CARDIAC IMAGING IN ATHLETES

Asaad A. Khan, M.D.; Lucy Safi, D.O.; Malissa Wood, M.D.

Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts

Abstract
Athletic heart syndrome refers to the physiological and morphological changes that occur in a human heart after repetitive
strenuous physical exercise. Examples of exercise-induced changes in the heart include increases in heart cavity dimensions,
augmentation of cardiac output, and increases in heart muscle mass. These cardiac adaptations vary based on the type of
exercise performed and are often referred to as sport-specific cardiac remodeling. The hemodynamic effects of endurance and
strength training exercise lead to these adaptations. Any abnormalities in chamber dilatation and left ventricular function usually
normalize with cessation of exercise. Athletic heart syndrome is rare and should be differentiated from pathologic conditions
such as hypertrophic cardiomyopathy, left ventricular noncompaction, and arrhythmogenic right ventricular dysplasia when
assessing a patient for athletic heart syndrome. This paper describes specific adaptations that occur in athletic heart syndrome
and tools to distinguish between healthy alterations versus underlying pathology.

Introduction characterized by increased peripheral vascular resistance and

Athletic heart syndrome is an umbrella term covering various normal or only slightly elevated cardiac output. This increase in
significant physiological and morphological changes that occur peripheral vascular resistance causes transient but potentially
in a human heart after repetitive strenuous physical exercise. marked systolic hypertension and LV afterload. American football,
This type of exercise results in increased maximal oxygen uptake weight lifting, and track and field throwing events are some
due to increased cardiac output and arteriovenous oxygen examples of sports involving isometric training.
difference. Prolonged intensive training induces hemodynamic Hemodynamic conditions, specifically changes in cardiac
effects on all cardiac chambers and the aorta. Endurance exercise output and peripheral vascular resistance, vary widely across
predominantly results in volume load on the left ventricle (LV), different sports. A previously accepted Morganroth hypothesis
whereas strength exercise produces pressure load.1 The mild was based on a study that compared M-mode echocardiographic
biventricular remodeling is seen more often in large male athletes LV measurements in wrestlers (strength training), swimmers
participating in endurance sports, with the greatest degree of LV (endurance training), and sedentary control subjects and found
wall thickening seen in athletes of African or Afro–Caribbean significant differences across these three groups. Athletes exposed
origin. A clear understanding of the broad spectrum of normal to strength training demonstrated concentric LV hypertrophy,
cardiac adaptations to exercise is required to differentiate healthy whereas individuals exposed to endurance training demonstrated
cardiac adaptations from potentially life-threatening cardiac eccentric LV enlargement with balanced increases in LV cavity size
pathology. and wall thickness. This study led to the concept of sport-specific
cardiac remodeling.6,7 Interestingly, many athletes today participate
Left Ventricular Adaptations in Athletic Heart Syndrome in sporting disciplines that involve a great deal of overlap between
Characteristic changes of an athlete’s heart include mild LV endurance and strength training.
hypertrophy and increased chamber dimensions.2,3 Cardiac However, subsequent studies indicated that the classification
output, the product of stroke volume and heart rate, may increase of LV hypertrophy in athletes as eccentric or concentric does not
5- to 6-fold during maximal exercise effort. Heart rate in the follow an absolute pattern but instead takes a relative course.8,9
athlete may range from 40 bpm at rest to ≥ 200 bpm in a young Frequent combined endurance and power training (such as soccer,
maximally exercising athlete. Heart rate increase is responsible lacrosse, basketball, hockey, and field hockey) result in both
for the majority of cardiac output augmentation during exercise. volume and pressure load.
Early studies with electrocardiography (ECG) demonstrated Although most amateur athletes have normal chamber
a high prevalence of increased cardiac voltage suggestive of dimensions following exercise training, in some cases pronounced
LV enlargement in trained athletes.4 Subsequent work with LV dilation can occur.10,11 Pellicia et al. found that approximately
2-dimensional echocardiography confirmed underlying LV 15% of highly trained athletes demonstrated significant LV dilation
hypertrophy and dilation.5 with LV chamber dimensions of > 60 mm. In their cohort of Italian
To help understand the physiological mechanisms involved athletes, the LV diastolic dimension exceeded normal values in 40%
in various exercises, they can be broadly classified as either of subjects. This chamber enlargement can be accompanied by a
“isotonic” or “isometric” based on the hemodynamic mechanisms relatively mild increase in absolute LV wall thickness that exceeds
that occur during these activities. Isotonic (endurance) exercise upper normal limits (from 13 to 15 mm).12 These cardiac adaptations
involves sustained elevations in cardiac output with normal or reverse following cessation of exercise. Athletes may also show
reduced peripheral vascular resistance. These exercises primarily relatively small increases of wall thickness and cavity size on
pose a volume challenge for the heart that affects all four echocardiography. Maron et al. showed that approximately 10% to
chambers. Isometric (strength training) exercise involves activity 20% of athlete hearts demonstrate a statistically significant increase

