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joint hyperextensibility, and scoliosis (De Paepe et al 1996) The major risks to an athlete with Marfan syndrome are associated with the cardiovascular abnormalities, which are brought about by the two primary defects: aortic root dilatation and mitral valve prolapse (MVP) Progressive dilatation of the aortic root or descending aorta predisposes to dissection and rupture, whereas MVP with associated mitral regurgitation or LV systolic dysfunction may occasionally predispose to ventricular arrhythmias and sudden death (Yetman et al 2003) The risk of aortic dissection is increased considerably when the greatest diameter of the aorta exceeds 5 55 cm and these patients should be referred for elective surgical aortic root reconstruction (Kouchoukos & Dougenis 1997) Prophylactic -adrenergic blockade is effective in slowing the rate of aortic dilatation and reducing the development of aortic complications in some patients with Marfan syndrome (Shores et al 1994).

the syncope that occurs in unacclimatized persons on rst exposure to exercise in the heat (Eichna et al 1945; Eichna & Horvath 1947) On the basis of these ndings, the authors have concluded that athletes collapse after exercise because they are unable to maintain their blood pressures when standing This is caused by the continuation into recovery of a state of high cardiac output and low peripheral vascular resistance with high rates of blood ow to the dependent limbs including the skin By suddenly stopping exercise, athletes remove the action of the lower limb muscle pump the second heart the function of which is to maintain the central blood volume and the right atrial lling pressure and the stroke volume, even when the peripheral vascular resistance is low and the cardiac output is high, as occurs during the rst few minutes after stopping exercise.

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The FDA can treat as substantially equivalent devices that have the same intended use and the same technology as an existing device or differ in design or technology from a predicate device but perform the same function and are shown to be as safe and effective O Reilly , supra note 19, at 1807 Ch 288, 37 Stat 309 (1912) (codified at 42 USC 201 et seq (1994)) FDAMA 123(d)(I) (codified at 21 USC 301 et seq (1994)) Lorrie Harrison McNeill, CBER Update Spring 2001, Update 2001, Spring 2001, at http://wwwfdliorg/pubs/Update/2001/Issue4/McNeill/printhtml O Reilly, supra note 19, at 1322 Safe Medical Devices Act of 1990, Pub L No 101-629, 16, 104 Stat 4511, 4526 (codified as amended at 21 USC 353 (1994) 21 CFR Part 3, Subpart A, 32 (e) FDAMA 416 United States v.

Weightlifting has been speci cally associated with aortic dissection in athletes with cystic medial necrosis (de Virgilio et al 1990) Congenital bicuspid aortic valve has also been associated with ascending aortic root dilatation and dissection, independent of Marfan syndrome (Ferencik & Pape 2003) Athletes with Marfan syndrome can participate in low and moderate static or low dynamic competitive sports if they do not have aortic root dilatation more than 4 cm, moderate to severe mitral regurgitation, or a history of dissection or SCD in a relative with Marfan syndrome (36th Bethesda Conference 2005) However, these athletes should have an echocardiographic measurement of the aortic root dimension every 6 months If one of the abovementioned conditions is present or there is chronic dissection of the aorta or prior surgical root reconstruction, athletic participation should be limited to low intensity competitive sports.

Additionally, athletes with Marfan syndrome, familial aortic aneurysm dilatation, or congenital bicuspid aortic valve with any degree of ascending aortic enlargement should not participate in sports with a potential for bodily collision (36th Bethesda Conference 2005)..

This is complicated by the effects of any sudden reduction in atrial pressure that occurs on exercise cessation This aggravates the already low peripheral vascular resistance by inducing an additional but atavistic vasodilatation in the exercising limbs the Barcroft Edholm re ex (Noakes 2003c) According to this theory, the treatment of collapsed runners must aim to increase the central blood volume and the right atrial pressure by reducing the volume of blood displaced into the dependent limbs The authors therefore began to experiment by treating collapsed athletes in the head-down position, with their feet elevated above the level of the heart, so that venous return to the heart and therefore right atrial pressure would be immediately increased The results were quite remarkable and very rapidly caused the blood pressures of collapsed athletes to stabilize with reversal of their hypotensive symptoms.

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