Medical History & Physical Examination
As with all of medicine, the most important element of evaluating athletes and their clinical findings is the medical history, and in the medical history, the most important element is what prompted the athlete to obtain medical evaluation. Abnormalities found on screening examinations in an asymptomatic athlete have far less import than abnormalities found during the evaluation of a symptomatic individual. In our clinical experience, most clinical abnormalities found during screening ultimately turn out to be normal variants of the athlete's heart syndrome. Consequently, dividing athletes into those with and without symptoms is an important initial approach to their evaluation.
The other key elements of the history are the athlete's exercise training history and his or her exercise performance. Marked changes in cardiac dimensions require considerable amounts of exercise training so that cardiac findings in an athlete with a short or low-level training history are of more concern than similar findings in an athlete with high volumes of training. It is also extremely useful to be able to assess the athlete's level of performance. Excellent endurance exercise performance requires a large cardiac stoke volume, so that excellent exercise capacity is reassuring but does not absolutely exclude important disease. Family history of cardiac disease or unexpected or unexplained sudden death (including drowning, unexplained car accidents, or sudden infant death syndrome) is also useful in evaluating young athletes since most conditions causing SCD during exercise in this group are congenital or inherited.
The evaluation of both symptomatic and asymptomatic athletes should include a thorough physical examination. Vital signs are usually notable for training bradycardia with a resting heart rate as low as 30 bpm in highly trained aerobic athletes. Asymptomatic adolescent athletes with heart rates in this range can participate without further evaluation. Athletes may also have an S3 and S4 gallop. Athletes frequently have classical flow murmurs related to their slower heart rates and concomitant increased stroke volume. These functional murmurs typically are systolic and less than IV/VI in intensity. They are typically present supine because of enhanced venous return in this position and absent with the athlete upright; they have no diastolic component and are associated with a normal physiologic split of the second heart sound. Because HCM is the most frequent cause of SCD in young athletes, auscultation during the Valsalva maneuver or after arising from the squatting position, either of which should decrease cardiac dimensions and increase the murmur of HCM, is useful.
Syncope is a common problem among athletes and a frequent reason for referral to a cardiologist. Syncopal events are significant if judged to be not neurocardiogenic (vasovagal) and if they occur during exercise. Postexertional syncope is a common phenomenon in athletes. It is usually benign and does not require further workup. Under normal circumstances, exercise increases cardiac output and decreases peripheral vascular resistance due to vasodilation. Syncope after exercise can occur because the increases in cardiac output and heart rate decrease more rapidly than does the peripheral vasodilation. The net effect when the individual stops exercising is an increase in vasodilation without the compensatory increase in heart rate and cardiac output, thus explaining postexertional syncope. In contrast, syncope during exercise usually suggests a cardiac origin, such as anomalous coronary artery anatomy or cardiac arrhythmias.
The American Heart Association (AHA) position on screening athletes before competition recommends a 12-point evaluation (Table 36–1). The historical elements are important, but young athletes often respond positively to many of these queries, again highlighting the importance of separating the evaluation of athletes with abnormalities found on screening from those presenting with symptoms.
Table 36–1. The 12-Element American Heart Association Recommendations for Preparticipation Cardiovascular Screening of Competitive Athletes ||Download (.pdf)
Table 36–1. The 12-Element American Heart Association Recommendations for Preparticipation Cardiovascular Screening of Competitive Athletes
1. Exertional chest pain/discomfort
2. Unexplained syncope/near-syncope†
3. Excessive exertional and unexplained dyspnea/fatigue, associated with exercise
4. Prior recognition of a heart murmur
5. Elevated systemic blood pressure
6. Premature death (sudden and unexpected, or otherwise) before age 50 years due to heart disease, in ≥1 relative
7. Disability from heart disease in a close relative < 50 years of age
8. Specific knowledge of certain cardiac conditions in family members: hypertrophic or dilated cardiomyopathy, long-OT syndrome or other ion channelopathies, Marfan syndrome, or clinically important arrhythmias
9. Heart murmur‡
10. Femoral pulses to exclude aortic coarctation
11. Physical stigmata of Marfan syndrome
12. Brachial artery blood pressure (sitting position)§
Many clinical and electrocardiographic (ECG) findings of concern in the general population are normal for athletes. The accuracy of the ECG interpretation is particularly difficult in young athletes due to ECG evolutionary changes that are related to age. Furthermore, there are inconsistencies in the definitions of ECG abnormalities and definite criteria for the diagnosis of several diseases. While the routine use of ECG for preparticipation screening remains controversial in young adults, its use remains a cornerstone of any cardiac evaluation in athletes with cardiac complaints. It is recommended as part of a routine evaluation for all masters athletes > 40 years of age since it occasionally identifies a prior MI.
Sinus bradycardia as low as 30 bpm, sinus arrhythmia, prolonged PR interval up to 300 ms, sinoatrial block, junction rhythms, and Wenckebach phenomenon are common in athletes due to a high resting parasympathetic tone and should not prompt further workup if the athlete is asymptomatic and has good exercise capacity and the abnormalities disappear during exercise.
