Competitive athletes are those who participate in an organized team or individual sport that requires regular competition against others. This definition is most easily applied to high school, college, and professional sports. Athletic competitions substantially increase the sympathetic drive, and the resulting increase in catecholamine levels increases blood pressure (BP), heart rate, and myocardial contractility, thereby increasing myocardial oxygen demand. The increase in sympathetic tone can cause arrhythmias and may aggravate existing myocardial ischemia. An athlete with a cardiac problem is at an increased risk of developing serious morbidity and even sudden death during athletic competition compared with nonathletes with similar cardiac problems.
Almost all U.S. states require some type of preparticipation screening of participants in organized sports. The most important reason to screen for heart disease is to prevent sudden unexpected death. Heart disease may also lead to sudden incapacity, which may result in injuries, and preexisting heart disease may be exacerbated by exercise. There are also legal and insurance requirements.
Most physicians encounter this issue in association with high school and college sports; therefore, physicians should be aware of cardiac conditions that may cause problems and have the knowledge base required to accomplish a physician’s role in school sports clearance. In addition, physicians should have a general understanding of the eligibility guidelines and the participation eligibility for patients with specific cardiovascular conditions.
The recommendations presented are mostly from the 36th Bethesda conference published in 2005 (36th Bethesda Conference, 2005 ). The following major areas will be presented in a table format for easy access of information.
- 1.
Causes of sudden expected death
- 2.
The American Heart Association’s (AHA’s) 12-point screening procedure, including the responsibilities of the general physician
- 3.
Classification of sports according to the type and intensity to help physicians select allowable types of sports
- 4.
Participation eligibility for athletes with different types of cardiovascular problems, presented in a table form for easy access of information
- 5.
Guidelines for athletes with hypertension
Sudden Unexpected Death in Young Athletes
Sudden unexpected death in young athletes is estimated to occur in about 1 per 200,000 high school sports participants per academic year. Most cases of unexpected sudden death in athletes are caused by unrecognized cardiovascular disease. Although rare, when a sudden unexpected death of an athlete due to a cardiac condition occurs, the public becomes disbelieving, suspicious, and even angry. Sometimes, these feelings have been directed at the physicians involved. It is, therefore, important for primary care physicians to have a good understanding of cardiac conditions that can result in sudden death in order to reduce that possibility and to know his or her responsibilities in recommending sports clearance.
Among a variety of congenital or acquired heart diseases that can cause sudden death during athletic competition, hypertrophic cardiomyopathy (HCM) and coronary artery anomalies or diseases are the two most important groups, accounting for nearly 2/3 of the cases. Table 34-1 shows previously implicated diseases for sudden cardiac death, which is derived from 690 cases of cardiovascular causes of sudden death (Maron et al, 2009).
- 1.
Hypertrophic cardiomyopathy. The single most common cardiovascular abnormality among the causes of sudden death in young athletes is HCM (36%) and its variants (8%), accounting for nearly half of the cases (see Table 34-1 ).
- 2.
Congenital anomalies and acquired diseases of the coronary arteries are the next important group of causes of sudden death, accounting nearly 25%, including congenital anomalies of the coronary artery and acquired coronary artery diseases such as atherosclerotic coronary artery disease or coronary artery stenosis resulting from Kawasaki disease.
- 3.
Myocarditis. Sudden cardiac death has been reported at rest and during exercise with both acute and chronic myocarditis (up to 6% of sudden death) by way of ventricular arrhythmias.
- 4.
Cardiac arrhythmias (from long QT syndrome, Wolff-Parkinson-White [WPW] syndrome, sinus node dysfunction, arrhythmogenic right ventricular dysplasia [ARVD]) are rare causes of sudden death.
- 5.
