This Article Extract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Maron, B. J. Articles by Spirito, P. Search for Related Content PubMed PubMed Citation Articles by Maron, B. J. Articles by Spirito, P. Pubmed/NCBI databases Medline Plus Health Information Cardiomyopathy Heart Disease in Women Heart Diseases

(Circulation. 1995;91:1596-1601.)
© 1995 American Heart Association, Inc.

Articles

Cardiac Disease in Young Trained Athletes

Insights Into Methods for Distinguishing Athlete's Heart From Structural Heart Disease, With Particular Emphasis on Hypertrophic Cardiomyopathy

Barry J. Maron, MD; Antonio Pelliccia, MD; Paolo Spirito, MD

From the Cardiovascular Research Division, Minneapolis Heart Institute Foundation, Minneapolis, Minn; the Institute of Sports Science, Rome, Italy; and the Cardiology Division, Ente Ospedaliero Ospedali, Galliera, Genoa, Italy.

Correspondence to Barry J. Maron, MD, Cardiovascular Research Division, Minneapolis Heart Institute Foundation, 920 E 28th St, Suite 40, Minneapolis, MN 55407.

	Introduction

Top Introduction Athlete's Heart Cardiovascular Causes of Sudden... Differential Diagnosis Between... References

 
In young competitive athletes,¹ the differential diagnosis between nonpathological changes in cardiac morphology associated with training (commonly referred to as "athlete's heart")^{2 3 4} and certain cardiac diseases with the potential for sudden death is an important and not uncommon clinical problem. Such crucial diagnostic distinctions most frequently involve hypertrophic cardiomyopathy (HCM), which is the most common cause of sudden death in young competitive athletes.^{5 6 7} Our awareness of this issue, as well as the parallel consideration of preparticipation athletic screening,^{8 9} has been heightened by several recent high-visibility catastrophies involving elite basketball players who died suddenly and unexpectedly from cardiovascular disease.^{10 11 12}

The distinction between athlete's heart and cardiac disease has particularly important implications, because identification of cardiovascular disease in an athlete may be the basis for disqualification from competition in an effort to minimize risk.¹³ By the same token, the improper diagnosis of cardiac disease in an athlete may lead to unnecessary withdrawal from athletics, thereby depriving that individual of the varied benefits of sport.

Consequently, interest in the application of noninvasive techniques that may aid in making such a diagnostic distinction and in planning subsequent clinical strategies has increased. Because this issue has not been examined in a comprehensive fashion, it is of value to assimilate the available data to develop a practical approach for the decision-making process directed toward the identification of cardiovascular disease in athletes.

	Athlete's Heart

Top Introduction Athlete's Heart Cardiovascular Causes of Sudden... Differential Diagnosis Between... References

 
While the entity of athlete's heart has been recognized for over 100 years,^{2 3 4} only in the past two decades has the application of echocardiography and other noninvasive imaging techniques permitted definition with some precision of the alterations in cardiac dimensions associated with athletic conditioning.^{14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33} Echocardiography has demonstrated that long-term athletic training leads to an increase in left ventricular mass due to increases in left ventricular diastolic cavity dimension, wall thickness, or both. These changes in cardiac morphology are relatively mild in absolute terms, and the differences between athlete and nonathlete populations are statistically significant but generally small.² Furthermore, cardiac alterations associated with training differ somewhat depending on the particular sport in which the individual athlete participates.^{2 3 21 31 32} In particular, the changes in left ventricular wall thickness, cavity dimension, or both associated with long-term athletic training may be more striking in certain sports such as distance running, swimming, cycling, and rowing/canoeing. The differential diagnosis with cardiac disease is more likely to be raised in athletes training in such sports.

	Cardiovascular Causes of Sudden Death

Top Introduction Athlete's Heart Cardiovascular Causes of Sudden... Differential Diagnosis Between... References

 
A variety of cardiovascular diseases have been identified as potential causes of sudden death in young competitive athletes (<35 years old).^{5 6 7 34 35 36} The vast majority of these deaths occur on the athletic field during severe exertion in the context of training or competition. Each of the responsible diseases is also known to cause sudden death in nonathletes. The most common cause of sudden death in young athletes appears to be HCM.^{5 6 7 34} Less common causes are a variety of congenital coronary artery anomalies, myocarditis, dilated cardiomyopathy, Marfan's syndrome, and right ventricular dysplasia (in one series).^{35 36} Uncommon but reported causes of these athletic field catastrophies include sarcoid, mitral valve prolapse, aortic valve stenosis, atherosclerotic coronary artery disease, and QT-interval prolongation syndromes.

	Differential Diagnosis Between Athlete's Heart and Cardiovascular Disease

Top Introduction Athlete's Heart Cardiovascular Causes of Sudden... Differential Diagnosis Between... References

 
Dilated Cardiomyopathy
In an important minority of athletes, the increase in left ventricular diastolic cavity dimension that occurs with training overlaps with that characteristic of certain known pathological entities. For example, while left ventricular end-diastolic cavity dimension in athletes is usually in the range of 53 to 58 mm, in some individuals it may extend into what may be regarded as the pathological range of >58 mm and thereby resemble dilated cardiomyopathy.²¹ However, the absence of left ventricular systolic dysfunction is usually sufficient to distinguish this physiological ventricular enlargement induced by training from that due to dilated cardiomyopathy.

Myocarditis
Myocarditis, a disorder associated with a heterogeneous clinical profile, has recently been incriminated as the possible cause of some highly publicized deaths in athletes.^{10 37} While myocarditis usually has an infectious origin, it can also be a consequence of drug abuse.^{38 39 40} Sudden cardiac death may occur in its active or healed phases as a consequence of complex arrhythmias that develop in the setting of an unstable myocardial electrical substrate. In an athlete with myocarditis, left ventricular cavity enlargement may be due to the disease, to athletic training, or to a combination of these, but the differential diagnosis with athlete's heart is usually resolved by the presence of clinically relevant and overt arrhythmias, cardiac symptoms such as syncope, presyncope and palpitations, or heart failure with systolic dysfunction. In some instances, the diagnosis may also be clarified by histological examination of myocardium obtained by endomyocardial biopsy.

