JACC Vol. 7. No I 231 January 1986:231-6

Mitral Valve Prolapse: Definition and Implications in Athletes

ROBERT M. JERESATY, MD, FACC Hartford and Farmington. Connecticut

Mitral valve prolapse is probably the most common car• and sudden . The symptoms and the complications diac valve disorder, affecting approximately 5 % of the are not usually related to physical activity. population. Although it is genetically determined, its A permissive attitude toward participation of patients clinical manifestations do not usually become evident with mitral valve prolapse in competitive athletics is before adulthood. In the setting of a referral probably warranted; however, it would appear reason• center, a mitral valve prolapse syndrome, consisting of able to disqualify athletes with mitral valve prolapse in nonspecific symptoms, repolarization changes on the the following circumstances: 1) history of ; 2) electrocardiogram and , has been identified. disabling ; 3) complex ventricular arrhyth• However, doubt has recently been expressed about the mias, particularly if induced or worsened by exercise; existence of such a syndrome. The prognosis of mitral 4) significant mitral regurgitation; 5) prolonged QT in• valve prolapse is generally favorable but infrequent com• terval; 6) Marfan's syndrome; and 7) family history of plications do occur and include transient ischemic at• sudden death. tacks, progression of mitral regurgitation with or with• (J Am Coil CardioI1986;7:231-6) out ruptured , infective

Mitral valve prolapse was first identified (1,2) as a clinical• ally become evident before adulthood (1). However, the pathologic entity in the mid 1960s when the midsystolic symptoms associated with mitral valve prolapse, particularly click and the late systolic murmur were correlated with the chest pain, fatigue and palpitation, and the serious yet un• demonstration of angiographic protrusion of the mitral leaf• common complications of this syndrome (especially sudden lets into the left and late systolic regurgitation. This death and ruptured chordae tendineae) have a definite bear• syndrome continues to generate great interest and remains ing on those who participate in athletics and on their possible the subject of an unprecedented information explosion. De• disqualification from strenuous and competitive activities. spite the outpouring of information, much of it remains incomplete, contradictory and controversial (1-3). More• over, careful studies of mitral valve prolapse in the athlete are notoriously lacking. In this report, the implications of Etiology and Basic Structural Definition mitral valve prolapse, as it relates to recommendations on The basic structural abnormality of mitral valve prolapse participation in competitive activities, will be formulated in is the systolic protrusion of the mitral valve leaflets or their the context of its cause, pathology and clinical findings and scallops beyond the mitral anulus into the left atrium as complications. demonstrated by angiography, and patho• logic examination. Although the cause of this syndrome Scope of the Problem remains controversial, two main theories have been pro• posed: the valvular theory stresses mitral valve abnormality Mitral valve prolapse is probably the most common car• as the cause and the myocardial theory ascribes this syn• diac valve disorder. Although the abnormality may be ge• drome to primary myocardial involvement (1). netically determined, its clinical manifestations do not usu- According to the valvular theory, myxomatous transfor• mation is the underlying mechanism responsible for mitral From the Section of Cardiology, Department of Medlcme, Samt Francis valve prolapse and the associated click. Myxomatous trans• Hospital and Medical Center, Hartford, Connecticut; and DIvision of Car• formation is characterized by disruption and loss of normal diology, University of Connecticut School of Medicine, Fannington. Connecticut valvular architecture with thickening of the spongiosa, which Manuscript received January 22, 1985; revised manuscrIpt received is rich in acid mucopolysaccarides. The thickened spongiosa March 26, 1985, accepted May 24, 1985 encroaches on the fibrosa, interrupting it focally and causing Address for reprints: Robert M. Jeresaty, MD, Director, Section of Cardiology, Saint Francis HospItal and Medical Center, 114 Woodland a basic weakness of this supporting structure, leading to Street, Hartford, Connecticut 06105. redundancy and prolapse (4). The mitral valve anulus is