Other rare causes of sudden death in athletes include severe obstructive lesions (e.g., aortic stenosis, pulmonary stenosis), Marfan’s syndrome (from ruptured aortic aneurysm), mitral valve prolapse (MVP), dilated cardiomyopathy, primary pulmonary hypertension (PH), unexpected blow to the chest (by such objects as baseball or hockey puck, termed commotion cordis ), sarcoidosis, and sickle cell trait.
| Cause | Proportion of all Causes (%) |
|---|---|
| Hypertrophic cardiomyopathy | 36 |
| Coronary artery anomalies | 17 |
| Possible hypertrophic cardiomyopathy ∗ | 8 |
| Myocarditis | 6 |
| Arrythmogenic right ventricular cardiomyopathy | 4 |
| Ion channel disease | 4 |
| Mitral valve prolapse | 3 |
| Bridged left anterior descending coronary artery | 3 |
| Atherosclerotic coronary artery disease | 3 |
| Aortic rupture | 3 |
| Aortic stenosis | 2 |
| Dilated cardiomyopathy | 2 |
| Wolff-Parkinson-White syndrome | 2 |
| Others | 5 |
∗ Findings suggestive but not diagnostic of hypertrophic cardiomyopathy.
Some patients die while they are sedentary or during mild exertion, but many collapse during or just after vigorous physical activity. On occasion, athletes may die suddenly without evidence of structural heart disease on autopsy. In such instances, it may be due to a noncardiac cause such as drug abuse.
Preparticipation Screening
The objective of preparticipation screening is to detect “silent” cardiovascular disease that can cause sudden cardiac death. There are, however, no cost-effective practical guidelines for the screening that have been proved to be effective in identifying the potential candidates for sudden death at this time. Prospective cardiovascular screening of a large athletic population is impractical. The total number of competitive athletes in the United States may be in the range of 8 to 10 million. Even with the use of specialized tools available to cardiologists, complete prevention of such death is nearly impossible, given the rarity of some of the causes of sudden expected death. Consequently, medical clearance for sports does not necessarily imply the absence of cardiovascular disease or complete protection from sudden death.
Customary screening for U.S. high school and college athletes is confined to history taking and physical examination, which is known to be limited in its power to consistently identify important cardiovascular abnormalities. The AHA has recommended its 12-point screening procedure as shown in Box 34-1 . As can be seen, eight of the 12 points are related to the history, and the remaining four are physical examination. Although the European Society of Cardiology (ESC) has recommended electrocardiography (ECG) with each evaluation, the AHA did not recommend other testing on a routine basis. The ESC believes that ECGs will detect most cases of HCM. Although that may be true, the AHA believes that the cost of doing ECGs versus the yield is prohibitive and that the cost of evaluating false-positive results is too great to make this practice cost effective. Currently, there are no comparative data using the two approaches, and there are few data to support that either approach significantly reduces the risk of sudden athletic death.
Family History
- 1.
Premature sudden cardiac death
- 2.
Heart disease in surviving relative younger than 50 years old
Personal History
- 3.
Heart murmur
- 4.
Systemic hypertension
- 5.
Fatigue
- 6.
Syncope or near syncope
- 7.
Excessive or unexplained exertional dyspnea
- 8.
Exertional chest pain
Physical Examination
- 9.
Heart murmur (supine or standing ∗
∗ In particular, to identify heart murmur consistent with dynamic obstruction to the left ventricular outflow tract.
)
- 10.
Femoral arterial pulses (to exclude coarctation of the aorta)
- 11.
Stigmata of Marfan syndrome
- 12.
Brachial blood pressure measurement (sitting)
History and Physical Examination
Although simple history and physical examination can raise the suspicion of cardiovascular disease in some at-risk athletes, they do not have sufficient power to guarantee detection of many critical cardiovascular abnormalities. However, the AHA’s screening method has the capability of raising the clinical suspicion of several cardiovascular abnormalities.
- 1.
History of syncope, chest pain, dyspnea, and fatigue, particularly when associated with exertion, is important.
- 2.
Family history of premature cardiac death, sudden unexpected death, and heritable diseases should be noted.
- 3.
Physical examination detects significant aortic or pulmonary stenosis or coarctation of the aorta.
- 4.
Identification of HCM by the standard history and physical examination is unreliable because (a) most patients with HCM have the nonobstructive form of the disease (and thus no audible heart murmur), and (b) most athletes with HCM do not experience exertional syncope or have a family history of the disease or premature sudden death.