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Figure 1. Parasternal long axis of an athletic heart. Figure 3. Normal septal tissue Doppler of an athletic heart showing e’
velocities ~ 0.12 m/s.

in wall thickness or cavity size. Importantly, they also demonstrated (DCM), and arrhythmogenic right ventricular dysplasia
that these values remain within accepted normal limits in most (ARVD) in our patients, some of whom may be athletes, and
athletes.13 Of note, LV systolic function is usually at the low end differentiating among these entities can be difficult. Knowledge
of normal in athletes; however, with exercise they demonstrate of some morphological distinguishing characteristics can prove
evidence of contractile reserve with improved LV and RV function. vital in diagnosing and managing these cases. The pattern
Use of 3-dimensional (3D) echocardiography improves of LV hypertrophy (LVH) may help to distinguish between
assessment of left- and right-ventricular volumes and helps to pathology and an athletic heart. In the athlete’s heart, LVH is
characterize different cardiovascular adaptations in athletes. 3D almost always symmetrical. Pathology such as HCM results
echocardiography takes into account differences in the length in asymmetric septal hypertrophy in approximately 60% and
and shape of the LV chamber and provides data on geometry apical hypertrophy in about 10% of patients. Importantly, in an
and function of the LV as well as synchronicity of LV contraction. athletic heart, concomitant LVH and cavity dilatation results in
These variables differ in patients with hypertrophic or dilated preservation of LV relative wall thickness or the ratio between
cardiomyopathy that do not show LV harmonic remodeling.14 posterior LV wall thickness and the LV end-diastolic diameter.
Studies using newer functional myocardial imaging techniques Patients with HCM have pathological hypertrophy that results in
in athletes, such as tissue Doppler echocardiography and strain a reduced LV cavity size. Additionally, abnormal morphology and
echocardiography, indicate that exercise training may lead to attachment of the papillary muscles to the mitral valve apparatus
changes in LV systolic function such as normal-to-high tissue can also be observed in HCM.17 Asymmetric septal hypertrophy
velocities and normal-to-low-normal tissue strain, respectively. or abnormal attachment of the papillary muscles can both lead to
These indices are not detected by assessment of a global index systolic anterior motion of the mitral valve and LV outflow tract
such as LV ejection fraction.15,16 obstruction,18 although the latter is typically not seen in an athletic
As cardiologists, we encounter pathologies such as heart. Overall, the LV ejection fraction is usually low-normal
hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy to normal in athletes but hyperdynamic in HCM. A significant

Figure 2. Four-chamber view of an athletic heart. Figure 4. Normal lateral tissue Doppler of an athletic patient with e’ of ~ 0.17
m/s.

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 reduction in systolic LV function should alert the physician to
the possibility of DCM, particularly if ejection fraction does not
augment with exercise.
Doppler assessment of mitral diastolic inflow patterns,
tissue Doppler imaging of the LV walls, and assessment of
tissue deformation can reveal impairment of relaxation and
longitudinal function that usually precede the development of
pathological LVH. On the contrary, early diastolic relaxation
velocities are usually normal or increased in athletes with
exercise-induced LVH.19 Studies by Afonso et al. have shown
that global longitudinal strain (GLS) is normal in athletes and
abnormal in HCM.20

The Right Ventricle

Exercise-induced cardiac remodeling is not confined to the
left ventricle. Endurance exercise requires both the left and right
ventricle (RV) to accept and eject relatively large quantities of
blood. In the absence of significant shunting, both chambers must
augment function to accomplish this task.
Figure 5. Parasternal long axis of a patient with hypertrophic cardiomyopathy.