© 1986 by the AmerIcan College of Cardiology 0735-1097/86/$350 232 lERESATY lACC Vol 7. No I MITRAL VALVE PROLAPSE DEFINITION AND IMPLICATIONS IN ATHLETI,S ldnUdfy 19X6 ~31-6

usually enlarged. The valvular theory has been confirmed symptom, is usually sharp, left precordial and either fleeting pathologically and surgically by the finding of myxomatous or of several hours' duration (2). It occurs in 6lo/c of our and redundant mitral cusps in more than 30 patients known patients (20) and, in about 89% of them, it is unrelated to to have had a mid systolic click (1,5,6). physical activity. Children and adolescents with mitral valve The myocardial theory is based primarily on angiographic prolapse may present with the same symptoms as adults and hemodynamic findings (1). In view of the high prev• (14,17,19) but at a lesser frequency. alence of mitral valve prolapse and the generally benign outlook of this syndrome (3), an important myocardial com• ponent would be highly unlikely. There is little evidence to Auscultatory Findings warrant the diagnosis of myocardial disease in the young There are seven major auscultatory manifestations of athlete with mitral valve prolapse. Autonomic dysfunction mitral valve prolapse: isolated mid-systolic click, mid-sys• with a predominant high adrenergic tone has been reported tolic click followed by a late systolic murmur, early systolic in mitral valve prolapse (7,8). click, isolated late systolic murmur, pansystolic murmur, precordial honk and "silent" form. Physiologic and pharmacologic maneuvers can alter the timing of the click Prevalence, Sex and Age Distribution and murmur (1,2). The prevalence of mitral valve prolapse increases with The mid- to late systolic click is generally accepted as age (9). To quote Leatham and Brigden (10), "the incidence the diagnostic hallmark of this syndrome and its mere pres• of mitral valve prolapse increases greatly with age, sug• ence on , preferably with phonocardiographic gesting a 'wear and tear' effect superimposed on a minor confirmation, would warrant, except in a few instances, the congenital abnormality of the cusps and chordal tissue." diagnosis of mitral valve prolapse (1). In the presence of a This syndrome has been reported in children and adolescents click, echocardiography, which is positive for mitral valve (11-19); however, with the exception of one survey (13), prolapse in 80% of patients with a click, is not required for its prevalence has been lower than in adults. In the aus• the diagnosis. However, in the absence of a click ("silent" cultatory survey by McLaren et aL (11), of 12,050 children form) and in patients with an early click, isolated late sys• in Soweto, South Africa, 1.5% were found to have a non• tolic murmur, honk or pansystolic murmur, the diagnosis ejection click. Chandraratna et aL (13) studied 100 clinically of mitral valve prolapse can only be established by means stable newborn infant girls and observed a 7% (3 infants of echocardiography or angiography. The "silent" form is with auscultatory and echocardiographic evidence and 4 the most uncommon in children: of 119 patients with mitral with isolated echocardiographic abnormalities) prevalence valve prolapse only 1 "silent case" was reported by Bisset of mitral valve prolapse. et aL (19). In my experience and that of others (1,9), mul• A female preponderance has been reported in this syn• tiple clicks and precordial honks in young patients have drome, women constituting approximately two-thirds of pa• sometimes been mistaken for a pericardial friction rub by tients with idiopathic mitral valve prolapse (1). The true referring physicians. prevalence of this disorder in the general population has not The general physical appearance in mitral valve prolapse yet been established and the results of surveys are variable. may be entirely normaL However, certain features, that is, A 6% prevalence is probably the most accurate for a young asthenic body habitus, high arched palate and thoracic skel• female population and, in view of the known female pre• etal abnormalities (straight back, and sco• ponderance, a 5% prevalence for the general population can liosis), are frequently noted and heighten suspicion of this be extrapolated (1). An autosomal form of inheritance with syndrome (2,22,23). incomplete penetrance and reduced expressivity in the male and the young has been noted in this syndrome (1). Electrocardiographic Findings changes. Electrocardiographic abnormalities, Symptomatology noted primarily in the inferior limb leads, consist of initially In the setting of a cardiology referral center, chest