If cardiovascular abnormalities are suspected by the AHA’s screening procedure, a physician should request specialty consultation or order additional testing. The athlete should be temporarily withdrawn from activities until the issue can be resolved. The utility of ECG and an echocardiographic study are briefly outlined below, although they are not routinely recommended by the AHA.
Electrocardiography
The 12-lead ECG is a practical and cost-effective strategic alternative to routine echocardiography.
- 1.
The ECG findings are abnormal in up to 75% to 95% of patients with HCM. Common ECG abnormalities in HCM include left ventricular hypertrophy (LVH), ST-T changes, and abnormally deep Q waves (owing to septal hypertrophy) with diminished or absent R waves in the left precordial leads. Occasionally, “giant” negative T waves are seen in the left precordial leads. Cardiac arrhythmias and first-degree atrioventricular (AV) block may be seen occasionally.
- 2.
Coronary artery abnormalities may show ST-T wave abnormalities or abnormal Q waves.
- 3.
It will also identify other abnormalities such as the long QT syndrome (prolonged QTc interval >0.46 sec), Brugada syndrome (right bundle branch block [RBBB] with ST-segment elevation), and other inherited syndromes associated with ventricular arrhythmias.
- 4.
It may also raise suspicion of myocarditis (premature ventricular contractions [PVCs], ST-T changes), or arrhythmogenic right ventricular (RV) cardiomyopathy (by T-wave inversion in leads V1 through V3, tall P waves, decreased RV potentials).
- 5.
However, abnormal ECG findings are seen in about 40% of trained athletes, and this may be the source of confusion. ECG abnormalities seen in trained athletes include increased R- or S-wave voltages, Q-wave and repolarization abnormalities, and frequent or complex ventricular tachyarrhythmias on Holter ECG monitors.
- 6.
On the other hand, normal ECG does not necessarily rule out significant cardiac abnormalities.
Echocardiography
Echocardiographic study is the principal diagnostic imaging modality for clinical identification of HCM and other cardiac abnormalities.
- 1.
HCM can be reliably diagnosed by two-dimensional echocardiography. Diastolic left ventricular (LV) wall thickness of 15 mm or greater (or on occasion, 13 or 14 mm), usually with LV dimension of less than 45 mm, is accepted for the clinical diagnosis of HCM in adults. For children, z-score of 2 or more relative to body surface area is theoretically compatible with the diagnosis.
The hearts of some highly trained athletes may show hypertrophy of the LV wall, making the differentiation between the physiologic hypertrophy and HCM difficult. An LV wall thickness of 13 mm or greater is very uncommon in highly trained athletes and is always associated with an enlarged LV cavity (with LV diastolic dimension >54 mm, ranging from 55–63 mm). Therefore, athletes with LV wall thickness greater than 16 mm and a nondilated LV cavity are likely to have HCM (Pelliccia et al, 1991) .
- 2.
Echocardiography is also expected to detect other congenital structural abnormalities, such as valvular heart disease (aortic stenosis, pulmonary stenosis), Marfan’s syndrome (aortic root dilatation, MVP), myocarditis, and dilated cardiomyopathy (LV dysfunction or enlargement).
- 3.
Definitive diagnosis of congenital coronary artery anomalies may not be accomplished by echo studies; it may require other tests such as computed tomography or coronary angiography.
Although the primary obligation of a physician to the athletes is their best medical interest, the physician must avoid unnecessary exclusion from sports. The physician should seek consultations from a specialist or order additional testing (e.g., ECG, echocardiography) to minimize unnecessary disqualification. The athlete should be temporarily withdrawn from activities until the issue can be resolved. After evaluation by a specialist, if the general physician and the specialist both agree that the patient’s condition requires disqualification, then they should not hesitate to disqualify the individual from participation. Such decisions, if based on a reasonable preparticipation evaluation, have generally been upheld in court cases. Also, there seems to be little liability risk if an asymptomatic condition is missed.
