Copyright © 2004, The European Society of Cardiology
Cardiac hypertrophy and how it may break an athlete's heart – the Cypriot case
aDepartment of Medicine, Middlesex Hospital, University College London Hospitals NHS Foundation Trust, Mortimer Street, London W1T 3AA, United Kingdom
bCardiovascular Diagnostic Centre, 1, Thassou Street, 1087 Nicosia, Cyprus
Received 16 March 2004; received in revised form 7 November 2004; accepted after revision 22 November 2004.
* Corresponding author. Tel.: +35722 760948; fax: +35722 760087. E-mail: anast@spidernet.com.cy
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Abstract |
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Aims This is a case report of an athlete whose professional football career was transiently terminated because of the presumed diagnosis of hypertrophic cardiomyopathy.
Methods and results The diagnosis was based on electrocardiographic repolarisation changes. The ECGs, treadmill exercise tests (Bruce protocol) and echo examinations at the time of his active training and several years after termination of his professional career are discussed. No hypertrophic cardiomyopathy was documented by ultrasound examination.
Conclusions The distinction between physiological athlete's heart and pathological conditions has critical implications for professional athletes. Criteria and guidelines for screening of athletes in competitive sports are recommended.
Keywords: Hypertrophic cardiomyopathy; Athlete's heart; Athletic heart syndrome; Repolarisation; Apical cardiomyopathy; M-mode and 2D-echocardiography
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Introduction |
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The heart undergoes morphological and functional changes in response to athletic training. The clinical, electrocardiographic and echocardiographic expression of these physiological alterations is known as the athletic heart syndrome. However, hypertrophic cardiomyopathy (HCM) may manifest with similar clinical and electrocardiographic findings. The clinical distinction between physiological athlete's heart and pathological conditions has critical implications for professional athletes.1,2 Echocardiography plays a crucial role in establishing the diagnosis of HCM. We report on an athlete whose career was nearly finished due to conflicting medical opinions.
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Examinations |
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A 23-year-old Caucasian, professional soccer player was evaluated in our clinic in 1990 after being diagnosed elsewhere as having an HCM. An electrocardiogram (ECG), a treadmill test (Bruce protocol), 2D-echo Doppler examination, a chest X-ray, 24h Holter monitor and cardiac catheterisation with coronary angiography were performed. His father and two brothers also underwent an echocardiographic examination. The opinion of two prestigious centres in Europe and the USA was also sought. Follow-up clinical and non-invasive evaluation at our cardiac laboratory has continued till the present time.
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Results |
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The athlete had been asymptomatic throughout his athletic training career. The physical examination was normal. The ECG (Fig. 1) showed left ventricular hypertrophy (LVH) by voltage criteria with a biphasic T-wave in V3 and inverted T-waves in leads II, III, aVF and V3–V6. Chest X-ray was normal and 24-h Holter monitoring revealed no arrhythmias. During the treadmill exercise test a peak heart rate of 173/min was reached and the blood pressure raised to 200/80mmHg, with progressive ‘normalization’ of the inverted T-waves as the heart rate increased (Fig. 2). No ischemic changes or arrhythmias were recorded. On M-mode and 2D-echo Doppler examination (Fig. 3), the findings were: left ventricle (LV) – normal cavity dimensions (end-systolic dimension: 30mm, end-diastolic dimension: 51mm), mild concentric hypertrophy (LV posterior wall: 13mm, inter-ventricular septum, IVS: 12mm), with thickening of the papillary muscles and good LV systolic function; right ventricle – normal; IVS – normal shape and motion; mitral valve – no thickening of the leaflets and no prolapse. Normal LV inflow velocities and no pressure gradients across any of the valves were recorded. On cardiac catheterisation, the LV angiogram showed a hypertrophied ventricle with large papillary muscles and normal contraction. The coronary arteries were large and smooth.
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Based on these data, we recommended that the patient should continue with his sporting activities. His soccer team, however, sought for a second opinion from a medical centre in the USA. Their results and recommendations were similar to ours. However, the athlete's medical data were also reviewed by another prominent medical group in Europe. The comments on the ECG were similar to ours but the echocardiography report described "a hypertrophied LV free wall and septum not confined to the apical region". Based on these findings, the possible diagnosis of HCM was accepted with the recommendation that the patient "should cease all violent competitive exercise" which was adopted by the Cyprus sports authorities. The young soccer player ceased all training and participation with his football team as well as the Cyprus National Team for a period of more than one year until our suggestion, backed by that from the USA Centre, was finally adopted.
This man has been followed until the end of his professional sports career. He never had any medical problems and no significant changes occurred in his ECG or echo. Consequently, the sports authorities issued the necessary health certificate at the end of his football career, about four years ago. Since then he has been working as a coach at a sports academy for young football talents. On a recent re-evaluation at our Centre, the physical findings remained unchanged. The ECG, however, showed more prominent T-wave inversions in the precordial leads V4–V6 and in leads II, III, aVF (Fig. 4). The treadmill exercise test, at peak effort, showed no "normalization" of the ST-T as compared to the changes that had occurred at the time of active training (Fig. 5). On 2D-echo Doppler examination the findings were the same as before, when he was in full training (Fig. 6). Detailed high-resolution (5MHz) apical imaging did not reveal any apical hypertrophy.