pain, inverted or totally inverted T waves with or without ST dyspnea, fatigue, dizziness, palpitation and neuropsychia• segment depression (20). These abnormalities may also be tric disorders are commonly encountered in patients with evident in the left precordial leads, and, in a few patients, mitral valve prolapse (I). In epidemiologic surveys, how• they may be widespread. Therefore, if abnormal T waves ever, most of the patients are asymptomatic and, recently, are noted on a routine electrocardiogram in a young athlete, doubt has been expressed about the existence of a distinct mitral valve prolapse should be kept in mind in the differ• mitral valve prolapse syndrome including symptoms, ential diagnosis. However, because biphasic or negative T electrocardiographic abnormalities and arrhythmias (21). waves are not uncommon in the athlete (24), they are not Chest pain, the most common and potentially disabling necessarily due to mitral valve prolapse when this syndrome JACC Vol 7, No I JERESATY 233 January 1986 231-6 MITRAL VALVE PROLAPSE DEFINITION AND IMPLICATIONS IN ATHLETES

is present. The finding of the high prevalence of mitral valve being induced by a high position, and masked by a low prolapse (4 patients) and hypertrophic (3 position. To be helpful in the diagnosis of mitral valve patients) in 12 top ranking athletes with pseudo-ischemic T prolapse, hammocking should be pronounced (2:3 mm). waves awaits further confirmation (25). Prolongation of the Two-dimensional echocardiography is probably indicated in QT interval has been reported, but its true prevalence and all patients who exhibit isolated hammocking and may be• significance have not been defined. Thallium 201 scintig• come the standard for the diagnosis of mitral valve prolapse, raphy, when results are normal, is helpful in eliminating particularly in controversial cases (30). It enables the rec• associated as a cause of repolari• ognition of the superior as well as of the strictly posterior zation abnormalities in mitral valve prolapse, prolapse. Moreover, it can identify structural abnormalities Arrhythmias. Ventricular and atrial arrhythmias are of the mitral valve consisting of thickening and redundancy. probably the most common manifestation of mitral valve Angiography. Left ventricular angiography is helpful in prolapse. Using ambulatory electrocardiographic monitor• the diagnosis but is not usually required. The angiographic ing in 31 patients with mitral valve prolapse, DeMaria et findings may be nonspecific and should, therefore, be cor• al. (26) observed premature ventricular complexes in 58%, related with the clinical and echocardiographic data before supraventricular arrhythmias in 35% and brady arrhythmias a diagnosis of idiopathic mitral valve prolapse can be made. in 29%, Winkle et al. (27) reported a 75% incidence of ventricular arrhythmias in mitral valve prolapse. In both investigations ambulatory monitoring was more sensitive Prognosis and Complications than stress testing in the detection of arrhythmias. A lower The prognosis in mitral valve prolapse is generally fa• prevalence of arrhythmias has been reported in the pediatric vorable (l ,3), particularly in children (16,19). Patients with age group. In 26 un selected pediatric patients with mitral an isolated click and those with the "silent" form constitute valve prolapse (age 7 to 18 years) studied with graded ex• a low risk group (I). Bisset et al. (19) studied 119 children ercise treadmill testing and 24 hour ambulatory electrocar• and adolescents for a mean follow-up period of 6 to 9 years. diographic monitoring, Kavey et al. (28) detected poten• No progression of mitral regurgitation was observed and tially serious ventricular arrhythmias in 6 (23%), of whom there were no sudden , One patient developed infec• 5 manifested the on exercise testing. Neither tive endocarditis and one had a cerebrovascular accident. standard electrocardiographic abnormalities nor clinical Complications. Despite its generally benign outlook, symptoms correlated with the arrhythmia. A similar prev• this syndrome may infrequently become complicated by alence of ventricular arrhythmias (21 %) was reported by transient ischemic attacks that are thought to be due to Bisset et al. (19) in 43 children. platelet and fibrin embolization originating from the mitral Bradyarrhythmias and conduction defects. These have valve (31) by ruptured chordae tendineae, progression of also been reported in this syndrome but have been rare. It mitral regurgitation, or sudden death. is of interest that mitral valve