Right Ventricular Dysplasia
Arrhythmogenic right ventricular dysplasia (or cardiomyopathy) is a heart muscle disorder of unknown cause that is characterized pathologically by fibrofatty replacement of the right ventricular myocardium.^{35 36 41} The clinical and phenotypic profile is variable but includes structural and functional abnormalities of the right ventricle, ventricular and supraventricular arrhythmias, familial occurrence, and the risk for sudden cardiac death.^{35 41} Indeed, it has been suggested that right ventricular dysplasia is an important cause of sudden death in the young, including competitive athletes, largely on the basis of reports from the northeastern (Veneto) region of Italy.^{35 36}

Because highly trained athletes may demonstrate right ventricular enlargement³³ and a variety of depolarization, repolarization, and conduction abnormalities on the ECG,^{3 4 42} the differential diagnosis between athlete's heart and right ventricular dysplasia may arise. Noninvasive identification of right ventricular dysplasia by echocardiography⁴³ may be difficult because of technical limitations in imaging right ventricular structure and assessing function in these patients and because the spectrum of the disease is broad and includes mild morphological forms with subtle manifestations.⁴¹ Magnetic resonance imaging, however, promises enhanced noninvasive diagnosis of this condition.⁴⁴ The demonstration of right ventricular segmental or global dysfunction or substantial right ventricular cavity enlargement would support the diagnosis of right ventricular dysplasia; alternatively, thickening or enlargement of the left ventricle would be most consistent with athlete's heart.^{2 3 4}

Hypertrophic Cardiomyopathy
The greatest difficulty in distinguishing clinically between athlete's heart and structural heart disease most frequently arises with respect to HCM, since many of the other cardiac disorders that cause sudden death in a young athletic population can be identified independently of any changes in cardiac morphology typically associated with training. The basic definition of HCM used here is that of a patient (or athlete) with evidence of a hypertrophied and nondilated left ventricle in the absence of another cardiac or systemic disease that could itself cause hypertrophy of the magnitude present in that individual.⁴⁵

Wall Thickness
In the vast majority of competitive athletes, absolute left ventricular wall thickness is normal or only mildly increased (12 mm).^{2 3 4 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33} In some athletes, however, the increase in left ventricular wall thickness may be more substantial, up to 16 mm, unavoidably raising the possibility of HCM.²¹ In patients with HCM, the increase in left ventricular wall thickness is usually marked; the average wall thickness reported in most echocardiographic studies of this disease is 20 mm,^{46 47 48 49} ranging to >50 mm.⁵⁰ However, an important minority of patients with HCM show relatively mild left ventricular hypertrophy with wall thickness values in the range of 13 to 15 mm, and many of these patients are asymptomatic.^{47 49 51 52 53} Therefore, a diagnostic dilemma arises in those athletes who fall into this morphological "gray zone" between physiological hypertrophy and HCM² (Fig 1). While this distinction cannot be resolved with certainty in some of these athletes, careful analysis of several echocardiographic and clinical features permits this diagnostic differentiation in most.

View larger version (91K): [in this window] [in a new window]   Figure 1. Echocardiograms in parasternal long-axis view from an elite athlete (Olympic rower) (left) and a young asymptomatic patient with hypertrophic cardiomyopathy (HCM) (right). Magnitude of anterior ventricular septal (VS) hypertrophy is similar in each, demonstrating the morphological gray zone into which a highly trained athlete may fall and the diagnostic ambiguity that may ensue. Calibration dots are 1 cm apart. Left panel is reprinted by permission of the New England Journal of Medicine (1991;324:295-301).

In highly trained athletes, although the region of predominant left ventricular wall thickening always involves the anterior septum, the thicknesses of other segments of the wall are similar (with differences in the range of 1 to 2 mm). In patients with HCM, while the anterior portion of the ventricular septum is usually the region of maximal wall thickening, the pattern of hypertrophy is often heterogeneous,^{47 48 52 53 54 55} asymmetry is prominent, and areas other than the anterior septum may show the most marked thickening.⁵⁵ In addition, contiguous portions of the left ventricle often show strikingly different wall thicknesses, and the transition between such areas is often sharp and abrupt. The diagnosis of HCM in asymptomatic athletes is frequently based solely on the echocardiographic assessment of the magnitude of hypertrophy and often on precise measurements of wall thickness in a single segment or region of the left ventricle. It should be emphasized that, in borderline cases, such circumstances present fertile ground for the overdiagnosis of HCM. This, in turn, creates considerable potential risk to the well-being of the athlete by possibly creating an unnecessary perception of heart disease.

Since a marked increase in left ventricular wall thickness often occurs during adolescence in patients with HCM,⁵⁶ young athletes with HCM (<18 years old) may not demonstrate their maximum magnitude of hypertrophy until full physical maturation and development is achieved. Therefore, an athlete with HCM may initially be evaluated with echocardiography when the hypertrophy is still only mild and within the borderline range. The differential diagnosis with athlete's heart may be difficult at that point in time. However, this uncertainty can be resolved by serial echocardiographic examinations, which, within months or years, may show more definite left ventricular wall thickening and confirm the diagnosis of HCM.

Cavity Dimension
An enlarged left ventricular end-diastolic cavity dimension (>55 mm) is present in more than one third of highly trained elite male athletes.^{21 32} Conversely, the diastolic cavity dimension is small, usually <45 mm, in most patients with HCM, and it is >55 mm only in those patients who evolve to the end-stage phase of the disease with progressive heart failure and systolic dysfunction.⁵⁷ Therefore, in some instances, it is possible to distinguish the athlete's heart from HCM solely on the basis of left ventricular diastolic cavity dimension. For example, a cavity >55 mm in an athlete with borderline wall thickness would constitute strong evidence against the presence of HCM; conversely, a cavity dimension <45 mm would be inconsistent with the athlete's heart. However, in those athletes in whom left ventricular cavity size falls between these extremes, this variable alone will not resolve the differential diagnosis.

ECG
Because of the wide variety of ECG alterations present in both athletes without cardiovascular disease^{42 58} and patients with HCM, the 12-lead ECG is not particularly useful in distinguishing between these two entities. However, unusual and bizarre ECG patterns with strikingly increased voltages, prominent Q waves, or deep, negative T waves are most characteristic of HCM and represent evidence favoring this diagnosis.^{59 60 61}

Doppler Transmitral Waveform
Abnormalities of left ventricular diastolic filling have been identified noninvasively with pulsed Doppler echocardiography or radionuclide angiography in many patients with a variety of cardiac diseases associated with left ventricular hypertrophy, such as systemic hypertension and HCM.^{62 63 64 65 66} Most patients with HCM, including those with relatively mild hypertrophy that could be confused with athlete's heart, show abnormal Doppler diastolic indexes of left ventricular filling independently of whether symptoms or outflow obstructions are present.^{65 66} Typically, the early peak of transmitral flow-velocity ("E," due to rapid filling) is decreased and deceleration time of the early peak is prolonged; the late peak ("A," due to atrial contraction) is increased, inverting the normal E/A ratio. On the other hand, trained athletes have invariably demonstrated normal left ventricular filling patterns.^{21 66 67 68 69 70 71 72} Consequently, in a trained athlete suspected of having HCM, a distinctly abnormal Doppler pattern of transmitral flow-velocity strongly supports this diagnosis, while a normal Doppler pattern is compatible with either HCM or athlete's heart.