Figure 6. Clip A shows a parasternal long axis of a patient with hypertrophic cardiomyopathy. Clip B shows anterior systolic motion of the anterior mitral leaflet.
Clip C is M mode through the mitral valve level showing extensive left ventricular hypertrophy and systolic anterior motion. Clip D is a normal patient.

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 Exercise-Induced
Chamber Pathology
Cardiac Adaptations
Right atrium Dilated Normal or dilated
Right ventricle Dilated Localized areas of akinesia, dyskinesia, or aneurysmal wall motion
Left atrium Dilated Variable
Left ventricle Dilated, symmetrical hypertrophy, preserved Wall thickness > 1.3-1.5 cm.40 Asymmetric hypertrophy, reduced
wall thickness/end-diastolic LV diameter ratio LV cavity size, LVOT obstruction
Tissue Doppler Increased Decreased
velocities
Global longitudinal Normal/low normal Abnormal
strain

Table 1. Echocardiographic findings comparing exercise-induced cardiac adaptations to pathology. LV: left ventricle; LVOT: left ventricular outflow tract.

Emerging data from Oxborough et al. and Teske et al.,21,22 Athletic adaptations of the heart need to be differentiated
supported by recent prospective studies, have stimulated interest from arrhythmogenic RV dysplasia (ARVD), where, unlike the
in RV adaptation to exercise.23,24 Additional data have provided symmetric remodeling and mild dilatation seen in the athlete
further insights into RV adaptation by showing that the RV has heart, localized areas of akinesia, dyskinesia, or aneurysmal wall
to endure a disproportionately higher increase in hemodynamic motion are usually seen. Newer echocardiographic techniques
afterload compared to the LV during intense exercise.25 Right such as tissue deformation imaging may reveal pathological strain
ventricular structure in collegiate endurance-trained (rowing) and patterns, including regional postsystolic shortening seen in ARVD
strength-trained (football) athletes was recently assessed before patients but not in healthy athletes.29
and after 90 days of team-based exercise training. There was a
statistically significant dilation of the RV in the endurance-trained Atria
athletes but not in the strength-trained athletes.26 Neilan et al. Left atrial remodeling is an important physiological adaptation
showed the dynamic nature of RV size and function in the setting present in highly trained athletes, most commonly those who
of marathon running,27 and they also showed myocardial injury engage in combined static and dynamic sports (i.e., cycling
and ventricular dysfunction related to training levels among non- and rowing), and is largely explained by associated LV cavity
elite participants in the Boston marathon. A recently published enlargement and volume overload.30 Larger left atria were first
study showed similar changes in the form of higher absolute RV noted in 1985 in a small study of endurance athletes.31 Another
diastolic area.28 These findings emphasize the notion of sports- study revealed left atrial enlargement in older individuals with a
specific alteration in RV morphology. significant history of exercise training.32

Figure 7. Strain rate imaging in an

athlete.

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 were deemed clinically insignificant. Therefore, marked aortic root
dilatation should be considered a pathological process in athletes.35