prolapse was noted in 3 of The risk of infective endocarditis warrants the use of anti• 10 top ranking athletes with Wenckebach second degree biotic prophylaxis in patients with mitral valve prolapse atrioventricular (A V) block (29). An immediate normaliza• when a regurgitant murmur is present. In our experience tion of A V conduction was obtained with reflex sympathetic (32) with 25 patients with surgically proved ruptured chor• stimulation, sympathomimetic or vagolytic drugs and phys• dae tendineae, idiopathic mitral valve prolapse was the un• iologic exercise. No deterioration of A V conduction was derlying anatomic lesion in 23 (92%). Current evidence noted and the prognosis of this vagally induced benign fea• indicates that myxomatous transformation of the mitral valve ture of the athlete's was judged to be favorable. is probably the most common cause of "spontaneous" chor• Ventricular is the probable mechanism of sud• dal rupture. None of our patients were in the young age den death, a rare occurrence in mitral valve prolapse (l). group and the rupture occurred during physical stress (chop• ping wood) in only one patient. Echocardiographic and Sudden death. This is the most feared complication of mitral valve prolapse, Fortunately, this catastrophic event Angiographic Findings is a rare complication of this syndrome and, to my knowl• Echocardiography. This procedure is, along with aus• edge, only 60 cases (1,5,6,9,33-38) have been reported, It cultation and angiography, an important diagnostic marker is possible that there is a larger number of patients with in mitral valve prolapse. Pansystolic sagging (hammocking) sudden death that go unreported. The age of these patients or late systolic dipping of the mitral valve echo are the ranged from 9 to 79 years; only four were 20 years or characteristic findings on M-mode echocardiography, Late younger (age 9,14,17,19 and 20, respectively). Two chil• systolic dipping is less sensitive but much more specific dren not included in this sudden death series developed than hammocking in the diagnosis of mitral valve prolapse. ventricular arrhythmia and and were success• Hammocking is affected by the position of the transducer, fully resuscitated (18), Among the four young patients who 234 JERESATY JACC Vol 7, No I MITRAL VALVE PROLAPSE DEFINITION AND IMPLICA nONS IN ATHLETES JanuaJ) 1986 231-6

died suddenly, I have included a 17 year old football player left ventriculography are only indicated when other forms (35) who had at necropsy alterations of the mitral valve of congenital heart disease are suspected or severe mitral consistent with mitral valve prolapse and a family history insufficiency is noted. of that disease, However, his heart weighted 530 g and the Holter monitoring and stress testing. In the presence "abnormality" of the mitral valve was relatively mild; of asymptomatic mitral valve prolapse, ambulatory electro• therefore, it was probably not responsible for significant cardiographic monitoring or stress testing is not indicated mitral regurgitation and the degree of left ventricular hy• as part of the work-up. However, in the presence of symp• pertrophy that was present. In addition, this athlete had toms, particularly palpitation, dizziness, near-syncope or severe narrowing of the artery to the A V node, which is syncope, and in the presence of premature beats on aus• not a known complication of mitral valve prolapse, cultation and , both Holter monitoring Death occurred during physical stress in only three pa• and stress testing are advisable for evaluation of the mech• tients; one, aged 39, died while mowing his lawn (39), the anism of the symptoms and to help the physician formulate second, aged 31, died after a game of tennis (40) and the a recommendation. It is important to recognize that patients third, a 17 year old boy, died during football scrimmage with mitral valve prolapse may have symptoms in the ab• (36). Only one of these three patients was a trained com• sence of arrhythmias or conduction defects and that symp• petitive athlete (36). Sudden death has been reported in only toms should be correlated with specific electrocardiographic one patient with "silent" mitral valve prolapse (37) and in changes (43). Although ambulatory monitoring may detect only a few patients with an isolated click (1,6,37). It would a higher prevalence of arrythmias (27) than does exercise seem that the patient with mitral valve prolapse and a late testing, the clinical value of these tests may be additive. or pansystolic murmur is at a higher risk of