Ultrasonic Myocardial Reflectivity (Integrated Backscatter Signal)
There has been interest in applying specialized ultrasound techniques to assessment of the acoustic properties of the myocardium for the purpose of resolving the differential diagnosis between athlete's heart and HCM.^{73 74} Initial observations suggest that most asymptomatic (or mildly symptomatic) patients with HCM show increased intensity of the ultrasound signal from the septum and posterior free wall (including patients with mild and localized hypertrophy),⁷³ while highly trained athletes with physiological hypertrophy show normal myocardial tissue reflectivity.⁷⁴ One limitation in the use of the backscatter technique is its availability, which is at present confined to a few research institutions. In addition, it is not known whether differences in the backscatter signal identified by group comparisons can be used to distinguish athlete's heart from cardiac disease in the individual subject.

Type of Sport Training
The specific nature of the athletic training itself has a major influence on the type and magnitude of the changes in left ventricular dimensions.^{20 21 22 23 24 25 26 27 28 29 30 31 32 33} For example, in a study of almost 1000 elite Italian athletes,²¹ only about 2% had a left ventricular wall thickness 13 mm (in the gray zone between physiological hypertrophy and HCM), and this subset was confined to rowing sports and cycling. Conversely, most other forms of training, including isometric (or power) sports such as weight-lifting or wrestling, were not associated with absolute increases in wall thickness beyond 12 mm.²⁰ Therefore, in assessing whether an athlete with increased wall thickness has HCM, detailed knowledge of the training regimen is relevant. It is also possible that the outer limits of left ventricular wall thickness are different in trained athletes of various ethnic and racial origins, although this issue has not yet been resolved.

Sex
Sex differences with regard to alterations in cardiac dimensions and left ventricular mass have been identified in trained athletes.^{75 76 77} Preliminary findings indicate that highly trained female athletes rarely show left ventricular wall thicknesses that are within the aforementioned gray zone between athlete's heart and HCM.⁷⁵ In a recent report, none of 600 elite women athletes had left ventricular wall thickness in the range compatible with the diagnosis of HCM (13 mm).⁷⁵ These observations suggest, therefore, that female athletes with "borderline" left ventricular wall thickness (in the presence of normal cavity size) are most likely to have HCM.

Regression of Left Ventricular Hypertrophy With Deconditioning
That increases in left ventricular cavity size or wall thickness are a physiological consequence of athletic training is shown by serial echocardiographic examinations demonstrating a decrease in cardiac dimensions and mass after athletic deconditioning.^{14 15 30 78} For example, elite athletes with left ventricular hypertrophy may show reduction in wall thickness (of about 2 to 5 mm) within 3 months of deconditioning.⁷⁸ Identification of such changes in wall thickness with deconditioning, however, requires (1) compliance from highly motivated competitive athletes to interrupt training and (2) serial echocardiographic studies of optimal technical quality. Similar changes in left ventricular wall thickness with deconditioning are inconsistent with the presence of pathological hypertrophy and HCM.

Familial Transmission and Genetics
The most definitive evidence for the presence of HCM in an athlete with a substantial increase in wall thickness probably comes from the demonstration of the disease in a relative.^{44 79 80} Therefore, in those athletes in whom the distinction between HCM and athlete's heart cannot be achieved definitively by other methods, one potential way of resolving this diagnostic uncertainty is the echocardiographic screening of family members. The absence of HCM in family members, however, does not exclude HCM, since the disease may be "sporadic" (ie, absent in relatives other than the index case), presumably as a result of de novo mutations.⁸¹

Recent advances in the understanding of the genetic alterations responsible for HCM raise the possibility of DNA diagnosis in athletes suspected of having this disease.^{79 80 81 82} The genetic abnormalities that cause HCM, however, are greatly heterogeneous. At present, mutations responsible for HCM have been identified in three genes located on chromosomes 14, 1, and 15; these genes encode the contractile proteins ß-myosin heavy chain, cardiac troponin T, and -tropomyosin, respectively.^{79 80} In addition, a fourth gene locus on chromosome 11 is known.⁸³ Thus, mutations of at least four different genes can cause HCM. This substantial genetic heterogeneity of the disease makes it extremely difficult and time consuming at present to use the techniques of molecular biology for the purpose of resolving clinically the differential diagnosis between athlete's heart and HCM.

Conclusions
In highly trained athletes with substantial left ventricular hypertrophy, it is of critical importance to clarify whether the increased left ventricular wall thickness represents the expression of the physiological adaptation of the heart to athletic training or a pathological condition such as HCM. While at present there is no single approach that will definitively resolve this question in all such athletes, several strategies are described here that alone or in combination offer a large measure of clarification in most instances for this often compelling diagnostic dilemma.

View larger version (31K): [in this window] [in a new window]   Figure 2. Chart showing criteria used to distinguish hypertrophic cardiomyopathy (HCM) from athlete's heart when the left ventricular (LV) wall thickness is within the shaded gray zone of overlap, consistent with both diagnoses. *Assumed to be the nonobstructive form of HCM in this discussion, since the presence of substantial mitral valve systolic anterior motion would confirm, per se, the diagnosis of HCM in an athlete. May involve a variety of abnormalities, including heterogeneous distribution of left ventricular hypertrophy (LVH) in which asymmetry is prominent, and adjacent regions may be of greatly different thicknesses, with sharp transitions evident between segments; also, patterns in which the anterior ventricular septum is spared from the hypertrophic process and the region of predominant thickening may be in the posterior portion of septum or anterolateral or posterior free wall.47 55 indicates decreased; LA, left atrial.

Received August 2, 1994; revision received September 26, 1994; accepted October 30, 1994.

	References

Top Introduction Athlete's Heart Cardiovascular Causes of Sudden... Differential Diagnosis Between... References

 
1. Maron BJ, Mitchell JH. Revised eligibility recommendations for competitive athletes with cardiovascular abnormalities: the introduction to Bethesda Conference #26. J Am Coll Cardiol. 1994; 24:846-848.

2. Maron BJ. Structural features of the athlete heart as defined by echocardiography. J Am Coll Cardiol. 1986;7:190-203. [Abstract]

3. Rost R. The athlete's heart. Eur Heart J. 1982;3(suppl A):193-198.

4. Hutson TP, Puffer JC, MacMillan W. The athlete heart syndrome. N Engl J Med. 1985;313:24-32. [Medline] [Order article via Infotrieve]

5. Maron BJ, Roberts WC, McAllister HA, Rosing DR, Epstein SE. Sudden death in young athletes. Circulation. 1980;62:218-229. [Abstract/Free Full Text]

6. Maron BJ, Epstein SE, Roberts WC. Causes of sudden death in the competitive athlete. J Am Coll Cardiol. 1986;7:204-214. [Abstract]

7. Maron BJ, Shirani J, Mueller FO, Cantu RC, Roberts WC. Cardiovascular causes of "athletic field" deaths: analysis of sudden death in 84 competitive athletes. Circulation. 1993;88(suppl I):I-50. Abstract.