The physician should resist pressure from competing interest such as the athlete, the family, the coach, and administrative officials of the educational institution. The importance of the player to the team should be a secondary factor; it is the player’s safety that should be the primary factor in making recommendations. After a decision has been made, the physician should report only to the patient and his or her parents; the referring doctor; and in some cases, the institutional officials when an institution is paying for the medical evaluation.
Classification of Sports
If cardiovascular or other abnormalities are found when evaluating an individual, the next step is to estimate how much physical exercise can be safely tolerated. Depending on the cardiac condition, the athlete may be able to safely engage in less demanding athletic activities. This requires knowledge of the type of exercise the individual will be doing, how much static and dynamic exertion is required, and how vigorous the training program is.
For the purpose of making recommendations on athletes’ participation eligibility, Task Force 8 of the 36th Bethesda Conference ( Fig. 34-1 ) has presented the following classification of sports. Sports can be classified according to the type and intensity of exercise performed and with regard to the danger of bodily injury from collision as well as the consequences of syncope. Sports are divided into two broad types, dynamic and static, and each sport is categorized by the level of intensity (low, medium, or high). This should not be regarded as a rigid classification but rather a spectrum in which some athletes in the same sport could possibly deserve placement in different categories.
Dynamic (isotonic) exercise involves changes in muscle length and joint movement with rhythmic contractions that develop relatively small intramuscular force; static (isometric) exercise involves development of relatively large intramuscular force with little or no change in muscle length or joint movement. Most sports activities are a combination of static and dynamic exercises. The terms dynamic and static exercise characterize activity on the basis of the mechanical action of the muscles involved and are different from the terms aerobic and anaerobic exercise. The latter characterizes activity on the basis of the type of muscle metabolism.
Dynamic exercise causes a marked increase in oxygen consumption with a substantial increase in cardiac output, heart rate, stroke volume, and systolic BP and a decrease in diastolic pressure and systemic vascular resistance. Static exercise, in contrast, causes a small increase in oxygen consumption, cardiac output, and heart rate and no change in stroke volume. There is a marked increase in systolic, diastolic, and mean arterial pressures and no appreciable change in total peripheral resistance. Thus, whereas dynamic exercise primarily causes a volume load on the left ventricle, static exercise causes a pressure load.
Eligibility Determination of Athletes with Cardiovascular Diseases
For the purpose of eligibility recommendations for athletes with cardiovascular abnormalities, recommendations for each specific condition are presented in table format for easy access of information.
- 1.
Acyanotic congenital heart defects (CHDs)
- 2.
Cyanotic congenital heart defects
- 3.
Coronary artery anomalies
- 4.
Valvular heart disease
- 5.
Cardiomyopathy, pericarditis, and other select cardiovascular diseases
- 6.
Cardiac arrhythmias
- 7.
AV or intraventricular block
- 8.
Systemic hypertension
Most of the recommendations are excerpts from the 36th Bethesda Conference (2005). These recommendations apply to athletes in high school and college. For middle school and elementary school children, less strict restriction may apply because of less strenuous training and sports activities. However, the above guidelines are still useful in making final recommendations for this group of athletes as well.
It should be noted that beta-blockers that are used to treat certain heart conditions and arrhythmias are expressly banned in sports like riflery (class IA) and archery (class IIA) in which the athlete would benefit from a slow heart rate. Putting athletes on beta-blockers would risk their having a positive drug test result.
Acyanotic Congenital Heart Defects
The participation eligibility of athletes with acyanotic heart diseases (which include left-to-right shunt lesions and obstructive lesions) is importantly determined by the level of pulmonary artery (PA) systolic pressure and the status of LV systolic function. Note that pressure levels shown below are those obtained in the cardiac catheterization laboratory (i.e., peak-to-peak pressure gradient): Doppler-derived pressure gradients are higher than these (see Chapter 29 ).
- 1.
PA systolic pressure
- a.
When PA systolic pressure is 30 mm Hg or less (or Doppler-estimated PA systolic pressure is <36 to 40 mm Hg), full participation in all competitive sports is allowed.
- b.