dying suddenly Moreover, observation of the athlete during exercise is in• and of developing ruptured chordae tendineae and bacterial valuable for adequate clinical assessment and sound endocarditis than is the patient with "silent" mitral valve recommendations, prolapse or isolated click (1,41), Marfan's syndrome. In evaluating the young athlete The rare occurrence of sudden death in mitral valve pro• with mitral valve prolapse, Marfan's syndrome should be lapse should not be mentioned to the patient or his or her ruled out because the risk of aortic rupture and dissection family for fear of arousing undue anxiety or possibly in• in this syndrome represents a contraindication to competitive ducing psychoneurosis. activities and contact sports, particularly if dilation of the ascending aorta is present. Mitral valve prolapse is common in Marfan's syndrome (44); however, oculoskeletal stigmata of Marfan's syndrome have been infrequent in large series Clinical Presentations in the Young and of cases of mitral valve prolapse, being present in only 4 Diagnostic Work-Up of the Athlete With of our 350 patients (1). Thus, despite the high prevalence Mitral Valve Prolapse of mitral valve prolapse in Marfan's syndrome, an uncom• mon disease, there is a rare occurrence of Marfan's syn• Clinical features. The clinical presentations of mitral drome in mitral valve prolapse, a common disorder. valve prolapse in the young are variable, This syndrome can present as an auscultatory complex of a click or murmur, or both, or a symptomatic complex characterized by chest pain, fatigue, dyspnea. syncope and palpitation. It may also Criteria for Disqualification of Athletes With manifest itself by the appearance of premature beats detected on auscultation and on a routine electrocardiogram by the Mitral Valve Prolapse From Competition occurrence of supraventricular or the detection The dearth of documented serious complications in mitral of repolarization changes, or both. In young patients with valve prolapse, particularly in the young, the lack of cor• these symptoms, particularly in those with atypical chest relation between symptoms (chest pain) and major compli• pain and ventricular or supraventricular arrhythmias, a thor• cations (ruptured chordae tendineae, sudden death) and the ough auscultation in various positions (supine, left decu• lack of correlation between these complications and physical bitus, sitting and standing, before and after squatting) should effort would warrant a permissive attitude toward partici• be carried out to detect a click or murmur, or both. The pation of patients with mitral valve prolapse in athletics. diagnosis of mitral valve prolapse is primarily clinical and However, hard data on which to base a judgment are not is based on the discovery of a nonejection click. In the yet available. The prognosis of both ventricular and supra• absence of a click, an echocardiogram is needed to establish ventricular arrhythmias detected with either exercise testing a diagnosis. or ambulatory electrocardiography in patients with mitral Diagnostic work-up. An electrocardiogram should be valve prolapse is unknown (45). However, the demonstra• part of the diagnostic studies performed to determine the tion of no, infrequent or benign premature ventricular com• presence of repolarization changes that may be associated plexes on Holter monitoring and the lack of occurrence of with complex arrhythmias (42). Cardiac catheterization and complex ventricular arrhythmias on stress testing would pro- JACC Vol 7. No I JERESATY 235 January 1986:231 ~6 MITRAL VALVE PROLAPSE DEFINITION AND IMPLICATIONS IN ATHLETES

vide the physician with objective evidence favoring a per• less common in the young, it is probably more common missive attitude toward athletic participation. It is more than any other cardiac condition and it is being reported difficult to arrive at a definitive recommendation regarding with increasing frequency in this age group. Its prognosis participation in athletic activities when apparently important is generally benign; however, progression of mitral regur• arrhythmias are documented. gitation, chordal rupture, infective endocarditis and sudden Reasons for disqualification from competition in death do occur and, although rare, have shattered the illusion strenuous activities. Recognizing the lack of definitive data of that mitral valve prolapse is an innocent disorder. at the present time, it would appear reasonable to consider Although a restrictive approach to the performance of disqualifying athletes with