[CR]Some Confente stuff...(Confente was not alone)


Example: Framebuilders:Chris Pauley

From: "JB Froke" <jbfroke@msn.com>
To: "classicrendezvous" <Classicrendezvous@bikelist.org>
Subject: [CR]Some Confente stuff...(Confente was not alone)
Date: Wed, 4 Jan 2006 13:36:33 -0800
Seal-Send-Time: Wed, 4 Jan 2006 13:36:33 -0800


Certainly Confente was not alone; and although utterly tragic, his early death was medically not so shocking. Two of my own friends, young athletes including a famous Olympian, died of heart maladies in their early thirties: One an equestrienne, the other (Flo Hyman of the '84 Olympic Team) a volleyball player. But ancient history taught us to watch out long before - In 490 BC, Phidippides, a young Greek messenger, ran 26.2 miles from Marathon to Athens delivering the news of the Greek victory over the Persians, and then he collapsed and died. This is probably the first recorded incident of sudden death of an athlete.

In our little community of Coto de Caza where Flo Hyman and Leslie Love lived and died (we hosted the Olympic women's volleyball team for three years, plus the '84 pentathlon event), we learned twice that sports, per se, are not a cause of enhanced mortality, but they can trigger sudden death in athletes with heart or blood vessel abnormalities by predisposing them to life-threatening heart irregularities.

Other well-known athletes who have been victims of sudden death include marathon runner Jim Fixx (1984), NBA basketball star Hank Gathers (1990), Olympic figure skater Sergei Grinkov (1995), all pro NFL player Korey Stringer with the Minnesota Vikings (2001), and Darryl Kile, all-star pitcher for the St. Louis Cardinals (2002).

The most common causes of sudden death are congenital abnormalities of the heart and blood vessels, or those that are present at birth. These abnormalities usually produce no symptoms and are disproportionately prevalent in African-American athletes. The most common cause of sudden death is hypertrophic cardiomyopathy, an excessive thickening of the heart muscle that can lead to an irregular heart rhythm called ventricular fibrillation. During VF, numerous chaotic electrical discharges to the chambers of the heart (400+ per minute) result in no blood being pumped.

The second most common cause of sudden death in athletes is abnormal coronary arteries (the blood vessels that supply oxygen to the heart muscle). Often, coronary arteries originate from an abnormal location or have an acute twisting angle that slows the blood flow. Other cardiac abnormalities that can cause sudden death are heart valve abnormalities, electrical conduction abnormalities of the heart, and rupture of the aorta (the large blood vessel that carries the blood from the heart to the body). Another cause of sudden death among athletes is Marfan syndrome. Marfan syndrome affects approximately 1 in 20,000 of the general population. People who have this medical condition are usually tall, slender, and loose-jointed. It is a hereditary disorder of the connective tissue, which is the basic substance that holds blood vessels, heart valves, and other structures together. Both of my friends, Flo and Leslie had Marfan syndrome. On June 8, 2004, Florida State basketball player Ronalda Pierce died from an aorta rupture that was a result of this syndrome.

Most sudden death in athletes over the age of 30 is due to a heart attack, or blockage of the coronary arteries. The otherwise normal arteries are occluded with lipid plaque. Athletes who are older than 30 are at increased risk for heart attack if they smoke, have high blood pressure, diabetes, elevated abnormal lipids, or a strong family history of heart disease. Darryl Kile, the Cardinal pitcher, died suddenly at age 33. (His father died of a heart attack at age 44).

Always on topic - Listers, if born before 1983, get a check-up.

-- Maron BJ. Sudden Death in Young Athletes. N Engl J Med. 2003:1064-1075. -- Maron BJ, Chaitman BE, Ackerman MJ, et al. Recommendations for Physical Activity and Recreational Sports Participation for Young Patients with Genetic Cardiovascular Disease. Circulation. 2004;109:2807-2816.

JB Froke, Pebble Beach CA