Other Imaging Modalities

In some cases, cardiac magnetic resonance imaging (CMR)
may provide additional diagnostic and prognostic information,
allowing for better visualization of the cardiac apex and lateral LV
wall compared to standard echocardiography. Administration of
gadolinium may demonstrate characteristic patterns of myocardial
fibrosis in HCM and DCM.36 The cardiovascular response to
exercise is a powerful discriminator between physiological
changes and a pathological disease process.
In healthy individuals, the blood pressure rises during exercise
as stroke volume is augmented. Individuals with cardiomyopathies
such as HCM are unable to demonstrate these changes and may
exhibit a flat response or even a fall in blood pressure during
exercise.37 In some cases, particularly with families in which a
Figure 8. Right ventricular dilatation seen in a marathon runner. definitive genetic mutation has already been identified, genetic
testing may be considered. However, this can create challenges in
Pelliccia et al. showed increased transverse left atrial dimensions terms of availability and expense, and test results generally may
(≥ 40 mm) in 20% of athletes and more substantially enlarged not be available for several weeks after ordering the exam.
dimensions (≥ 45 mm) in approximately 2%.30 Importantly, left
atrial enlargement appeared benign and largely confined to Long-Term Consequences
endurance training. Despite the left atrial enlargement, atrial Concern exists regarding long-term sequelae of significant
fibrillation is rarely associated with atrial enlargement (< 1% of LV remodeling evident in some highly trained athletes.
athletes evaulated in a small study).33 In an athletic heart, the left Approximately 15% of these athletes show striking LV cavity
atrium may measure large but should remain proportional to the enlargement (end-diastolic dimensions ≥ 60 mm) similar in
LV cavity size. Atrial dilation is less likely to occur in HCM patients magnitude to that evident in pathological forms of dilated
compared to patients with exercise-induced LV remodeling. Caselli cardiomyopathy. One longitudinal echocardiographic study
et al. found that a left atrial transverse diameter measurement > reported incomplete reversal of extreme LV cavity dilatation with
40 mm was highly reliable in excluding HCM (sensitivity 92% and deconditioning; significant chamber enlargement persisted in 20%
specificity 71%).34 of retired and deconditioned former elite athletes after 5 years.38
There is no current evidence showing a correlation between an
Aorta athlete’s remodeled heart and long-term prognosis, cardiovascular
The aorta experiences a significant hemodynamic load during disability, or sudden cardiac death.39
exercise, and the nature of this load is dependent on the type of
sport. Endurance activity causes high-volume aortic flow with Conclusion
modest systemic hypertension and strength activity, resulting in Athlete heart syndrome encompasses a variety of cardiac
normal-volume aortic flow with potentially profound systemic morphological changes, some of which are still not well
hypertension. A meta-analysis by Iskandar et al. showed that elite understood. The variation from normal cardiac physiology found
athletes have a small but significantly larger aortic root diameter at within the athletic population is similar to some of the other
the sinuses of Valsalva and aortic valve annulus. These differences conditions discussed above. Familiarity with the differentiating

Figure 9. Focused right ventricular view of a patient with

arrhythmogenic right ventricular cardiomyopathy.