8. Lewis JF, Maron BJ, Diggs JA, Spencer JE, Mehrotra PP, Curry CL. Preparticipation echocardiographic screening for cardiovascular disease in a large predominantly black population of collegiate athletes. Am J Cardiol. 1989;64:1029-1033. [Medline] [Order article via Infotrieve]

9. Maron BJ, Bodison S, Wesley Y, Tucker E, Green KJ. Results of screening a large population of intercollegiate athletes for cardiovascular disease. J Am Coll Cardiol. 1987;10:1214-1222. [Abstract]

10. Maron BJ. Sudden death in young athletes: lessons from the Hank Gathers affair. N Engl J Med. 1993;329:55-57. [Free Full Text]

11. Kassirer JP. Diagnosis in the public domain. N Engl J Med. 1993;329:50-51. [Free Full Text]

12. The death of Reggie Lewis: a search for answers. Boston Globe, September 12, 1993:69-76.

13. Maron BJ, Mitchell JH. 26th Bethesda Conference: recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. J Am Coll Cardiol. 1994;24:845-899. [Medline] [Order article via Infotrieve]

14. Ehsani AA, Hagberg JM, Hickson RC. Rapid changes in left ventricular dimensions and mass in response to physical conditioning and deconditioning. Am J Cardiol. 1978;42:52-56. [Medline] [Order article via Infotrieve]

15. Fagard R, Aubert A, Lysens R, Staessen J, Vanhees L, Amery A. Noninvasive assessment of seasonal variations in cardiac structure and function in cyclists. Circulation. 1983;67:896-901. [Free Full Text]

16. Shapiro LM. Physiological left ventricular hypertrophy. Br Heart J. 1984;52:130-135. [Abstract/Free Full Text]

17. Shapiro LM, Kleinebenne A, McKenna WJ. The distribution of left ventricular hypertrophy in hypertrophic cardiomyopathy: comparison of athletes and hypertensives. Eur Heart J. 1985;6:967-974. [Abstract/Free Full Text]

18. Milliken MC, Stray-Gundersen J, Peshock RM, Katz J, Mitchell JH. Left ventricular mass as determined by magnetic resonance imaging in male endurance athletes. Am J Cardiol. 1988;62:301-305. [Medline] [Order article via Infotrieve]

19. Douglas PS, O'Toole ML, Hiller DB, Reichek N. Left ventricular structure and function by echocardiography in ultraendurance athletes. Am J Cardiol. 1986;58:805-809. [Medline] [Order article via Infotrieve]

20. Pelliccia A, Maron BJ, Spataro A, Caselli G. Absence of left ventricular hypertrophy in athletes engaged in intense power training. Am J Cardiol. 1993;72:1048-1054. [Medline] [Order article via Infotrieve]

21. Pelliccia A, Maron BJ, Spataro A, Proschan MA, Spirito P. The upper limit of physiologic cardiac hypertrophy in highly trained elite athletes. N Engl J Med. 1991;324:295-301. [Abstract]

22. Nishimura T, Yamada Y, Kawai C. Echocardiographic evaluation of long-term effects of exercise on left ventricular hypertrophy and function in professional bicyclists. Circulation. 1980;61:832-840. [Abstract/Free Full Text]

23. Morganroth J, Maron BJ, Henry WL, Epstein SE. Comparative left ventricular dimensions in trained athletes. Ann Intern Med. 1975;82:521-524.

24. Gilbert CA, Nutter DO, Felner JM, Perkins JV, Heymsfield SB, Schlant RC. Echocardiographic study of cardiac dimensions and functions in the endurance-trained athlete. Am J Cardiol. 1977;40:528-533. [Medline] [Order article via Infotrieve]

25. Keul J, Dickhuth H-H, Simon G, Lehmann M. Effect of static and dynamic exercise on heart volume, contractility, and left ventricular dimensions. Circ Res. 1981;48(suppl I):I-162-I-170.

26. Ikaheimo MJ, Palatsi IJ, Takkunen JT. Noninvasive evaluation of the athletic heart: sprinters versus endurance runners. Am J Cardiol. 1979;44:24-30. [Medline] [Order article via Infotrieve]

27. Longhurst JC, Kelly AR, Gonyea WJ, Mitchell JH. Chronic training with static and dynamic exercise: cardiovascular adaptation and response to exercise. Circ Res. 1981;48(suppl I):I-171-I-178.

28. Bekaert I, Pannier JL, Van de Weghe C, Van Durme JP, Clement DL, Pannier R. Non-invasive evaluation of cardiac function in professional cyclists. Br Heart J. 1981;45:213-218. [Abstract/Free Full Text]

29. Longhurst JC, Kelly AR, Gonyea WJ, Mitchell JH. Echocardiographic left ventricular masses in distance runners and weight lifters. J Appl Physiol. 1980;48:154-162. [Abstract/Free Full Text]

30. Shapiro LM, Smith RG. Effect of training on left ventricular structure and function: an echocardiographic study. Br Heart J. 1983;50:534-539. [Abstract/Free Full Text]

31. Fisher AG, Adams TD, Yanowitz FG, Ridges JD, Orsmond G, Nelson AG. Noninvasive evaluation of world class athletes engaged in different modes of training. Am J Cardiol. 1989;63:337-341. [Medline] [Order article via Infotrieve]

32. Spirito P, Pelliccia A, Proschan MA, Granata M, Spataro A, Caselli G, Biffi A, Vecchio C, Maron BJ. Morphology of the "athlete's heart" assessed by echocardiography in 947 elite athletes representing 27 sports. Am J Cardiol. 1994;74:802-806. [Medline] [Order article via Infotrieve]

33. Hauser AM, Dressendorfer RH, Vos M, Hashimoto T, Gordon S, Timmis GC. Symmetric cardiac enlargement in highly trained endurance athletes: a two-dimensional echocardiographic study. Am Heart J. 1985;109:1038-1044. [Medline] [Order article via Infotrieve]

34. Burke AP, Farb A, Virmani R, Goodin J, Smialek JE. Sports-related and non-sports-related sudden cardiac death in young athletes. Am Heart J. 1991;121:568-575. [Medline] [Order article via Infotrieve]

35. Thiene G, Nava A, Corrado D, Rossi L, Penelli N. Right ventricular cardiomyopathy and sudden death in young people. N Engl J Med. 1988;318:129-133. [Abstract]

36. Corrado D, Thiene G, Nava A, Rossi L, Pennelli N. Sudden death in young competitive athletes: clinicopathologic correlations in 22 cases. Am J Med. 1990;89:588-596. [Medline] [Order article via Infotrieve]

37. Maron BJ, Garson A. Arrhythmias and sudden cardiac death in elite athletes. Cardiol Rev. 1994;2:26-32.

38. Isner JM, Estes NAM, Thompson PD, Costanza-Nordin MR, Subramanian R, Miller G, Katsas G, Sweeney K, Sturner WQ. Acute cardiac events temporally related to cocaine abuse. N Engl J Med. 1986; 315:1438-1443.