QRS axis varies with age, but in athletes, mild right or left axis deviations should not trigger further evaluation unless there is history of pulmonary disease or systemic hypertension. An acceptable rage is between –30 and +115 degrees.
Incomplete right bundle branch block is extremely common in athletes. In contrast, complete block of either bundle, even in asymptomatic athletes, should prompt further investigation. Increased QRS amplitude is present in up to 80% of the athletes, but if the increased voltage is not accompanied by axis changes, repolarization changes, atrial abnormalities, or increased QRS width, it does not warrant further evaluation.
Small q waves may be present in athletes. The ECG in patients with HCM may also show q waves, but these “septal q's” are often seen in the inferior and/or lateral leads and suggest HCM if they are > 3 mm in depth and/or > 40 ms duration in at least two leads. Athletes with pathologic Q waves should be referred for further evaluation to exclude HCM (Table 36–2).
Table 36–2. Electrocardiogram Abnormalities that Require Further Evaluation ||Download (.pdf)
Table 36–2. Electrocardiogram Abnormalities that Require Further Evaluation
|Any QRS >120 ms|
|QRS axis deviation|
More leftward than −30°
More rightward than 115°
>470 ms in males
>480 ms in females
<340 ms in any athlete
|Brugada pattern||Presence of Type 1 pattern: coved ST segment in V1 and V2 gradually descending into inverted T wave|
|Pre-Excitation||Delta wave and PR interval <120 ms|
|Ventricular extrasystoles, heart block, and supraventricular arrhythmia||Atrial fibrillation/flutter, supraventricular tachycardia, complete heart block or ≥2 PVCs in one 12 lead ECG|
Early repolarization in V3–V6 with an elevated J point and peaked upright T waves is common in athletes and especially in those of African descent. The repolarization pattern may also include a domed ST segment followed by a biphasic or inverted T wave. These benign repolarization changes must be distinguished from the Brugada ECG pattern commonly present in leads V1–V2.
Other Noninvasive Cardiovascular Evaluations
ECG and echocardiography are indicated when clinical, historical, or physical findings suggest the possibility of structural heart disease (valvular disease, HCM, arrhythmogenic right ventricular cardiomyopathy, or prior MI). Tilt table testing is often positive in athletes because of their resting bradycardia and large venous capacitance and thus should not be used or should be used cautiously in athletes to evaluate lightheadedness, syncope, or presyncope.
Echocardiography in highly trained endurance athletes may show evidence of four-chamber cardiac enlargement. Left ventricular end-diastolic dimensions can exceed 60 mm in 15% of athletes. Left ventricular wall thickness can occasionally exceed the upper normal limit of 12 mm. Values of 13–15 mm may be seen in normal athletes, although marked enlargement of > 16 mm is unusual, and the ratio of the septal to posterior wall thickness does not exceed 1.2. The left ventricular cavity in HCM typically has asymmetric wall thickening, although symmetric wall enlargement may occur and the cavity dimensions are usually small and < 45 mm. In contrast, the athlete's heart typically has symmetric mild increases in left ventricular wall thickness and an increase in left ventricular chamber size of 55 mm or greater.
Left atrial enlargement in athletes is also common, and anterior-posterior diameters > 40 mm, the upper limit of normal, exist in 20% of high-performance athletes. This increased atrial size may contribute to the observation that atrial fibrillation is more common in older athletes than in age-matched nonathletes.
Left ventricular diastolic function measured by tissue Doppler is normal in athletes despite the hypertrophy, and normal diastolic function can help distinguish the athlete's heart from pathologic hypertrophy. The systolic anterior motion (SAM) of the mitral valve and mitral leaflet elongation can help with the diagnosis of HCM. These changes could happen in HCM even when the walls are not severely thickened. Stress echocardiography could provoke SAM and can provide more information than at rest.
Cardiac MRI can also help distinguish athlete's heart from HCM. A left ventricular diastolic wall thickness–to–cavity volume ratio of < 0.15 mm/m2/mL is useful in diagnosing athlete's heart. In HCM, intravenous gadolinium used in contrast-enhanced MRI is taken up by areas of myocardium with extra expanded cellular space indicating areas of fibrosis and scarring, also referred to as “late gadolinium enhancement” (LGE). LGE is not typical of the athlete's heart, especially in young athletes, but has been observed in older athletes with a history of life-long, intense exercise training.
Finally, detraining is another approach that could help to distinguish the athlete's heart from HCM. Three months of detraining should be sufficient to reverse the left ventricular hypertrophy of the athlete's heart and to distinguish this condition from HCM, although some studies suggest 6 months may be required. A decrease of > 2 mm in left ventricular wall thickness with detraining relative to peak training is more consistent with athlete's heart since patients with HCM should not demonstrate a change with deconditioning.
Corrado D, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur Heart J
Petersen SE, et al. Differentiation of athlete's heart from pathological forms of cardiac hypertrophy by means of geometric indices derived from cardiovascular magnetic resonance. J Cardiovasc Magnetic Res
Scharhag J, et al. Right and left ventricular mass and function in male endurance athletes and untrained individuals determined by magnetic resonance imaging. J Am Coll Cardiol
Uberoi A, et al. Interpretation of the electrocardiogram of young athletes. Circulation