Park's Pediatric Cardiology for Practitioners, 6th Ed.

Athletes with Cardiac Problems

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.

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.

TABLE 34-1



Proportion of all Causes (%)

Hypertrophic cardiomyopathy


Coronary artery anomalies


Possible hypertrophic cardiomyopathy




Arrythmogenic right ventricular cardiomyopathy


Ion channel disease


Mitral valve prolapse


Bridged left anterior descending coronary artery


Atherosclerotic coronary artery disease


Aortic rupture


Aortic stenosis


Dilated cardiomyopathy


Wolff-Parkinson-White syndrome




 Findings suggestive but not diagnostic of hypertrophic cardiomyopathy.

From Balady GJ and Ades PA. Exercise and Sports Cardiology, IN Braunwald’s Heart Disease. Eds, Robert O. Bonow, Douglas L. Mann, Douglas P. Zipes, and Peter Libby, ed9, Saunders, Philadelphia, 2012.

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.

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.

BOX 34-1 American Heart Association Consensus Panel Recommendations for Preparticipation Athlete Screening

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)

10. Femoral arterial pulses (to exclude coarctation of the aorta)

11. Stigmata of Marfan syndrome

12. Brachial blood pressure measurement (sitting)

 In particular, to identify heart murmur consistent with dynamic obstruction to the left ventricular outflow tract.

Maron BJ, Thompson PD, Puffer JC, et al: Cardiovascular preparticipation screening of competitive athletes. Circulation 94:850-856, 1996.

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.


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.


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.


FIGURE 34-1 Classification of sports. Max O2, maximal oxygen uptake; MVC, maximal voluntary contraction; Danger of bodily collision; Increased risk if syncope occurs. Modified from Mitchel JH, Haskel W, Snell P, Van Camp SP: Task Force 8: Classification of sports. J Am Coll Cardiol 45:1364-1367, 2005.

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.

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.

Detailed participation recommendations for specific left-to-right shunt lesion and obstructive lesion are presented in Table 34-2.

Cyanotic Congenital Heart Defects

In patients with arterial oxygen desaturation from cyanotic CHD, moderate to severe restriction in sports participation is recommended.

1. Patients with cyanotic CHDs, which are unoperated or for which palliative procedures have been done, can only participate in low-intensity competitive sports, such as class IA.

2. Most patients with cyanotic CHDs for which surgical repair have been done can only participate in low-intensity sports.

3. Patients who have received an excellent result from the surgical repair of tetralogy of Fallot or arterial switch operation for transposition of the great arteries may participate in all competitive sports.

Detailed recommendations are provided for specific cyanotic heart defects in Table 34-3.

Coronary Artery Abnormalities

For most patients with congenital abnormalities of the coronary arteries or after Kawasaki’s disease, moderate to severe restriction in sports participation is recommended. Children who had no coronary artery involvement during the acute phase of Kawasaki’s disease may participate in all sports 6 to 8 weeks after the illness. Stress testing is often required before prescribing participation eligibility. Detailed participation recommendations for specific conditions with coronary artery abnormalities are presented in Table 34-4.

Valvular Heart Diseases

The severity of the valvular lesion determines the eligibility of participation in competitive sports.

1. With mild valvular lesions (e.g., mitral stenosis, mitral regurgitation, atrial stenosis, and atrial regurgitation), participation in all competitive sports is allowed.

2. With moderate valvular lesions, participation is limited to low to moderate-intensity sports.

3. With severe obstructive lesions such as atrial stenosis, participation in competitive sports is not permitted.

4. With valvular lesions that produce significant PH, no participation in competitive sports is permitted.

5. For patients with prosthetic valve and taking warfarin, no sports involving the risk of bodily contact is allowed.

Detailed participation recommendations for specific valvular heart disease are presented in Table 34-5.

TABLE 34-2



AS, Aortic (valve) stenosis; ASD, atrial septal defect; AV, atrioventricular; COA, coarctation of the aorta; EST, exercise stress test; LV, left ventricle; MR, mitral regurgitation; PA, pulmonary artery; PDA, patent ductus arteriosus; PH, pulmonary hypertension; PR, pulmonary regurgitation; PS, pulmonary (valve) stenosis; RV, right ventricle; SP, systolic pressure; SVT, supraventricular arrhythmia; VSD, ventricular septal defect.

Adapted from Graham TP, Driscoll DJ, Gerosny WM, et al: 36th Bethesda Conference: Eligibility recommendations for competitive athletes with cardiovascular abnormalities. Task Force 2: Congenital heart disease. J Am Coll Cardiol 45:1326-1333, 2005.