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 5. Roeske WR, O’Rourke RA, Klein A, Leopold G, Karliner JS.
Noninvasive evaluation of ventricular hypertrophy in professional
athletes. Circulation. 1976 Feb;53(2):286-91.
6. Morganroth J, Maron BJ, Henry WL, Epstein SE. Comparative
left ventricular dimensions in trained athletes. Ann Intern Med.
1975 Apr;82(4):521-4.
7. Gilbert CA, Nutter DO, Felner JM, Perkins JV, Heymsfield SB,
Schlant RC. Echocardiographic study of cardiac dimensions and
function in the endurance-trained athlete. Am J Cardiol. 1977
Oct;40(4):528-33.
8. Fagard RH. Athlete’s heart: a meta-analysis of the echocardiographic
experience. Int J Sports Med. 1996 Nov;17 Suppl 3:S140-4.
9. Pluim BM, Zwinderman AH, van der Laarse A, van der Wall EE.
The athlete’s heart. A meta-analysis of cardiac structure and
function. Circulation. 2000 Jan 25;101(3):336-44.
10. Utomi V, Oxborough D, Whyte GP, et al. Systematic review and
meta-analysis of training mode, imaging modality and body size
influences on the morphology and function of the male athlete’s
heart. Heart. 2013 Dec;99(23):1727-33.
Figure 10. Short axis of the left and right ventricles showing profound 11. Pelliccia A, Culasso F, Di Paolo FM, Maron BJ. Physiologic left
enlargement of the right ventricle in a patient with arrhythmogenic right
ventricular cavity dilatation in elite athletes. Ann Intern Med. 1999
ventricular cardiomyopathy.
Jan 5;130(1):23-31.
factors will help discriminate at-risk individuals from those with 12. Pelliccia A, Maron BJ, Spataro A, Proschan MA, Spirito P. The
athletic adaptations. Pathologic conditions such as HCM, DCM, upper limit of physiologic cardiac hypertrophy in highly trained
and arrhythmogenic RV dysplasia are important differentials to elite athletes. N Engl J Med. 1991 Jan 31;324(5):295-301.
consider when assessing a patient for athletic heart syndrome. 13. Maron BJ. Structural features of the athlete heart as defined by
echocardiography. J Am Coll Cardiol. 1986 Jan;7(1):190-203.
Key Points: 14. Vitarelli A, Capotosto L, Placanica G, et al. Comprehensive
• Athletic heart syndrome is an umbrella term covering assessment of biventricular function and aortic stiffness in
various significant physiological and morphological changes athletes with different forms of training by three-dimensional
that occur in a human heart after repetitive strenuous echocardiography and strain imaging. Eur Heart J Cardiovasc
physical exercise. Imaging. 2013 Oct;14(10):1010-20.
• Isotonic (endurance) exercise poses a volume challenge for 15. Baggish AL, Yared K, Wang F, et al. The impact of endurance
the heart, whereas isometric (strength training) exercise exercise training on left ventricular systolic mechanics. Am J
causes a transient pressure challenge for the heart. Physiol Heart Circ Physiol. 2008 Sep;295(3):H1109-H1116.
• Left ventricular hypertrophy, left atrial enlargement, and 16. Cardim N, Oliveira AG, Longo S, et al. Doppler tissue imaging:
right ventricular enlargement may occur in the athletic heart; regional myocardial function in hypertrophic cardiomyopathy
however, the overall heart remains proportional in size. and in athlete’s heart. J Am Soc Echocardiogr. 2003
• An athlete’s heart may share similar characteristics Mar;16(3):223-32.
to pathologic conditions such as HCM, DCM, and 17. Cavalcante JL, Barboza JS, Lever HM. Diversity of mitral valve
arrhythmogenic right ventricular dysplasia, and it is abnormalities in obstructive hypertrophic cardiomyopathy. Prog
important to exclude these pathologic entities when Cardiovasc Dis. 2012 May-Jun;54(6):517-22.
assessing a patient for athletic heart syndrome. 18. Gersh BJ, Maron BJ, Bonow RO, et al.; American College
of Cardiology Foundation/American Heart Association Task
Conflict of Interest Disclosure: The authors have completed and submitted Force on Practice Guidelines. 2011 ACCF/AHA Guideline for
the Methodist DeBakey Cardiovascular Journal Conflict of Interest Statement the Diagnosis and Treatment of Hypertrophic Cardiomyopathy:
and none were reported. a report of the American College of Cardiology Foundation/
Keywords: athletic heart syndrome, isotonic exercise, isometric exercise, American Heart Association Task Force on Practice Guidelines.
cardiac adaptations, cardiac remodeling Developed in collaboration with the American Association for
Thoracic Surgery, American Society of Echocardiography,
References American Society of Nuclear Cardiology, Heart Failure Society
1. Maron BJ, Pelliccia A. The heart of trained athletes: cardiac of America, Heart Rhythm Society, Society for Cardiovascular
remodeling and the risks of sports, including sudden death. Angiography and Interventions, and Society of Thoracic
Circulation. 2006 Oct 10;114(15):1633-44. Surgeons. J Am Coll Cardiol. 2011 Dec 13;58(25):e212-60.
2. Maron BJ. Structural features of the athlete heart as defined by 19. Pelà G, Bruschi G, Montagna L, Manara M, Manca C. Left
echocardiography. J Am Coll Cardiol. 1986 Jan;7(1):190-203. and right ventricular adaptation assessed by Doppler tissue
3. La Gerche A, Taylor AJ, Prior DL. Athlete’s heart: the potential for echocardiography in athletes. J Am Soc Echocardiogr. 2004
multimodality imaging to address the critical remaining questions. Mar;17(3):205-11.
JACC Cardiovasc Imaging. 2009 Mar;2(3):350-63. 20. Afonso L, Kondur A, Simegn M, et al. Two-dimensional
4. Arstila M, Koivikko A. Electrocardiographic and vectorcardiographic strain profiles in patients with physiological and pathological
signs of left and right ventricular hypertrophy in endurance athletes. hypertrophy and preserved left ventricular systolic function: a
J Sports Med Phys Fitness. 1966 Sep;6(3):166-75. comparative analyses. BMJ Open. 2012 Aug 17;2(4).

