Recently, there have been a number of high-profile athletes who have died sudden and frightening deaths. Basketball stars Reggie Lewis, Hank Gathers, Pistol Pete Maravich, and volleyball standout Flo Hyman remain vividly in our memories not only because of their athletic achievements, but also because of their untimely exits from this world.

Thus, the risk is extremely low. However, along with this low risk is the reality that most athletic trainers - and many team doctors - may not be knowledgeable about cardiac disease. They don't always screen their athletes for cardiac problems in preseason physicals and may not be aware of the warning signs. The challenge, therefore, is trying to identify those individuals who are at high risk.

Table One lists the most common cardiac causes of sudden death in athletes under the age of 35. At the head of the list is cardiomyopathy, of which there are two types, hypertrophic and obstructive. In hypertrophic cardiomyoathy, which doctors believe was the cause of Reggie Lewis' death, there is a thickened cardiac muscle, no evidence of chamber enlargement, and extensive myocardial scarring.

People who die from this condition are thought to have an increased frequency of ventricular arrhythmia (a disturbance in the rhythm of the heartbeat) as was the case with Hank Gathers. In these cases, the cardiac enlargement is concentric (symmetric) and there is no evidence of obstruction of the outflow tract in the left ventricle. Athletes with this condition often complain of cardiac palpitation or cardiac flutter and may have syncopal or fainting episodes, in which the athlete collapses after a strenuous workout. It can be screened for with an echocardiogram

Obstructive cardiomyopathy has been described under a number of different names over the past 30 years, including hypertrophic obstructive cardiomyopathy. The key features are asymmetric hypertrophy of the cardiac muscle and enlargement of the cardiac muscle on the septum of the heart, which obstructs blood flow during exercise. This obstruction beneath the aortic valve causes the mitral valve to prolapse and to work inappropriately, and can be easily recognized on an echocardiogram. During a physical exam, this obstruction is recognized by harsh systolic heart murmur that is atypical in nature; when the athlete is asked to perform maneuvers that make the left ventricle smaller and this increase the obstruction, the murmur increases. In addition, there is often a family history of sudden death in athletes with this condition.

In the condition of anomalous (atypical) origin of the coronary artery, the blood vessels that run to the heart do so in an irregular manner. In some cases, the patient has a single blood vessel instead of two, as was the case with Pete Maravich. A more common condition in that one of the two main blood vessels which run to the heart originates from a different site than normal. For example, the anomalous vessel may go between the aorta and pulmonary artery. Anomalous origin of vessels are dangerous because the course of the coronary vessels becomes compromised. During exercise, those blood vessels can come closer together and squeeze or obstruct the coronary artery; the coronary artery could also become obstructed because it has a more torturous or unusual course. People with anomalous origin of the coronary artery often complain of chest pain or chest discomfort upon exertion. To diagnose this abnormality, a resting and exercise cardiogram is very helpful.

Aortic rupture from Marfan's syndrome - nicknamed Abe Lincoln's disease - is seen in people who are tall. In these people, there is an abnormality of the connective tissue that results in weakening the structure of the aorta and cardiac valves. The weakened connective tissue can lead to a rupture of the aortic blood vessel or a rupture of the aortic valve as happened to Flo Hyman, who was 6"5". This condition may be initially screened for by simple measurement. When the athlete's arm span is greater than his or her height, this disease may be present. People with this abnormality also have increased flexibility of finger joints, a high arch palate, and long, slender fingers.

Coronary artery disease, a disease more common in older populations, can also occur among young athletes. It involves a narrowing of the blood vessels and symptoms include chest discomfort and shortness of breath. It is screened for through an electrocardiogram.

Sudden death can also occur due to non-cardiac causes. Table Two lists these causes.

Alcohol has a number of effects on the body. In combination with barbiturates, for example, it is often lethal, and by itself, it can cause cardiac arrhythmias. The most common cardiac arrhythmia is atrial fibrillation. A typical story is that after a major athletic event, such as winning a championship, there is a great deal of celebration and alcohol ingestion that precipitates the cardiac arrhythmia.

The symptoms present with an overdose of cocaine are often similar to the cardiac causes of sudden death. Pathologic reports have showed cerebral aortic and myocardial effects of cocaine. Death could be due to cerebral vascular accident, rupture of the aorta, or a myocardial infarction.

Amphetamines or "speed" can cause cardiac arrhythmias. These drugs were introduced during World War II to keep pilots awake during long bombing missions. More recently, they have been used by athletes to increase endurance.

Erythropoietin, or EPO, stimulates red blood cell production. With more red blood cells, athletes are able to carry more oxygen in their blood and enhance endurance. In 1985, synthetic erythropoietin became available through specialized recombinant DNA technology. Although it was developed to be used in the treatment of patients who have anemia resulting from relative or absolute erythropoietin deficiency, erythropoietin was soon used by athletes, particularly in Europe (where is was first approved for clinical use), as a ergogenic aid. Since 1987, approximately 20 Dutch and Belgian amateur and professional cyclists have died unexpectedly, and these deaths were all thought to be cardiac in origin. Although none of these deaths have been conclusively linked to erythropoietin, which is illegal but cannot be detected by any current drug testing, rumors abound in the cycling community that it is the cause.

The mechanism of death due to EPO is thought to be increased hematocrit (red blood cells). The erythropoietin will increase the hematocrit to high levels in any endurance event. Dehydration will push the hematocrit even higher, causing clotting in the blood vessels to the brain or to the heart could cause death.

The challenge to the medical profession is to find a cost effective way to screen and identify preventable causes of sudden death in athletes. It is obvious that if the risk is 1 in 280,000, mass electrocardiogram screening cannot be done because it is too costly. However, all persons who exercise should be given a history and physical exam. If they have any of the following risk factors, 1) a family history of sudden death or heart disease, 2) personal history of external chest pain or fainting or 3) on physical exam - heart murmurs, high blood pressure or Marfan's syndrome they should go on to the next level of screening which is a rest and exercise electrocardiogram. The exercise electrocardiogram should be a maximal effort exercise test. The routine exercise tests done in most doctor offices are submax and does not stress the heart and lungs to the same anerobic intensity which athletes routinely perform.

Herman Falsetti, M.D., is a board-certified cardiologist with Health Corp., in Irvine, California. 949 727 1900. A former professor of cardiology and team physician at the University of Iowa, he has also served as team physician to several elite racing teams, including members of the 1984, '88, '92 and '96 U.S. Olympic cycling teams.

1. Hypertrophic cardiomyopathy

2. Obstructive cardiomyopathy

3. Anomalous origin of coronary artery

4. Aortic rupture (Marfan's syndrome)

5. Coronary artery disease

6. Right venticular dysplasia

7. Electricalconduction system abnormalities

8. Aortic stenosis

9. Myocarditis

1. Alcohol

2. Cocaine

3. Amphetamine

4. Erythropoietin (EPO)

5. Vascular event

6. Head trauma