When PA systolic pressure is greater than 30 mm Hg (or Doppler-estimated PA systolic pressure of >36 to 40 mm Hg), a full evaluation will determine limitations in participation eligibility. With mild PH, low-intensity sports (IA) are permitted. With pulmonary vascular obstructive disease (PVOD), no competitive sports are allowed.
- a.
- 2.
Left ventricular (LV) systolic function
- a.
When LV systolic function is normal (with ejection fraction [EF] ≥50%), full participation is allowed.
- b.
With mild LV dysfunction (EF 40%–50%), low-intensity static sports (class IA, IB, and IC) are allowed.
- c.
With moderate to severe LV dysfunction (EF <40%), no competitive sports are allowed.
- a.
Detailed participation recommendations for specific left-to-right shunt lesion and obstructive lesion are presented in Table 34-2 .
| Heart Defect | Clinical Status | Can Participate in |
|---|---|---|
| ASD, untreated | Small ASD with normal PA pressure | All competitive sports |
| Moderate to large ASD with mild PH | Class IA sports | |
| Large ASD with severe PH (cyanosis) | No competitive sports | |
| ASD, closed by surgery or device | Postclosure ASD in the absence of PH, symptomatic arrhythmias, or second- or third-degree AV block | All sports (3–6 mo after closure) |
| Athletes with PH, arrhythmias, or AV block | Determined by level of PH and Table 34-7 recommendations | |
| VSD, untreated | VSD with normal PA pressure | All competitive sports |
| Large VSD (without marked PH) requires surgery | All competitive sports (3–6 mo after surgical repair) | |
| VSD, closed | Asymptomatic, no or small residual defect, and no PH | All sports (3–6 mo after closure) |
| Symptomatic arrhythmias, or second- or third-degree AV block | See Table 34-7 recommendations | |
| Persistent severe PH | No competitive sports | |
| PDA | Small PDA | All competitive sports |
| Moderate to large PDA: requires surgery | All competitive sports (3–6 mo after surgical repair) | |
| Moderate or large PDA with severe PH and cyanosis | No competitive sports | |
| PDA, closed | Asymptomatic with no PH and no LV enlargement | All sports (after 3 mo) |
| Residual PH | Class IA or no competitive sports | |
| PS, untreated | Mild PS (peak Doppler gradient <40 mm Hg) and normal RV function | All competitive sports; annual reevaluation needed |
| Moderate PS (peak Doppler gradient, 40–60 mm Hg) and severe PS (peak gradient >60 mm Hg) | Class IA and IB until balloon valvuloplasty is performed | |
| PS, treated | No or mild residual PS and normal ventricular function | All competitive sports (2–4 wk after balloon or 3 mo after surgery) |
| Residual Doppler gradient >40 mm Hg | Class IA and IB | |
| Severe PR with marked RV enlargement | Class IA and IB | |
| AS, untreated | Mild AS (peak Doppler gradient <40 mm Hg), with normal ECG, normal EST, no symptoms, and no symptomatic arrhythmias | All competitive sports |
| Moderate AS (peak Doppler gradient, 40–70 mm Hg), asymptomatic, with mild or no LVH (echocardiography); no strain pattern on ECG; normal EST | Class IA, IB, and IIA | |
| Moderate AS with SVT or multiple or complex ventricular arrhythmias at rest or with exercise | Class IA and IB | |
| Severe AS (peak Doppler gradient >70 mm Hg) | No competitive sports | |
| AS, treated by surgery or balloon | Residual mild, moderate, or severe AS | Same as untreated AS |
| Moderate to severe AR | See Table 34-5 recommendations | |
| COA, untreated | Mild COA (no aortic root dilatation, normal EST, arm-to-leg SP gradient at rest <20 mm Hg, and arm SP <230 mm Hg with exercise) | All competitive sports |
| Arm-to-leg SP gradient >20 mm Hg or exercise-induced hypertension with arm SP >230 mm Hg | Only class IA until treated | |
| COA, treated by surgery or balloon | Arm-to-leg SP gradient <20 mm Hg at rest and normal arm SP during rest and exercise | All competitive sports 3 mo after repair |
| Significant aortic dilatation, wall thinning, or aneurysm formation | Class IA and IB |
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