TABLE 34-3



AV, Atrioventricular; BP, blood pressure; CHD, congenital heart defects; ECG, electrocardiogram; EF, ejection fraction; EST, exercise stress test; LV, left ventricle; PR, pulmonary regurgitation; RV, right ventricle; SP, systolic pressure; SVT, supraventricular tachycardia; TGA,transposition of the great arteries; TOF, tetralogy of Fallot; TR, tricuspid regurgitation; VSD, ventricular septal defect.

TABLE 34-4



CA, Coronary artery; EF, ejection fraction; EST, exercise stress test; LV, left ventricle; MI, myocardial infarction.

Adapted from Graham TP, Driscoll DJ, Gerosny WM, et al: 36th Bethesda Conference: Eligibility recommendations for competitive athletes with cardiovascular abnormalities. Task Force 2: Congenital heart disease. J Am Coll Cardiol 45:1326-1333, 2005.

TABLE 34-5




AF, Atrial fibrillation; AR, aortic regurgitation; AS, aortic stenosis; BAV, bicuspid aortic valve; EST, exercise stress test; LV, left ventricle or ventricular; LVE, left ventricular enlargement; MR, mitral regurgitation; MS, mitral stenosis; PA, pulmonary artery; PH, pulmonary hypertension; SP,systolic pressure.

Adapted from Graham TP, Driscoll DJ, Gerosny WM, et al: 36th Bethesda Conference: Eligibility recommendations for competitive athletes with cardiovascular abnormalities. Task Force 2: Congenital heart disease. J Am Coll Cardiol 45:1326-1333, 2005.

Cardiomyopathy, Pericarditis, and Other Myocardial Diseases

Detailed participation recommendations for specific disorders of the myocardium, pericardium, and other related cardiovascular diseases are presented in Table 34-6.

1. Athletes who have either confirmed or probable diagnosis of HCM or arrhythmogenic RV dysplasia are excluded from most competitive sports, with the possible exception of class IA sports.

2. Athletes with myocarditis or pericarditis of any etiology should be excluded from all competitive sports during the acute phase. After complete recovery from these illnesses, they may gradually participate in sports.

TABLE 34-6



EF, Ejection fraction; EST, exercise stress testing; FH, family history; HCM, hypertrophic cardiomyopathy; ICD, implantable cardioverter-defibrillator; LV, left ventricle; LVOT, left ventricular outflow tract; MI, myocardial infarction; MR, mitral regurgitation; MVP, mitral valve prolapse; RV,right ventricle; SD, standard deviation; SVT, supraventricular tachycardia; VT, ventricular tachycardia.

3. Athletes with Marfan’s syndrome can participate only in class IA or IB sports.

4. Athletes with MVP who have any symptoms or abnormalities in ECG, LV function, or arrhythmias are permitted to participate only in low-intensity sports.

5. Athletes with myocardial bridging without ischemia at rest and during exercise may participate in all sports.

Detailed participation recommendations for specific valvular heart disease are presented in Table 34-6.

Cardiac Arrhythmias and Sports

Although sudden unexpected death in young athletes is rare, a significant portion of these deaths occurs in relation to exercise, and it is probably related to cardiac arrhythmias. Cardiac arrhythmias occurring while playing sports, however, manifest more often with syncope or near syncope than sudden death. A cardiac arrhythmia should be considered a possible cause of syncope, particularly when it occurs during or immediately after exercise, and a thorough evaluation is required. Although syncope may signal the presence of a serious cardiac problem, it may also be due to a benign mechanism such as vasovagal syncope, which is a common finding in highly trained athletes. However, the diagnosis of such a benign mechanism should not be made without first excluding underlying structural disease or electrical disorders (see Chapter 31 for further description).

Arrhythmias may be associated with a variety of structural heart disease. In the absence of identifiable structural abnormalities of the heart, it may be due to primary electrical disorders, such as an supraventricular tachycardia (SVT) associated with WPW preexcitation or ventricular tachycardia (VT) secondary to long QT syndrome. A number of stimulant-containing drinks that are popular among young athletes can trigger certain arrhythmias. Abuse with drugs such as cocaine or ephedra can precipitate life-threatening arrhythmias.

Young athletes with an arrhythmia who are permitted to engage in athletic activities should be reevaluated at 6- to 12-month intervals to determine whether the training process affected the arrhythmia. Follow-up evaluation should be done to check on compliance of antiarrhythmic drugs. Use of certain drugs, such as β-adrenergic blocking agents, is banned in some competitive sports, such as archery and riflery, in which athletes benefit from slow heart rates.