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Discussion |
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This athlete was diagnosed with HCM on the basis of marked T-wave inversion and pathological Q-waves, which are suggestive of HCM.3,4 Some studies have stressed that deep T-wave inversion, ST depression, prolonged QT interval and abnormal Q-waves should raise the suspicion of underlying cardiac pathology.3,4 Sierra-Grima et al.5 reported that the ST-T changes simulating ‘pseudo-ischemia’ tended to normalize during exercise in all athletes.
Echocardiography is an important tool in defining the morphology of the athlete's heart and differentiating it from cardiac pathology especially when confusion is created by ECG changes. A large study3 has shown that in the absence of pathological conditions, the major determinant of altered ECG patterns was the morphological cardiac remodelling induced by physical training. Athletes with the most marked ECG abnormalities showed the greatest increase in LV cavity size, wall thickness, and mass on 2D-echo. Furthermore, there are echocardiographic features that differentiate the athlete's heart and HCM.6 In the athlete's heart, there is a maximal LV wall thickness of less than 16mm, concentric LVH, large LV cavity size, normal diastolic function and left atrial size. In HCM, the LV wall thickness is greater than 16mm, there is variable LVH or asymmetrical septal hypertrophy, a small LV cavity size and impaired diastolic function with dilated left atrium.
In certain cases posing difficult dilemmas, discontinuation of the training may help to distinguish between the athletic heart and HCM. Detraining produces a rapid and progressive normalization of morphology, and repeat echocardiography will show normalized wall thickness in athletes, but not in individuals with HCM.2 While during the training period, the ECG shows few changes in the repolarisation abnormalities, a large number of these abnormal ECGs return to normal, or become less abnormal over a long-term follow-up.7 In our case, the grossly abnormal repolarisation changes present during the active training period did not normalize but became more prominent both in the resting ECG and the treadmill test. There was also no normalization of the ST-T changes with increasing heart rate on effort, two years after termination of his professional football career contrary to what was observed during his professional career. Obviously, this observation does not comply with the current prevailing thought on the athlete's heart syndrome. These findings would more logically apply to an HCM. The possibility of an apical hypertrophic cardiomyopathy may be considered. Maron described in 1990 its purest morphologic form as relatively mild in extent and confined to the most distal portion of the left ventricle.8 We performed echocardiographic studies of the apex in the apical views using high-resolution apical imaging. No abnormalities were found. Current knowledge and experience indicate a benign clinical course of apical HCM which may remain in relatively stable condition without symptoms for a long period of time.9
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Acknowledgements |
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The authors are grateful to James B. Seward MD, Professor of Medicine, Cardiology and Paediatrics, Mayo Clinic, Rochester, Minnesota, USA, for his suggestions and discussion of the case with the student-authors.
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Notes |
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1 Medical students at the Royal Free and University College Medical School, London, UK, on elective rotation at the Cardiovascular Diagnostic Centre, Nicosia, Cyprus.
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References |
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- Hutter A.M. Jr. Cardiovascular abnormalities in the athlete: role of the physician. J Am Coll Cardiol (1994) 24:851–853.[Web of Science][Medline]
- Maron B.J., Pelliccia A., Spirito P. Cardiac disease in young trained athletes: insights into methods for distinguishing athlete's heart from structural heart disease, with particular emphasis on hypertrophic cardiomyopathy. Circulation (1995) 91:1596–1601.
[Free Full Text] - Pelliccia A., Maron B.J., Culasso F., Di Paolo F.M., Spataro A., Biffi A. Clinical significance of abnormal electrocardiographic patterns in trained athletes. Circulation (2000) 102:278–284.
[Abstract/Free Full Text] - Firoozi S., Sharma S., McKenna W.J. Risk of competitive sport in young athletes with heart disease. Heart (2003) 89:710–714.
[Abstract/Free Full Text] - Serra-Grima R., Estorch M., Carrio I., Subirana M., Berna L., Prat T. Marked ventricular repolarization in highly trained athletes' electrocardiograms: clinical and prognostic implications. J Am Coll Cardiol (2000) 36:1310–1316.
[Abstract/Free Full Text] - Pelliccia A., Maron B.J., Spataro A., Proschan M.A., Spirito P. The upper limit of physiologic cardiac hypertrophy in highly trained elite athletes. N Engl J Med (1991) 324:295–301.[Abstract]
- Pelliccia A. What constitutes adequate and cost-effective cardiac screening prior to vigorous activity for collegiate athletes and older adults? Dialogues Cardiovasc Med (2002) 7:165–171.
- Maron B.J. Apical hypertrophic cardiomyopathy: the continuing saga. J Am Coll Cardiol (1990) 15:91–93.[Web of Science][Medline]
- Webb J.G., Sasson Z., Rakowski A., Liu P., Wigle E.D. Apical hypertrophic cardiomyopathy: clinical follow-up and diagnostic correlates. J Am Coll Cardiol (1990) 15:83–90.[Abstract]
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