)
4) Khalid Khannouchi (2:12:34)

Should Dathan Ritzenheim qualify for the 10000 m event, he has indicated that he might forgo his spot on the marathon team as he is more interested in the 10,000 m. This would allow Khannouchi the opportunity to compete for the USA in the marathon, which is something to which he has aspired since the pre-Sydney trials, but has been hampered by injury.

Sad news from the race - death of Ryan Shay

In the meantime, the breaking news from the trials is the sudden death of Ryan Shay, who apparently collapsed around the five-mile mark. We are working hard to find out details, and you can be sure that we will have a full analysis of the physiology behind this tragic event.

See our other posts on sudden death during exercise:
Death at the Chicago Marathon
Autopsy report from Chicago Marathon
Analysis of a hospitalized runner
No evidence of dehydration in Chicago Marathon death

Scientisits engineer a "Lance Armstrong mouse": How scientific and journalistic integrity goes bad

US scientists have successfully managed to 'engineer' a line of mice that display remarkable physical prowess and ability. In some English newspapers, it was referred to as "The Mouse that Shook the World", and of course, many have termed it Mighty Mouse.

Being scientists, we have no problem with that, and the achievement of the scientists, led by Professor Richard Hanson, in creating the mice by injecting a gene for an enzyme called PEP-CK is a remarkable one (we won't go into the details here).

But what is unfortunate is how the scientific and journalistic integrity of exercise science and physiology was then compromised by what can only be described as very bad and very scientifically inaccurate attempts to translate this information for the public, by both the scientists and the media.

Now, we have no issue with this - we feel very strongly at The Science of Sport that complex science should be 'packaged' in a more easy to understand, entertaining form, but unfortunately, what Professor Hanson and the media have done is compromise exercise physiology through their sensationalist explanations...

It is not a Lance Armstrong mouse

Take the following two statements, for example:

"...the physical performance of the supermouse can only be compared to supremely fit athletes like the cyclist Lance Armstrong, who won the Tour de France seven consecutive times from 1999 to 2005. The genetic alteration to a gene involved in glucose metabolism appears to stimulate the efficient use of body fat for energy production. At the same time, the mice do not suffer from a build up of lactic acid – which causes muscle cramps – a feature also seen in the best endurance athletes." (source)

"They are metabolically similar to Lance Armstrong biking up the Pyrenees; they utilize mainly fatty acids for energy and produce very little lactic acid," said Hanson" (Source)

A few points:

What does "metabolically similar" mean? An incorrect starting point

Firstly, this is pure conjecture, and irresponsible, incorrect conjecture at that. Professor Hanson has never monitored any cyclist cycling up the Pyrenees, let alone Lance Armstrong, and so the comparison is laughable. In fact, I doubt they even measured the metabolic characteristics of their mice. Can we define "metabolically similar"? The answer of course is no, because we don't even know what to look for. Perhaps the mice have similar oxygen consumptions, or lactate levels? Meaningless information, quite frankly.

It's not lactate - exercise physiologists have known this for a while

Secondly, the scientific basis for the argument is entirely incorrect. The lactic acid which is blamed as the cause of muscle cramping, is in fact a source of fuel and is in no way responsible for cramps. Poor lactic acid (or lactate, which is the more correct term) is blamed for many of the problems associated with fatigue during exercise. The truth is, it's actually used by the muscle as a source of fuel.

So in fact, when the scientists claim that Lance Armstrong produces less lactate (a claim made by Armstrong as well, incidentally), they are probably incorrect. If anything, Lance Armstrong's difference lies in the fact that he is able to USE lactate more effectively than untrained people. Without going into too much detail (this is something we can tackle in a future series, perhaps), lactate is produced as a result of a metabolic pathway called glycolysis.

The lactate is then released into the blood, and taken up by other muscles and tissues (including the heart, incidentally), where it is used as a form of energy. So what elite athletes can do is use lactate. As a result, when you measure the lactate levels, what you are measuring is the balance between release and uptake. For that reason, you cannot simply make the statement that the mice are "producing less lactate." Similarly, you cannot say this about Lance Armstrong.

Now the problem here is that in exercise physiology, this type of information is known by MOST people, but not necessarily by biochemists. So just as medical doctors delivering verdicts on dehydration are coming from their paradigm which may not be appropriate for exercise, so too biochemistry is not necessarily as cut and dried as this.

Oversimplifying human performance - Lance Armstrong is not different either

Finally, and perhaps most significantly, this entire sensational media report makes the startling assumption that Lance Armstrong himself is different from the rest of the population against whom he competes, which is not true from a scientific point of view. All this does is propagate this oversimplification of a myth that one athlete can be physiologically and vastly superior from others at an elite level. Clearly, Armstrong was superior on the bike - he won the race 7 times in a row, so from a results point of view, no argument, but that is not what I am referring to. Instead, I'm referring to the oversimplification of the reasons BEHIND that success. And I do not believe that this type of irresponsible reporting or translation of the science (by journalists or scientists who frankly should know better) does anything to help advance our understanding or appreciation of exercise science.

The reality is that to suggest that a cyclist is "unique" merely contributes to an inaccurate physiological stereotype. The most tested (and published) cycling teams in the professional ranks are Spanish teams, who have been extensively researched, with some very interesting data. The truth is that if we showed you a table of the results of 10 professional cyclists, including their VO2max values, lactate values, heart rates and "metabolic" markers, you would be completely unable to tell which of those cyclists is the best! Lucia et al, in 2004 in Medicine and Science in Sports and Exercise, published the results of their testing on the Banesto team, which included former podium finishers in the Tour de France and a winner of the Vuelta Espana, as well as domestiques and "back-of-pack" riders (in the pro peleton). And the most interesting thing of all is that the best rider, the one who achieved Grand Tour victories, had very average physiological data! It was some of the domestiques, the climbers, who were good for perhaps a few stage wins and some solid finishes, who produced the "best" results.

Now, from a scientific point of view, adopting the paradigm of the Mighty Mouse scientists, it would be an open and shut case to say who would win. But the results contradict this, for they suggest that there is something we cannot measure that accounts for success in competition.

As for the case of Armstrong, it is indeed unfortunate that highly educated people like Professor Hanson propagate myths and urban legends suggesting a "genetic superiority" because that is not what exercise physiology tells us. Unfortunately, most viewers of the Tour and of sport in general believe this, for it comes from an educated source. But the truth of the matter is that neither Lance Armstrong, nor any other athlete for that matter, possess characteristics that stand out from the rest of the elite sportspeople they compete against. What is the difference between Gebrselassie and Tergat? Well, 29 seconds, of course, but you cannot measure it! The difference between Asafa Powell and Tyson Gay? Maybe 3/100th of a second, also can't be measured physiologically!

This is in fact one of the most fascinating things in all of exercise science - what determines success? People will tell you its a high VO2max, good running economy, low lactate levels etc. All these are theories, undoubtedly contributing to the whole, but not one thing exists, or even a package of things exists, that can explain why Athlete A beats Athlete B. Often, the science would have predicted that Athlete B would win!

So the point is that this type of sensational science does little for the field of exercise physiology, and in this specific case, merely builds a false legend that perhaps should be examined somewhat differently.

Ross