Diagnostic Workup

In general, all athletes with possible cardiac arrhythmias being considered for athletic activity should have a careful history and cardiac examination, a 12-lead ECG, and an echocardiogram. In most cases, a 24-hour Holter recording and exercise stress testing (EST) are also indicated.


The screening questionnaires recommended by the AHA (see Box 34-1) are useful starting points in eligibility evaluation. However, review of athlete’s medical history and careful cardiac examination are often negative. The following are some important findings from the history, which should prompt one to consider the possibility of arrhythmia in an athlete.

• History of syncope, near syncope, dizziness or lightheadedness, seizures, palpitation, chest pain, or pallor

• History of known heart disease (congenital or acquired) and medications or surgery for it

• Family history of arrhythmias or sudden death

Certain medications or drugs of abuse (e.g., tricyclic antidepressant, inhalants, or cocaine)

Physical Examination

Physical examination may reveal an irregularity of the heart rate, but a regular heart rate on examination does not rule out arrhythmias.

Recording of the Electrocardiogram

Normal ambulatory ECG monitoring findings do not provide absolute safety or absence of arrhythmias because arrhythmias are commonly evanescent, often disappearing unpredictably for long periods of time in some cases.

Although most high school and college athletes are not fully trained athletes, it is important to understand the range of normal heart rate and rhythm for trained athletes recorded on 24-hour Holter ECG recordings.

1. Heart rates of 25 beats/min and sinus pauses for longer than 2 seconds may be found.

2. Mobitz type I second-degree AV block and single uniform PVCs each may occur in about 40% of trained athletes.

3. Complex ventricular arrhythmias (including multiform PVCs, couplets, and nonsustained VT) are rarely present without adverse clinical events (Marion et al, 2006).

Exercise Stress Test

An EST is often needed to document the appearance or disappearance of arrhythmias with exercise. Arrhythmias that disappear or reduce in their frequency during exercise are usually benign. Those that appear with exercise or those that increase their frequency are more significant. EST may be indicated to document the efficacy of medical treatment or ablation of arrhythmias.

Eligibility Recommendations for Cardiac Arrhythmias

Detailed participation recommendations are provided in Table 34-7 for arrhythmias based on the 36th Bethesda Conference (Zipes et al, 2005). The following are general statements regarding participation eligibility for athletes with cardiac arrhythmias.

1. The presence of a symptomatic cardiac arrhythmia requires exclusion from physical activity until this problem can be adequately evaluated and controlled by a cardiologist.

2. Sinus arrhythmias and premature atrial contractions (PACs) are benign if the heart is structurally normal; these individuals can participate in all competitive sports.

3. Asymptomatic athletes with atrial flutter or fibrillation and structurally normal hearts may participate in competitive sports when the arrhythmias are fully under control either by medication or ablation.

4. Athletes with SVT and structurally normal hearts may participate in all competitive sports when the SVT is in full control with medication or after successful ablation.

5. For athletes with structurally normal hearts who have PVCs or more complex arrhythmias, an EST is a useful technique. If the PVCs disappear when the heart rate reaches 140 to 150 beats/min, the PVCs are benign, and full participation may be permitted.

6. Athletes with VT who had successful treatment to prevent recurrence of the arrhythmias may participate in sports, provided that VT is not inducible by EST or electrophysiologic study (EPS).

7. Asymptomatic adult athletes with WPW preexcitation with no history of SVT may participate in all competitive sports, but children with the same diagnosis require in-depth evaluation.

8. Athletes with long QT syndrome can only participate in class IA sports.

9. Athletes who had a successful ablation for any of the arrhythmias may participate in all competitive sports after verification of the success by appropriate tests.

Eligibility Recommendations for Atrioventricular Block and Intraventricular Blocks

Detailed participation recommendations are provided in Table 34-8 for AV and intraventricular blocks. The following are general statements regarding participation eligibility for athletes with these abnormalities.

1. Athletes with first-degree AV block or Mobitz type 1 second-degree AV block can participate in all sports provided the block does not worsen with exercise.

TABLE 34-7





AF, Atrial fibrillation; AVJT, atrioventricular junctional tachycardia; EPS, electrophysiologic study; EST, exercise stress test; HD, heart disease; HR, heart rate; ICD, implantable cardioverter-defibrillator; LQTS, long QT syndrome; VT, ventricular tachycardia; WPW, Wolff-Parkinson-White.