mitral valve prolapse from com• "exhaustive and highly competitive physical exercise" has petition or other strenuous activities if they fall into any of been advocated by some investigators (2), a permissive at• the following categories: titude would seem warranted by the available evidence. However, this attitude should be modified by the presence 1) Patients with a history of syncope. Since syncope may of disabling chest pain, syncope, prolonged QT interval, be due to an arrhythmia, a vasovagal reaction or or• complex ventricular arrhythmias, significant mitral regur• thostatic hypotension, it is advisable to evaluate with gitation, Marfan's syndrome and a family history of sudden Holter monitoring and exercise testing all patients with death. Most athletes presenting with these findings should mitral valve prolapse with a history of syncope. probably be disqualified from strenuous and competitive 2) Patients with disabling chest pain, particularly if the pain activities. is made worse by exercise. 3) Patients with complex ventricular arrhythmias (frequent, multifocal, occurring as pairs or runs or Ron T beats). References These arrhythmias are especially of concern if they are 1. lere,aty RM. MItral Valve Prolapse. New York: Raven Press, induced or made worse by exercise. 1979:4.19.38;45.76,187. 4) Patients with significant mitral regurgitation associated 2. Cnley 1M. Heger 1. Prolapsed mItral leaflet syndrome In: Roberts with moderate to marked (46). However, Wc, ed: CongenItal Heart Disease in Adults: Cardiovascular Clinics. in patients with a late systolic murmur or a pansystolic PhIladelphIa: F.A DaVIS, 1979:213-33 murmur with no cardiomegaly and no exertional symp• 3 Barlow JB, Pocock WA. The mItral valve prolapse enIgma-two decades later Mod Concepts Cardlovasc DIS 1984;53: 13-7 toms, all recreational activities can probably be allowed 4 Guthrie RB. Edwards lE. Pathology of the myxomatous mItral valve: (46). nature, ,econdary change, and complicatIOns. Minn Med 5) Patients with a prolonged QT interval. These patients 1976;59:637-47 may be at a higher risk of complex arrhythmias and 5. Bharatl S. Granston AS. Liebson PRo Loeb HS. Rosen KM, Lev M. sudden death. The conductIon system in mItral valve prolapse syndrome WIth sudden death. Am Heart J 1980;100:667-70. 6) Patients with Marfan's syndrome and associated mitral 6. Malr Wl Sudden death In young famIlies with floppy mItral valve valve prolapse because of the risk of aortic rupture and syndrome. Aust NZ J Med 1980;10:221-3. dissection. 7. Coghlan HC. Phares P. Cowley M. Copley D. James TN. Dysauto• 7) Patients with a family history of sudden death due to nomIa In mItral valve prolapse. Am J Med 1979;67.236-44. mitral valve prolapse. 8 Boudoulas H. Reynold, JC, Mazzafern E. Wooley CF. Metabolic studies in mitral valve prolapse syndrome. CirculatIOn 1980;61.1200-5. Risk of chordae tendineae rupture. Theoretically, pa• 9 DaVIe, MJ. Moore BP. Bralmbndge MV. The floppy mitral valve. tients with mitral valve prolapse and underlying mitral valve Study of InCIdence. pathology. and complications In surgical. nec• roP'y. and foren;ic material. Br Heart J 1978.40;468-81. disease (regurgitant murmur, redundant leaflet and mitral 10 Leatham A. Bngden w. Mild mItral regurgItatIOn and the mItral pro• anular dilation on echocardiography) may be at risk of de• lap,e fiasco (letter) Am Heart J 1980; 100:942. veloping ruptured chordae tendineae during strenuous ac• II McLaren Ml. HawkInS DM. Lachman AS. et al. Non-ejectIOn clicks tivities, particularly those associated with isometric strain and mItral systolic murmurs In black school children of Soweto. Jo• and body contact. However, except for anecdotal experience hannesburg. Br Heart J 1976;38.718-24 (32), evidence for this increased risk is lacking and, thus, 12 PIckoff AS, Gelband H, Ferrer P. Cama O. Tamer D. Premature ventricular contractIons as the presentIng feature of mItral valve pro• no recommendation can be made at this time to restrict lapse In childhood. J Pedlatr 1979;94615-7. athletic activities in patients with mitral valve prolapse to 13 Chandraratna PAN. Vlahovlch G. Kong Y. WIlson D. Incidence of prevent ruptured chordae tendineae. mItral valve prolapse in one hundred clInically stable newborn baby gIrls: an echocardlOgraphlc study. Am Heart 1 1979;98:312-4. 14. Brown LM Mitral valve prolapse In chIldren. Adv Pediatr 1978;25.327-48. 15 FiddlerGi. Scott O. Heart murmurs audible across the room in children Conclusion WIth mItral valve prolapse Br Heart 1 1980;44:201-3. Idiopathic mitral valve prolapse has emerged during the 16. Cohen M. Pocock WA. LakIer lB. McLaren MJ. Lachman AS, Bar• low JB Four years follow-up of black school children WIth non• past decade as the most common valvular disorder, affecting ejectIon systolIc clicks and mItral systolIc munnurs Am Heart J approximately 5% of the population. Although relatively 1978.95.697-701. 236 JERESATY JACC Vol 7, No I MITRAL VALVE PROLAPSE DEFINITION AND IMPLICATIONS IN ATHLETES January 1986231-6

