Dipartimento di Medicina Generale, Clinica “Athena” Villa dei Pini – Piedimonte Matese (CE)
Athletic heart syndrome is a constellation of structural and functional changes that occur in the heart of people who train for > 1 h most days. The syndrome is asymptomatic.
A regular training programme causes favourable changes in skeletal muscle performance (the realm of the sports physiologist) and two clear cut cardiovascular effects—namely, enlargement of the heart and a slow pulse rate at rest. These are the components of a characteristic clinical picture known as the “athlete’s heart”. Regular training causes the heart to enlarge. This is the result of a combination of left ventricular cavity enlargement (dilatation) and increased wall thickness (hypertrophy). It is widely held that resistance or isometric training (weight lifting, etc) stimulates hypertrophy with normal cavity dimensions (concentric), whereas aerobic, isotonic training (running, etc) stimulates hypertrophy and cavity dilatation (eccentric).
Athlete’s heart is a diagnosis of exclusion; it must be distinguished from disorders that cause similar findings but are life threatening (eg, hypertrophic or dilated cardiomyopathies, ischemic heart disease, arrhythmogenic right ventricular dysplasia).
Signs vary but may include bradycardia; an left ventricular impulse that is laterally displaced, enlarged, and increased in amplitude; a systolic ejection (flow) murmur at the left lower sternal border; a 3rd heart sound (S3) due to early, rapid diastolic ventricular filling; a 4th heart sound (S4), heard best during resting bradycardia because diastolic filling time is increased; and hyperdynamic carotid pulses. These signs reflect structural cardiac changes
The ECG is usually normal, but left ventricular hypertrophy on voltage criteria is common.
Many abnormal ECG patterns have been described. Two of the most common are illustrated here:
– Pronounced left ventricular hypertrophy on voltage with inferolateral T wave changes
– Early depolarisation changes with biphasic T waves in the anterior leads.
The second pattern presents a particularly characteristic biphasic T wave morphology with early repolarisation, convex proximally.
These changes reflect non-homogenous repolarisation caused by reduced resting sympathetic drive and resolve rapidly on exercise.
Incomplete RBBB, deep anterolateral T wave inversion, and “left ventricular hypertrophy and strain” pattern are described elsewhere. The latter is rare. Various slow rhythms as previously mentioned may be present (TAB. 1).
The ECG is a constant source of confusionin athletes with numerous variations on thebasic patterns. The changes are related to the extent of training and vary in athletes whose training is seasonal. Even quite gross changes may not indicate cardiovascular disease, though thorough further evaluation will often be needed to prove this point. The unpredictability and variability of the ECG in athletes seriously limits its value in screening for cardiac disease in these subjects.
Cardiac ultrasound will frequently reveal a modest uniform increase in wall thickness seldom to more than 1.6 cm and usually less than 1.3 cm. Mild left ventricular cavity dilatation is also observed. Trivial regurgitation of mitral and tricuspid valves is reported more frequently than in the sedentary population.
Indices of systolic and diastolic function are normal. In some extreme cases, however, a pattern indistinguishable from hypertrophic cardiomyopathy is observed, even though exhaustive further investigations of the subject and immediate family yield no confirmatory evidence. Echocardiographic features of other confounding conditions may be present.
24 hour ECG
Dynamic ECG monitoring may show some of the bradycardic features mentioned above. Complete heart block and ventricular tachycardia (sustained or unsustained) are not features of the athlete’s heart and should be investigated thoroughly. Premature atrial and ventricular contractions are common, and more complex forms are seen, especially in the elderly.
Stress testing reveals an outstanding exercise capacity with rapid recovery of heart rate in the resting phase. The heart rate response is slower than in untrained people, but the eventual maximum rate is the same. Previously abnormal early repolarisation changes (thought to be related to reduced resting sympathetic tone) and T wave inversion will usually “normalise”.
It is widely known that patients with coronary disease may develop pseudonormalisation of T wave changes on exercise, but in the context of a fit young athlete this response is reassuring. The blood pressure response is normal which may be a helpful distinguishing feature from hypertrophic cardiomyopathy.
Radionuclide studies, cardiac catheterisation, and magnetic resonance imaging provide useful insight into the athlete’s heart but, in clinical practice, are largely reserved for specific cases where some suspected cardiac pathology requires elucidation. Multiple gated imaging shows that the increment in stroke volume on exercise in athletes is the result of a normal ejection fraction and increased end diastolic volume, rather than any demonstrable enhancement in contractility.
Vigorous exercise can cause elevation in cardiac enzymes including creatine phosphokinase (CPK). Small rises in MB CPK have also been reported. This can be confusing if an athlete is admitted having collapsed. The rises are modest, however, and the time scale of enzyme release is not typical of myocardial infarction. Troponin T and I are more specific and should be used in cases of doubt.
PROGNOSIS AND TREATMENT
Although gross structural changes resemble those in some cardiac disorders, no adverse effects are apparent. In most cases, structural changes and bradycardia regress with detraining, although up to 20% of elite athletes have residual chamber enlargement, raising questions, in the absence of long-term data, about whether the athletic heart syndrome is truly benign. No treatment is required, although 3 mo of deconditioning may be needed to monitor left ventricular regression as a way of distinguishing this syndrome from cardiomyopathy. Such deconditioning can greatly interfere with an athlete’s life and may meet with resistance.
Athletes are a challenging group for the cardiologist both in terms of diagnosis and management. The stakes are high. The cardiovascular system is going to be pushed to the limit. The consequences of an erroneous diagnosis are potentially devastating, be it the death of the athlete or a career and way of life in ruins. These patients always merit the most careful evaluation. When still in doubt, the physician is well advised to seek help from others. The author of this paper certainly does!
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Dottor Luigi Ferritto
Dipartimento di Medicina Generale – Ambulatorio di Fisiopatologia dello Sport
Clinica “Athena” Villa dei Pini – Piedimonte Matese (CE)