Adapted from Zipes DP, Ackerman MJ, Estes MAM, et al: Task Force 7: Arrhythmias, 36th Bethesda Conference: Eligibility Recommendations for Competitive Athletes with Cardiovascular Abnormalities. J Am Coll Cardiol 45:1354-1363, 2005.

TABLE 34-8



AF, Atrial fibrillation; AV, atrioventricular; EPS, electrophysiologic study; HD, heart disease; HR, heart rate; LBBB, left bundle branch block; PVC, premature ventricular contraction; RBBB, right bundle branch block; VT, ventricular tachycardia; WPW, Wolff-Parkinson-White.

Adapted from Zipes DP, Ackerman MJ, Estes MAM, et al: Task Force 7: Arrhythmias, 36th Bethesda Conference: Eligibility Recommendations for Competitive Athletes with Cardiovascular Abnormalities, J Am Coll Cardiol 45:1354-1363, 2005.

2. Athletes with Mobitz type 2 second-degree AV block or complete heart block usually require pacemaker implantation before being permitted to participate in any sports.

3. Athletes who have a pacemaker implanted and those who are on anticoagulation (usually for atrial flutter or fibrillation) should not be permitted to engage in activities with danger of bodily collision. Participation in class IA sports is usually permitted.

4. Asymptomatic athletes with RBBB or left bundle branch block (LBBB) who do not have ventricular arrhythmias or develop AV block during exercise can participate in all sports. However, patients with LBBB who have an abnormal prolongation of HV interval on EPS should receive pacemakers.

Athletes with Systemic Hypertension

Reports of cerebrovascular accident during maximal exercise have raised concerns that the rise in BP accompanying strenuous activity may cause harm. However, changes in BP depend on the type of exercise in which they are engaged. For example:

1. Dynamic exercise causes a substantial increase in systolic pressure, heart rate, stroke volume, and cardiac output. A moderate increase in mean arterial pressure and a decrease in diastolic pressure occur, with a marked decrease in total peripheral resistance.

2. Static exercise, in contrast, causes a small increase in 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.

Correct diagnosis of hypertension is very important before recommending restrictions. On each occasion, two or more BP readings should be taken, and when the readings vary by greater than 5 mm Hg, additional readings should be taken until two consecutive readings are close. When the initial office BP readings are high, an out-of-office measurement of BP may be needed to exclude “white-coat” hypertension. The diagnosis of hypertension should be made only after several elevated BP readings are obtained on separate occasions. When the diagnosis of hypertension is confirmed, an evaluation including a history, thorough physical examination, and appropriate laboratory testing should be performed (see Chapter 28).

Task Force 5: Systemic Hypertension, 36th Bethesda Conference on Eligibility Recommendations for competitive sports has recommended the following (Kaplan et al, 2005).

1. Athletes with prehypertension (BP levels between the 90th and 95th percentiles or 120–139/80–89 mm Hg):

a. May participate in physical activity but should be encouraged to modify their lifestyles

b. If prehypertension persists, echocardiography studies are done to see if there is LVH (beyond that seen with “athletes’ heart”).

c. If LVH is present, athletic participation is limited until the BP is normalized by appropriate drug therapy.

2. Athletes with stage 1 hypertension (BP levels between the 95th and 99th percentiles or 140–159/90–99 mm Hg):

a. May participate in any competitive sports in the absence of target organ damage, including LVH or concomitant heart disease. However, hypertension should be checked every 2 to 4 months (or more frequently) to monitor the impact of exercise.

b. If LVH is present, athletic participation is limited until the BP is normalized by appropriate drug therapy.

3. Athletes with stage 2 (severe) hypertension (BP level ≥5 mm Hg above the 99th percentile or >160/100 mm Hg): Even in the absence of target organ damage (e.g., LVH), athletic participation should be restricted, particularly from high-static sports (class IIIA, IIIB, and IIIC), until the hypertension is controlled by either lifestyle modification or drug therapy.

All drugs being taken must be registered with appropriate governing bodies to obtain a therapeutic exemption. When hypertension coexists with another cardiovascular disease, eligibility for participation in competitive sports is usually based on the type and severity of the associated condition.

With respect to the treatment of hypertension, beta-blockers are not banned for most sports, including football and basketball, but they are banned for riflery or archery. However, athletes with essential hypertension do not tolerate beta-blockers well because they reduce their maximum performance. Therefore, one should avoid treating hypertensive athletes with beta-blockers. Instead, angiotensin-converting enzyme (ACE) inhibitors or calcium channel blockers are preferred. One should be aware of the potential teratogenic effects of ACE inhibitors if they are taken during pregnancy.