Quoted post said:Originally posted by labicci
The problem most people have, including myself until the recent years, is to assume that young and physically active people should be healthy and should therefore be less susceptible to heart attack.
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(snip)... In the city that I live, there have been numerous reported cases of sudden deaths from heart attack to physically active young men (yes mostly male) such as policemen, firemen etc. who are very unlikely to use any performance-enhancing drugs. The stresses from modern city life is believed to be the cause in these cases. Professional cyclists, just like anyone else, are also likely to have mental stresses from their social life. Combined with the physical stresses from their training and racing, and the pressure to have good results in order to have new contracts, it is therefore not surprising they are susceptible to heart attack too.
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Whether Lance Armstrong should be banned from racing due to the fact that he used EPO as a part of his cancer treatment is outside the scope of this discussion. However I think that the public should at least have the right to know more about his use of drug, i.e. what drugs are allowed and have been used, his level of hemaetocrit and testerone and how does these compared to other racers, etc.
I've commented on the misconceptions regarding heart attacks on another thread already but perhaps it would be helpful if more people understood what a heart attack actually is and perhaps more importantly, what it isn't.
Stress, gender, age, smoking and a number of other factors certainly can affect one's odds of having a heart attack but a heart attack is caused by a buildup of placques inside the arteries that feed the heart. The heart is basically just a muscle and like any other, it needs to receive nutrients and oxygen in order to perform its job. Deprived of the blood that brings the oxygen and nutrients to the muscle, the muscle dies.
When placques build up to the point of completely blocking an artery, the muscle tissue fed by that portion of the circulatory system is deprived of blood. If the deprivation lasts long enough, the muscle tissue will die.
This is why doctors refer to a heart attack as an "M.I." or "myocardial infarction". The "myocardium" is heart muscle and "infarction" basically means death. The important thing to remember is that to qualify as a heart attack, this death must be the result of a coronary occlusion (blockage of a coronary artery). Stress doesn't, in and of itself, provide the components which make up the placque which lend to or creates the occlusion.
This placque has been examined and analyzed in thousands of cases and it always contains a high degree of fats and cholesterol. The correlation between high cholesterol levels and risk of heart attack isn't quite as linear as one might expect. There are other factors such as homocystene levels, genetics, etc. People who exercise regularly have a tendency to reduce the buildup of placques on the artery walls. People who consume fewer fats and cholesterol also have less tendency to show the build up of these placques. To take the importance of ingestion levels to the extreme; in the U.S. where the average person is eating more fats than ever before in the history of the country, the risk of dying of a heart attack for the average male is over 50%. The risk for someone who has adopted a vegetarian diet is listed, last I saw, at about 4%. Obviously what you eat affects your risk.
Having said all that, my point is this; a heart attack isn't something that simply happens or is triggered by some short-term event. A heart attack is a long, slow progressive event which starts as a slight build-up, grows to a significant build-up and eventually becomes a complete or nearly complete blockage. The final step might be caused by a blood clot, an embolism or a sudden increased need for nutrients by the heart muscle such as is the case when someone is severely frightened and as a result, suffers a heart attack. In such cases the heart attack was imminent. The condition already existed and all that was needed was the final blocking of the artery or a sudden need for increased circulation leading to a rapid rise in work for the heart.
As for the treatment of Pantani, it certainly sounds as though the UCI had singled him out to make an example of him or simply treat him differently than many others are treated. For what it's worth, the "official" explanation that I read as to why he wasn't in the Tour de France was that he was the only rider on his team with any recent performances of a degree which would place them in the league of riders found in the Tour. The claim was that they couldn't invite just him and felt that his team was below the level desired for the most prominent of cycling races.
As for Armstrong and EPO, any affects from the drug that he took to counter the destruction of red blood cells, (erythrocytes), which occurred during his chemotherapy would have subsided a long, long time ago. I threw the question out because it would seem that some people aren't aware of what EPO does, (increases the body's production of red, oxygen carrying, blood cells), or how it improves an athletes performance. I may be wrong but I get the idea that some think that the EPO he took while fighting cancer might still be giving him some kind of unfair edge. Erythrocytes have a lifespan of about 120 days in the circulatory system so any enhanced oxygen carrying qualities would have faded away within months of his final treatments.