39. Kloner RA, Hale S, Alker K, Rezkalla S. The effects of acute and chronic cocaine use on the heart. Circulation. 1992;85:407-419. [Abstract/Free Full Text]

40. Tazelaar HD, Karch SB, Stephens BG, Billingham ME. Cocaine and the heart. Hum Pathol. 1987;18:195-199. [Medline] [Order article via Infotrieve]

41. McKenna WJ, Thiene G, Nava A, Fontaliran F, Blomstrom-Lundqvist C, Fontaine G, Camerini F, on behalf of the Task Force of the Working Group Myocardial and Pericardial Disease of the European Society of Cardiology and of the Scientific Council on Cardiomyopathies of the International Society and Federation of Cardiology. Diagnosis of arrhythmogenic right ventricular dysplasia/cardiomyopathy. Br Heart J. 1994;71:215-218. [Free Full Text]

42. Zehender M, Meinertz T, Keul J, Just H. ECG variants and cardiac arrhythmias in athletes: clinical relevance and prognostic importance. Am Heart J. 1990;119:1378-1379. [Medline] [Order article via Infotrieve]

43. Robertson JH, Bardy GH, German LD, Gallagher JJ, Kisslo J. Comparison of two-dimensional echocardiographic and angiographic findings in arrhythmogenic right ventricular dysplasia. Am J Cardiol. 1985;55:1506-1508. [Medline] [Order article via Infotrieve]

44. Ricci C, Longo R, Pagnan L, Dalla Palma L, Pinamonti B, Camerini F, Bussani R, Silvestri F. Magnetic resonance imaging in right ventricular dysplasia. Am J Cardiol. 1992;70:1589-1595. [Medline] [Order article via Infotrieve]

45. Maron BJ, Epstein SE. Hypertrophic cardiomyopathy: a discussion of nomenclature. Am J Cardiol. 1979;43:1242-1244. [Medline] [Order article via Infotrieve]

46. Maron BJ, Nichols PF, Pickle LW, Wesley YE, Mulvihill JJ. Patterns of inheritance in hypertrophic cardiomyopathy: assessment by M-mode and two-dimensional echocardiography. Am J Cardiol. 1984;53:1087-1094. [Medline] [Order article via Infotrieve]

47. Maron BJ, Gottdiener JS, Epstein SE. Patterns and significance of the distribution of left ventricular hypertrophy in hypertrophic cardiomyopathy: a wide-angle, two-dimensional echocardiographic study of 125 patients. Am J Cardiol. 1981;48:418-428. [Medline] [Order article via Infotrieve]

48. Wigle ED, Sasson Z, Henderson MA, Ruddy TD, Fulop J, Rakowski H, Williams WG. Hypertrophic cardiomyopathy: the importance of the site and extent of hypertrophy: a review. Prog Cardiovasc Dis. 1985;28:1-83. [Medline] [Order article via Infotrieve]

49. Spirito P, Chiarella F, Carratino L, Berisso MZ, Bellotti P, Vecchio C. Clinical course and prognosis of hypertrophic cardiomyopathy in an outpatient population. N Engl J Med. 1989;320:749-755. [Abstract]

50. Louie EK, Maron BJ. Hypertrophic cardiomyopathy with extreme increase in left ventricular wall thickness: clinical significance, functional and morphologic features. J Am Coll Cardiol. 1986;8:57-65. [Abstract]

51. Spirito P, Maron BJ, Bonow RO, Epstein SE. Severe functional limitation in patients with hypertrophic cardiomyopathy and only mild localized left ventricular hypertrophy. J Am Coll Cardiol. 1986;8:537-544. [Abstract]

52. Maron BJ, Bonow RO, Cannon RO, Leon MB, Epstein SE. Hypertrophic cardiomyopathy: interrelation of clinical manifestations, pathophysiology, and therapy. N Engl J Med. 1987;316:780-789,844-852. [Medline] [Order article via Infotrieve]

53. Klues HG, Schiffers A, Maron BJ. Patterns of hypertrophy and morphologic spectrum in 600 patients with hypertrophic cardiomyopathy. Circulation. 1993;88(suppl I):I-211. Abstract.

54. Ciró E, Nichols PF, Maron BJ. Heterogeneous morphologic expression of genetically transmitted hypertrophic cardiomyopathy: two-dimensional echocardiographic analysis. Circulation. 1983;67:1227-1233. [Free Full Text]

55. Maron BJ, Gottdiener JS, Bonow RO, Epstein SE. Hypertrophic cardiomyopathy with unusual locations of left ventricular hypertrophy undetectable by M-mode echocardiography: identification by wide-angle, two-dimensional echocardiography. Circulation. 1981;63:409-418. [Abstract/Free Full Text]

56. Maron BJ, Spirito P, Wesley Y, Arce J. Development and progression of left ventricular hypertrophy in children with hypertrophic cardiomyopathy. N Engl J Med. 1986;315:610-614. [Abstract]

57. Spirito P, Maron BJ, Bonow RO, Epstein SE. Occurrence and significance of progressive left ventricular wall thinning and relative cavity dilatation in patients with hypertrophic cardiomyopathy. Am J Cardiol. 1987;60:123-129. [Medline] [Order article via Infotrieve]

58. Klemola E. Electrocardiographic observations of 650 Finnish athletes. Ann Med Intern Fenn. 1951;40:121-132.

59. Lemery R, Kleinebenne A, Nihoyannopoulos P, Aber V, Alfonso F, McKenna WJ. Q waves in hypertrophic cardiomyopathy in relation to the distribution and severity of right and left ventricular hypertrophy. J Am Coll Cardiol. 1990;16:368-374. [Abstract]

60. Alfonso F, Nihoyannopoulos P, Stewart J, Dickie S, Lemery R, McKenna WJ. Clinical significance of giant negative T waves in hypertrophic cardiomyopathy. J Am Coll Cardiol. 1990;15:965-971. [Abstract]

61. Maron BJ, Wolfson JK, Ciró E, Spirito P. Relation of electrocardiographic abnormalities and patterns of left ventricular hypertrophy identified by two-dimensional echocardiography in patients with hypertrophic cardiomyopathy. Am J Cardiol. 1983;51:189-194. [Medline] [Order article via Infotrieve]