17. Schmaltz AA, Ibrahim ZI, Apltz J. ClinIcal and angio- and echocar• 32. Jeresaty RM, Edwards JE, Chawla SK. Mitral valve prolapse and diographic findings in 45 children with mitral valve prolapse syn• ruptured chordae tendmeae. Am J Cardiol 1985;55:138-42. drome. Eur J Cardiol 1978;7:49-58. 33. Anderson RC. Idiopathic mitral valve prolapse and sudden death (let• 18. Rocchini AP, Chun PO, Dick M. in children. ter). Am Heart J 1980;100:941-2. Am J Cardiol 1981;47:1091-7. 34. Kleid n. Sudden death and the floppy mitral valve syndrome. An• 19. Bisset GS, Schwartz DC, Meyer RA, James FW, Kaplan S. Clinical giology 1976;27:734-7. spectrum and long-term follow-up of isolated mitral valve prolapse in 119 children. Circulation 1980;62:423-9. 35. Maron BJ, Roberts WC, McAllister HA, Rosing DR, Epstein SE. 20. Jeresaty RM. Mitral valve prolapse-click syndrome. Prog Cardiovasc Sudden death in young athletes. Circulation 1980;62:218-29. Dis 1973;15:623-52. 36. Bharati S, Bauernfeind R, Miller LB, Strasberg B, Lev M. Sudden 21. Hancock EW. Is there a mitral valve prolapse syndrome? Int J Cardiol death in three teenagers: conduction system studies. J Am Coli Cardiol 1982;1:443-4. 1983;13:879-86. 22. Bon Tempo CP, Ronan JA, deLeon AC, et al. Radiographic appear• 37. Chesler E, King RA, Edwards JE. The myxomatous mitral valve and ance of the thorax in systolic click-late systolic murmur syndrome. sudden death. Circulation 1983;67:632-9. Am J Cardiol 1975;36:27-31. 38. Pocock WA, Bosman CK, Chesler E, Barlow JB, Edwards JE. Sudden 23. Davies MK, Mackintosh P, Cayton RM, Page AJF, Shiu MF, Littler death in primary mitral valve prolapse. Am Heart J 1983;107:378-82. WA. The straight back syndrome. Q J Med 1980;49:443-60. 39. Barlow JB, Bosman CK, Pocock WA, Marchand P. Late systolic 24. Morganroth J, Maron BJ. The athlete's heart syndrome: a new per• murmurs and non-ejection (mid-late) systolic clicks. An analysis of spective. Ann NY Acad Sci 1977;301:931-41. 90 patients. Br Heart J 1968;30:203-18. 25. Zeppilli P, Pirraml MM, Sassara M, Fenici R. T wave abnormalities in fop ranking athletes: effects of isoproterenol, atropine, and physical 40. Cobbs BW, King SB. Ventricular buckling: a factor in the abnormal exercise. Am Heart J 1980;100:213-22. ventriculogram and peculiar hemodynamics associated with mitral valve prolapse. Am Heart J 1977;93:741-58. 26. DeMaria AN, Amsterdam EA, Vismara LA, Neumann A, Mason DT. Arrhythmias 10 the mitral valve prolapse syndrome. Ann Intern Med 41. Jeresaty RM. Sudden death in the mitral valve prolapse-click syn• 1976;84:656-60. drome. Am J Cardiol 1976;37:317-8. 27. Winkle RA, Lopes MG, Fitzgerald JW, et al. Arrhythmias in patients 42. Campbell RWF, Godman MG, Fiddler GI, et al. Ventricular arrhyth• with mitral valve prolapse. Circulation 1975;52:73-81. mias in syndrome of ballooning deformity of mitral valve: definition 28. Kavey RW, Sondheimer HM, Blackman MS. Detection of dysrhyth• of possible high risk group. Br Heart J 1976;38: 1053-7. mia in pediatric patients with mitral valve prolapse. Circulation 43. Schlant RC, Feiner JM, Miklozek CL, Lutz JF, Hurst JW. Mitral 1980;62:582-7. valve prolapse. DM 1980;26:3-51. 29. Zeppili P, Fenici R, Sassara M, Pirrami MM, Caselli G. Wenckebach 44. Brown OR, DeMots H, Kloster FF, et al. Aortic root dilatatIOn and second degree A-V block in top ranking athletes: an old problem mitral valve prolapse in Marfan's syndrome. Circulation 1975;52:651-7. revisited. Am Heart J 1980;100:281-94. 30. Morganroth J, Mardelli TJ, Naito M, Chen Cc. Apical cross-sectional 45. Kennedy HL. Comparison of ambulatory electrocardiography and ex• echocardlOgraphy. Standard for the diagnosis of idiopathiC mitral valve ercise testmg. Am J Cardiol 1981;47:1359-65. prolapse syndrome. Chest 1981 ;79:23-8. 46. Statement by Ad Hoc Committee on Rehabilitation of the Young 31. Barnett HJ, Jones MW, Boughner DR, et al. Cerebral ischemic events Cardiac (American Heart Association). Activity gUidelines for young associated with prolapsing mitral valve. Arch Neurol 1976;33:777-82. patIents with heart disease. Phys Sport Med 1976;4:47-52.