MDCVJ | XII (2) 2016 houstonmethodist.org/debakey-journal 91

21. Oxborough D, Sharma S, Shave R, et al. The right ventricle of 30. Pelliccia A, Maron BJ, Di Paolo FM, et al. Prevalence and clinical
the endurance athlete: the relationship between morphology and significance of left atrial remodeling in competitive athletes. J Am
deformation. J Am Soc Echocardiogr. 2012 Mar;25(3):263-71. Coll Cardiol. 2005 Aug 16;46(4):690-6.
22. Teske AJ, Prakken NH, De Boeck BW, Velthuis BK, Doevendans 31. Hauser AM, Dressendorfer RH, Vos M, Hashimoto T, Gordon
PA, Cramer MJ. Effect of long term and intensive endurance S, Timmis GC. Symmetric cardiac enlargement in highly trained
training in athletes on the age related decline in left and endurance athletes: a two-dimensional echocardiographic study.
right ventricular diastolic function as assessed by Doppler Am Heart J. 1985 May;109(5 Pt 1):1038-44.
echocardiography. Am J Cardiol. 2009 Oct 15;104(8):1145-51. 32. Höglund C. Enlarged left atrial dimension in former endurance
23. Poh KK, Ton-Nu TT, Neilan TG, Tournoux FB, Picard MH, Wood athletes: an echocardiographic study. Int J Sports Med. 1986
MJ. Myocardial adaptation and efficiency in response to intensive Jun;7(3):133-6.
physical training in elite speedskaters. Int J Cardiol. 2008 Jun 33. Mont L, Sambola A, Brugada J, et al. Long-lasting sport
6;126(3):346-51. practice and lone atrial fibrillation. Eur Heart J. 2002
24. Baggish AL, Wang F, Weiner RB, et al. Training-specific changes Mar;23(6):477-82.
in cardiac structure and function: a prospective and longitudinal 34. Caselli S, Maron MS, Urbano-Moral JA, Pandian NG, Maron BJ,
assessment of competitive athletes. J Appl Physiol (1985). 2008 Pelliccia A. Differentiating left ventricular hypertrophy in athletes
Apr;104(4):1121-8. from that in patients with hypertrophic cardiomyopathy. Am J
25. La Gerche A, Heidbüchel H, Burns AT, et al. Disproportionate Cardiol. 2014 Nov 1;114(9):1383-9.
exercise load and remodeling of the athlete’s right ventricle. Med 35. Iskandar A, Thompson PD. A meta-analysis of aortic root size in
Sci Sports Exerc. 2011 Jun;43(6):974-81. elite athletes. Circulation. 2013 Feb 19;127(7):791-8.
26. King G, Wood MJ. The right ventricle of the elite high end 36. O’Hanlon R, Grasso A, Roughton M, et al. Prognostic
endurance athlete cannot be underestimated. J Am Soc significance of myocardial fibrosis in hypertrophic
Echocardiogr. 2012 Mar;25(3):272-3. cardiomyopathy. J Am Coll Cardiol. 2010 Sep 7;56(11):867-74.
27. Neilan TG, Januzzi JL, Lee-Lewandrowski E, et al. Myocardial 37. Kawasaki T, Azuma A, Kuribayashi T, et al. Vagal enhancement
injury and ventricular dysfunction related to training levels among due to subendocardial ischemia as a cause of abnormal blood
nonelite participants in the Boston marathon. Circulation. 2006 pressure response in hypertrophic cardiomyopathy. Int J Cardiol.
Nov 28;114(22):2325-33. 2008 Sep 16;129(1):59-64.
28. Utomi V, Oxborough D, Ashley E, et al. The impact of chronic 38. Pelliccia A, Maron BJ, De Luca R, Di Paolo FM, Spataro A,
endurance and resistance training upon the right ventricular Culasso F. Remodeling of left ventricular hypertrophy in elite
phenotype in male athletes. Eur J Appl Physiol. 2015 athletes after long-term deconditioning. Circulation. 2002 Feb
Aug;115(8):1673-82. 26;105(8):944-9.
29. Yoerger DM, Marcus F, Sherrill D, et al.; Multidisciplinary Study 39. Maron BJ, Pelliccia A. The heart of trained athletes: cardiac
of Right Ventricular Dysplasia Investigators. Echocardiographic remodeling and the risks of sports, including sudden death.
findings in patients meeting task force criteria for arrhythmogenic Circulation. 2006 Oct 10;114(15):1633-44.
right ventricular dysplasia: new insights from the multidisciplinary 40. Baggish AL, Yared K, Weiner RB. Differences in cardiac
study of right ventricular dysplasia. J Am Coll Cardiol. 2005 Mar parameters among elite rowers and subelite rowers. Med Sci
15;45(6):860-5. Sports Exerc. 2010 Jun;42(6):1215-20.

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