62. Stoddard MF, Pearson AC, Kern MJ, Ratcliff J, Mrosek DG, Labovitz AJ. Left ventricular diastolic function: comparison of pulsed Doppler echocardiographic and hemodynamic indexes in subjects with and without coronary artery disease. J Am Coll Cardiol. 1989;13:327-336. [Abstract]

63. Phillips RA, Coplan NL, Krakoff LR, Yeager K, Ross RS, Gorlin R, Goldman ME. Doppler echocardiographic analysis of left ventricular filling in treated hypertensive patients. J Am Coll Cardiol. 1987;9:317-322. [Abstract]

64. Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow velocity patterns to left ventricular diastolic function: new insights from a combined hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol. 1988;12:426-440. [Abstract]

65. Maron BJ, Spirito P, Green KJ, Wesley YE, Bonow RO, Arce J. Noninvasive assessment of left ventricular diastolic function by pulsed Doppler echocardiography in patients with hypertrophic cardiomyopathy. J Am Coll Cardiol. 1987;10:733-742. [Abstract]

66. Lewis JF, Spirito P, Pelliccia A, Maron BJ. Usefulness of Doppler echocardiographic assessment of diastolic filling in distinguishing "athlete's heart" from hypertrophic cardiomyopathy. Br Heart J. 1992;68:296-300. [Abstract/Free Full Text]

67. Colan SD, Sanders SP, MacPherson D, Borow KM. Left ventricular diastolic function in elite athletes with physiologic cardiac hypertrophy. J Am Coll Cardiol. 1985;6:545-549. [Abstract]

68. Granger CB, Karuimeddini MK, Smith VE, Shapiro HB, Katz AM, Riba AL. Rapid ventricular filling in left ventricular hypertrophy, I: physiologic hypertrophy. J Am Coll Cardiol. 1985;5:862-868. [Abstract]

69. Pearson AC, Schiff M, Mrosek D, Labovitz AJ, Williams GA. Left ventricular diastolic function in weight lifters. Am J Cardiol. 1986;58:1254-1259. [Medline] [Order article via Infotrieve]

70. Fagard R, Van den Broeke C, Bielen E, Vanhees L, Amery A. Assessment of stiffness of the hypertrophied left ventricle of bicyclists using left ventricular inflow Doppler velocimetry. J Am Coll Cardiol. 1987;9:1250-1254. [Abstract]

71. Finkelhor RS, Hanak LJ, Bahler RC. Left ventricular filling in endurance-trained subjects. J Am Coll Cardiol. 1986;8:289-293. [Abstract]

72. Nixon JV, Wright AR, Porter TR, Roy V, Arrowood JA. Effects of exercise on left ventricular diastolic performance in trained athletes. Am J Cardiol. 1991;68:945-949. [Medline] [Order article via Infotrieve]

73. Lattanzi F, Spirito P, Picano E, Mazzarisi A, Landini L, Distante A, Vecchio C, L'Abbate A. Quantitative assessment of ultrasonic myocardial reflectivity in hypertrophic cardiomyopathy. J Am Coll Cardiol. 1991;17:1085-1090. [Abstract]

74. Lattanzi F, Di Bello V, Picano E, Caputo MT, Talarico L, Di Muro C, Landini L, Santoro G, Giusti C, Distante A. Normal ultrasonic myocardial reflectivity in athletes with increased left ventricular mass: a tissue characterization study. Circulation. 1992;85:1828-1834. [Abstract/Free Full Text]

75. Pelliccia A, Maron BJ, Spataro A, Biffi A, Caselli G, Culasso F. Physiological limits of "athlete's heart" in women. Circulation. 1993;88(suppl I):I-57. Abstract.

76. Milliken MC, Stray-Gundersen J, Peshock RM, Katz J, Mitchell JH. Left ventricular mass as determined by magnetic resonance imaging in male endurance athletes. Am J Cardiol. 1988;62:301-305.

77. Riley-Hagen M, Peshock RM, Stray-Gundersen J, Katz J, Ryschon TW, Mitchell JH. Left ventricular dimensions and mass using magnetic resonance imaging in female endurance athletes. Am J Cardiol. 1992;69:1067-1074. [Medline] [Order article via Infotrieve]

78. Maron BJ, Pelliccia A, Spataro A, Granata M. Reduction in left ventricular wall thickness after deconditioning in highly trained Olympic athletes. Br Heart J. 1993;69:125-128. [Abstract/Free Full Text]

79. Geisterfer-Lowrance AAT, Kass S, Tanigawa G, Vosberg H-P, McKenna WJ, Seidman CE, Seidman JG. A molecular basis for familial hypertrophic cardiomyopathy: a ß-cardiac myosin heavy chain gene missense mutation. Cell. 1990;62:999-1006. [Medline] [Order article via Infotrieve]

80. Thierfelder L, Watkins H, MacRae C, Lamas R, McKenna WJ, Vosberg H-P, Seidman JG, Seidman CE. -Tropomyosin and cardiac troponin T mutations cause familial hypertrophic cardiomyopathy: a disease of the sarcomere. Cell. 1994;77:701-712. [Medline] [Order article via Infotrieve]

81. Watkins H, Thierfelder L, Hwang DS, McKenna WJ, Seidman JG, Seidman CE. Sporadic hypertrophic cardiomyopathy due to de novo myosin mutations. J Clin Invest. 1992;90:1666-1671.

82. Watkins H, Rosenzweig A, Hwang D-S, Levi T, McKenna WJ, Seidman CE, Seidman JG. Characteristics and prognostic implications of myosin missense mutations in familial hypertrophic cardiomyopathy. N Engl J Med. 1992;326:1108-1114. [Abstract]

83. Carrier L, Hengstenberg C, Beckmann JS, Guicheney P, Dufour C, Bercovici J, Dausse E, Berebbi-Bertrand I, Wisnewsky C, Pulvenis D, Fetler L, Vignal A, Weissenbach J, Hillaire D, Feingold J, Bouhour J-B, Hagege A, Desnos M, Isnard R, Dubourg O, Komajda M, Schwartz K. Mapping of a novel gene for familial hypertrophic cardiomyopathy to chromosome 11. Nature Genet. 1993;4:311-317.[Medline] [Order article via Infotrieve]

This article has been cited by other articles:

				A. La Gerche, A. J. Taylor, and D. L. Prior Athlete's Heart: The Potential for Multimodality Imaging to Address the Critical Remaining Questions. J. Am. Coll. Cardiol. Img., March 1, 2009; 2(3): 350 - 363. [Abstract] [Full Text] [PDF]

				G S Soor, A Luk, E Ahn, J R Abraham, A Woo, A Ralph-Edwards, and J Butany Hypertrophic cardiomyopathy: current understanding and treatment objectives J. Clin. Pathol., March 1, 2009; 62(3): 226 - 235. [Abstract] [Full Text] [PDF]

				M. Martin, J. J. R. Reguero, M. G. Castro, E. Coto, E. Hernandez, A. Carro, D. Calvo, and C. M. de la Tassa Hypertrophic cardiomyopathy and athlete's heart: a tale of two entities Eur J Echocardiogr, January 1, 2009; 10(1): 151 - 153. [Abstract] [Full Text] [PDF]

				A. Magalski, B. J. Maron, M. L. Main, M. McCoy, A. Florez, K. J. Reid, H. W. Epps, J. Bates, and J. E. Browne Relation of race to electrocardiographic patterns in elite American football players. J. Am. Coll. Cardiol., June 10, 2008; 51(23): 2250 - 2255. [Abstract] [Full Text] [PDF]

				S. Basavarajaiah, A. Boraita, G. Whyte, M. Wilson, L. Carby, A. Shah, and S. Sharma Ethnic differences in left ventricular remodeling in highly-trained athletes relevance to differentiating physiologic left ventricular hypertrophy from hypertrophic cardiomyopathy. J. Am. Coll. Cardiol., June 10, 2008; 51(23): 2256 - 2262. [Abstract] [Full Text] [PDF]

				S. Basavarajaiah, M. Wilson, G. Whyte, A. Shah, W. McKenna, and S. Sharma Prevalence of hypertrophic cardiomyopathy in highly trained athletes: relevance to pre-participation screening. J. Am. Coll. Cardiol., March 11, 2008; 51(10): 1033 - 1039. [Abstract] [Full Text] [PDF]

				A. Pelliccia, F. M. Di Paolo, F. M. Quattrini, C. Basso, F. Culasso, G. Popoli, R. De Luca, A. Spataro, A. Biffi, G. Thiene, et al. Outcomes in Athletes with Marked ECG Repolarization Abnormalities N. Engl. J. Med., January 10, 2008; 358(2): 152 - 161. [Abstract] [Full Text] [PDF]

				S. Basavarajaiah, M. Wilson, R. Naghavi, G. Whyte, M. Turner, and S. Sharma Physiological upper limits of left ventricular dimensions in highly trained junior tennis players Br. J. Sports Med., November 1, 2007; 41(11): 784 - 788. [Abstract] [Full Text] [PDF]

				B. J. Maron and A. Pelliccia The Heart of Trained Athletes: Cardiac Remodeling and the Risks of Sports, Including Sudden Death Circulation, October 10, 2006; 114(15): 1633 - 1644. [Full Text] [PDF]

				A. Pelliccia, F. M. Di Paolo, D. Corrado, C. Buccolieri, F. M. Quattrini, C. Pisicchio, A. Spataro, A. Biffi, M. Granata, and B. J. Maron Evidence for efficacy of the Italian national pre-participation screening programme for identification of hypertrophic cardiomyopathy in competitive athletes Eur. Heart J., September 2, 2006; 27(18): 2196 - 2200. [Abstract] [Full Text] [PDF]

				S Basavarajaiah, M Wilson, S Junagde, G Jackson, G Whyte, S Sharma, and W O Roberts Physiological left ventricular hypertrophy or hypertrophic cardiomyopathy in an elite adolescent athlete: role of detraining in resolving the clinical dilemma * Commentary Br. J. Sports Med., August 1, 2006; 40(8): 727 - 729. [Abstract] [Full Text] [PDF]

				T. E. Paterick, T. J. Paterick, G. F. Fletcher, and B. J. Maron Medical and Legal Issues in the Cardiovascular Evaluation of Competitive Athletes JAMA, December 21, 2005; 294(23): 3011 - 3018. [Abstract] [Full Text] [PDF]

				B J Maron Distinguishing hypertrophic cardiomyopathy from athlete's heart: a clinical problem of increasing magnitude and significance Heart, November 1, 2005; 91(11): 1380 - 1382. [Abstract] [Full Text] [PDF]

				W. D. Binder, M. A. Fifer, M. E. King, and J. R. Stone Case 26-2005 - A 48-Year-Old Man with Sudden Loss of Consciousness while Jogging N. Engl. J. Med., August 25, 2005; 353(8): 824 - 832. [Full Text] [PDF]

				C.E. Chee, C.P. Anastassiades, A.G. Antonopoulos, A.A. Petsas, and L.C. Anastassiades Cardiac hypertrophy and how it may break an athlete's heart - the Cypriot case Eur J Echocardiogr, August 1, 2005; 6(4): 301 - 307. [Abstract] [Full Text] [PDF]

				B. J. Maron, P. S. Douglas, T. P. Graham, R. A. Nishimura, and P. D. Thompson Task Force 1: Preparticipation screening and diagnosis of cardiovascular disease in athletes J. Am. Coll. Cardiol., April 19, 2005; 45(8): 1322 - 1326. [Full Text] [PDF]

				X. Liu, F. Ouyang, H. Mavrakis, C. Ma, J. Dong, S. Ernst, D. Bänsch, M. Antz, and K.-H. Kuck Complete pulmonary vein isolation guided by three-dimensional electroanatomical mapping for the treatment of paroxysmal atrial fibrillation in patients with hypertrophic obstructive cardiomyopathy Europace, January 1, 2005; 7(5): 421 - 427. [Abstract] [Full Text] [PDF]

				B. J. Maron, J.G. Seidman, and C. E. Seidman Proposal for contemporary screening strategies in families with hypertrophic cardiomyopathy J. Am. Coll. Cardiol., December 7, 2004; 44(11): 2125 - 2132. [Abstract] [Full Text] [PDF]

				A. Biffi, B. J. Maron, L. Verdile, F. Fernando, A. Spataro, G. Marcello, R. Ciardo, F. Ammirati, F. Colivicchi, and A. Pelliccia Impact of physical deconditioning on ventricular tachyarrhythmias in trained athletes J. Am. Coll. Cardiol., September 1, 2004; 44(5): 1053 - 1058. [Abstract] [Full Text] [PDF]

				K. Soejima and W. G. Stevenson Athens, athletes, and arrhythmias: The cardiologist's dilemma J. Am. Coll. Cardiol., September 1, 2004; 44(5): 1059 - 1061. [Full Text] [PDF]

				E. Kasikcioglu and H. Akhan Echocardiographic limits of left ventricular remodeling in athletes J. Am. Coll. Cardiol., July 21, 2004; 44(2): 469 - 470. [Full Text] [PDF]

				B. J. Maron, W. J. McKenna, G. K. Danielson, L. J. Kappenberger, H. J. Kuhn, C. E. Seidman, P. M. Shah, W. H. Spencer III, P. Spirito, F. J. Ten Cate, et al. American College of Cardiology/European Society of Cardiology Clinical Expert Consensus Document on Hypertrophic Cardiomyopathy: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines J. Am. Coll. Cardiol., November 5, 2003; 42(9): 1687 - 1713. [Full Text] [PDF]

				Writing Committee Members, B. J. Maron, W. J. McKenna, G. K. Danielson, L. J. Kappenberger, H. J. Kuhn, C. E. Seidman, P. M. Shah, W. H. Spencer III, P. Spirito, et al. American College of Cardiology/European Society of Cardiology Clinical Expert Consensus Document on Hypertrophic Cardiomyopathy: A report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines Eur. Heart J., November 1, 2003; 24(21): 1965 - 1991. [Full Text] [PDF]

				B. J. Maron Sudden Death in Young Athletes N. Engl. J. Med., September 11, 2003; 349(11): 1064 - 1075. [Full Text] [PDF]

				W. B. Abernethy III, J. K. Choo, and A. M. Hutter Jr Echocardiographic characteristics of professional football players J. Am. Coll. Cardiol., January 15, 2003; 41(2): 280 - 284. [Abstract] [Full Text] [PDF]

				S. Sharma, B. J. Maron, G. Whyte, S. Firoozi, P. M. Elliott, and W. J. McKenna Physiologic limits of left ventricular hypertrophy in elite junior athletes: Relevance to differential diagnosis of athlete's heart and hypertrophic cardiomyopathy J. Am. Coll. Cardiol., October 16, 2002; 40(8): 1431 - 1436. [Abstract] [Full Text] [PDF]

				B. J. Maron Hypertrophic Cardiomyopathy: A Systematic Review JAMA, March 13, 2002; 287(10): 1308 - 1320. [Abstract] [Full Text] [PDF]

				S.G. Priori, E. Aliot, C. Blomstrom-Lundqvist, L. Bossaert, G. Breithardt, P. Brugada, A.J. Camm, R. Cappato, S.M. Cobbe, C. Di Mario, et al. Task Force on Sudden Cardiac Death of the European Society of Cardiology Eur. Heart J., August 2, 2001; 22(16): 1374 - 1450. [PDF]

				D J R Hildick-Smith and L M Shapiro Echocardiographic differentiation of pathological and physiological left ventricular hypertrophy Heart, June 1, 2001; 85(6): 615 - 619. [Full Text]

				S. Sharma, P. M. Elliott, G. Whyte, N. Mahon, M. S. Virdee, B. Mist, and W. J. McKenna Utility of metabolic exercise testing in distinguishing hypertrophic cardiomyopathy from physiologic left ventricular hypertrophy in athletes J. Am. Coll. Cardiol., September 1, 2000; 36(3): 864 - 870. [Abstract] [Full Text] [PDF]

				A. Pelliccia, B. J. Maron, F. Culasso, F. M. Di Paolo, A. Spataro, A. Biffi, G. Caselli, and P. Piovano Clinical Significance of Abnormal Electrocardiographic Patterns in Trained Athletes Circulation, July 18, 2000; 102(3): 278 - 284. [Abstract] [Full Text] [PDF]

				A. Pelliccia, F. Culasso, F. M. Di Paolo, and B. J. Maron Physiologic Left Ventricular Cavity Dilatation in Elite Athletes Ann Intern Med, January 5, 1999; 130(1): 23 - 31. [Abstract] [Full Text] [PDF]

				F. C. Basilico Cardiovascular Disease in Athletes Am. J. Sports Med., January 1, 1999; 27(1): 108 - 121. [Abstract] [Full Text] [PDF]

				B. J. Maron, J. H. Moller, C. E. Seidman, G. M. Vincent, H. C. Dietz, A. J. Moss, J. A. Towbin, H. M. Sondheimer, R. E. Pyeritz, G. McGee, et al. Impact of Laboratory Molecular Diagnosis on Contemporary Diagnostic Criteria for Genetically Transmitted Cardiovascular Diseases: Hypertrophic Cardiomyopathy, Long-QT Syndrome, and Marfan Syndrome : A Statement for Healthcare Professionals From the Councils on Clinical Cardiology, Cardiovascular Disease in the Young, and Basic Science, American Heart Association Circulation, October 6, 1998; 98(14): 1460 - 1471. [Full Text] [PDF]

				D. Corrado, C. Basso, M. Schiavon, and G. Thiene Screening for Hypertrophic Cardiomyopathy in Young Athletes N. Engl. J. Med., August 6, 1998; 339(6): 364 - 369. [Abstract] [Full Text] [PDF]

				P. Spirito, C. E. Seidman, W. J. McKenna, and B. J. Maron The Management of Hypertrophic Cardiomyopathy N. Engl. J. Med., March 13, 1997; 336(11): 775 - 785. [Full Text] [PDF]

				P. Melacini, M. Fanin, G.A. Danieli, C. Villanova, F. Martinello, M. Miorin, M.P. Freda, M. Miorelli, M.L. Mostacciuolo, G. Fasoli, et al. Myocardial Involvement Is Very Frequent Among Patients Affected With Subclinical Becker's Muscular Dystrophy Circulation, December 15, 1996; 94(12): 3168 - 3175. [Abstract] [Full Text]

				B. J. Maron, P. D. Thompson, J. C. Puffer, C. A. McGrew, W. B. Strong, P. S. Douglas, L. T. Clark, M. J. Mitten, M. H. Crawford, D. L. Atkins, et al. Cardiovascular Preparticipation Screening of Competitive Athletes: A Statement for Health Professionals From the Sudden Death Committee (Clinical Cardiology) and Congenital Cardiac Defects Committee (Cardiovascular Disease in the Young), American Heart Association Circulation, August 15, 1996; 94(4): 850 - 856. [Full Text]

				A. Pelliccia, B. J. Maron, F. Culasso, A. Spataro, and G. Caselli Athlete's Heart in Women: Echocardiographic Characterization of Highly Trained Elite Female Athletes JAMA, July 17, 1996; 276(3): 211 - 215. [Abstract] [PDF]

				A. Pelliccia, B. J. Maron, R. De Luca, F. M. Di Paolo, A. Spataro, and F. Culasso Remodeling of Left Ventricular Hypertrophy in Elite Athletes After Long-Term Deconditioning Circulation, February 26, 2002; 105(8): 944 - 949. [Abstract] [Full Text] [PDF]

				G. Derumeaux, P. Mulder, V. Richard, A. Chagraoui, C. Nafeh, F. Bauer, J.-P. Henry, and C. Thuillez Tissue Doppler Imaging Differentiates Physiological From Pathological Pressure-Overload Left Ventricular Hypertrophy in Rats Circulation, April 2, 2002; 105(13): 1602 - 1608. [Abstract] [Full Text] [PDF]

This Article Extract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Maron, B. J. Articles by Spirito, P. Search for Related Content PubMed PubMed Citation Articles by Maron, B. J. Articles by Spirito, P. Pubmed/NCBI databases Medline Plus Health Information Cardiomyopathy Heart Disease in Women Heart Diseases