Almost all states in the United States require some type of preparticipation screening of participants in organized sports. The major reason for this screening is to help prevent sudden unexpected death. Most physicians encounter this issue in association with high school and college sports, and therefore physicians should have a general understanding of the eligibility guidelines and the participation eligibility for patients with specific CV conditions. Athletic competitions substantially increase the sympathetic drive. The resulting increase in catecholamine levels increases blood pressure (BP), heart rate (HR), and myocardial contractility and increases oxygen demand. The increase in sympathetic tone can cause arrhythmias and may aggravate existing myocardial ischemia.
The recommendations presented are mostly from American Heart Association (AHA) and American College of Cardiology (ACC) Scientific Statement (2015) and some are from the 36th Bethesda conference (2005). The following areas are presented.
Causes of sudden unexpected death
AHA/ACC) 14-element screening procedure (of 2014)
Classification of sports according to the type and intensity to help physicians select allowable types of sports
Overview of participation eligibility for athletes with different types of CV problems
Guidelines for athletes with hypertension
I. Sudden Cardiac Death In Young Athletes
A. Statistics Of Sudden Unexpected Death
Sudden cardiac death (SCD) occurs in about 1 per 200,000 high school sports participants per academic year. It is far more common in boys than in girls. In the United States, football and basketball are the sports most frequently associated with SCD.
The two most important groups of heart disease that cause SCD are hypertrophic cardiomyopathy (HCM) and coronary artery anomalies or diseases, accounting for nearly 70% of the cases (see Table 25.1 ).
Coronary artery anomalies, congenital and acquired
Possible hypertrophic cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy
Ion channel disease
Mitral valve prolapse
a Original data from Maron, B. J., Doerer, J. J., Haas, T. S., Tierney, D. M., & Mueller, F. E. (2009). Sudden deaths in young competitive athletes: analysis of 1866 deaths in the United States, 1980-2006. Circulation, 119 (8), 1085-1092.
B. Common Causes Of SCD
HCM (up to 36%) and its variant (8%) account for nearly half of the unexpected SCD cases (see Table 25.1 ).
Anomalies of the coronary arteries, both congenital and acquired (atherosclerotic or the result of Kawasaki disease), is the next important group of causes of SCD, accounting for 23%.
Myocarditis and dilated cardiomyopathy are found in up to 8% of SCDs.
Cardiac arrhythmias (caused by long QT syndrome, WPW syndrome, sinus node dysfunction, arrhythmogenic right ventricular dysplasia [ARVD]) account for 10% of SCD.
Other rare causes of SCD in athletes include severe AS or PS, Marfan syndrome (from ruptured aortic aneurysm), MVP, dilated cardiomyopathy, primary pulmonary hypertension, “commotio cordis,” sarcoidosis, and sickle cell trait.
C. Preparticipation Screening
The most important reason for the screening is to detect “silent” CVD that can cause SCD. Detailed prospective CV screening of a large athletic population is impractical, because there are 8 to 10 million competitive athletes in the United States. Even with the use of specialized cardiologic tools, complete prevention of SCD is nearly impossible. Thus, medical clearance for sports does not necessarily imply the absence of CVD or complete protection from sudden death.
Recommended 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 CV abnormalities. In 2014, the AHA and ACC recommended using a 14-element screening procedure (formerly a 12-point screening) as shown in Box 25.1 . Ten of the 14 points are related to the history and the remaining 4 to physical examination.
Medical History a
a Parental verification is recommended for high school and middle school athletes.
Chest pain/discomfort/tightness/pressure to exertion
Unexplained syncope/near syncope b
b Judged not to be of neurocardiogenic (vasovagal) origin, of particular concern when occurring during or after physical exertion.
Excessive and unexplained dyspnea/fatigue or palpitations, associated with exercise
Prior recognition of heart murmur
Elevated systemic blood pressure
Prior restriction from participation in sports
Prior testing for the heart, ordered by a physician
Premature death (sudden and unexpected, or otherwise) before 50 years of age attributable to heart disease in ≥1 relative
Disability from heart disease in close relative <50 years of age
Hypertrophic or dilated cardiomyopathy, long-QT syndrome, or other ion channelopathies, Marfan syndrome, or clinically significant arrhythmias, specific knowledge of genetic cardiac conditions in family members.
Heart murmur c
c Refers to heart murmurs judged likely to be organic and unlikely to be innocent; auscultation should be performed with the patient in both the supine and standing positions (or with Valsalva maneuver), specifically to identify murmurs of dynamic left ventricular outflow tract obstruction.
Femoral pulse to exclude aortic coarctation
Physical stigmata of Marfan syndrome
Brachial artery blood pressure (sitting position) d
d Preferably taken in both arms.
Although the European Society of Cardiology has recommended an electrocardiogram (ECG) with each evaluation, the AHA/ACC does not recommend it. The ECG may detect most cases of HCM, but the cost of obtaining ECGs versus the yield is prohibitive, and the cost of evaluating false-positive results is too great to make this practice cost-effective. The ECG is used only for those patients in whom a potentially lethal CVD is suspected based on the 14-element screening.
History and physical examination. Although simple history and physical examination can raise suspicion of CVD in some at-risk athletes, they do not have sufficient power to guarantee detection of many critical CV abnormalities. However, the AHA’s screening method has the capability of raising the clinical suspicion of several CV abnormalities.
History of chest pain, discomfort, tightness, or pressure to exertion.
Unexplained syncope or near syncope, except for vasovagal syncope.
Excessive and unexplained dyspnea or fatigue or palpitation, associated with exercise.
Prior recognition of heart murmur.
Elevated systemic blood pressure.
Prior restriction from participation in sports.
Prior testing for the heart, ordered by a physician.
Premature death (sudden and unexpected, or otherwise) before 50 years of age attributable to heart disease in one or more relative.
Disability from heart disease in close relative younger than 50 years.
Hypertrophic or dilated cardiomyopathy, long QT syndrome, or other ion channelopathies, Marfan syndrome, or clinically significant arrhythmias, specific knowledge of genetic cardiac conditions in family members.
Heart murmur (likely to be organic, not likely to be innocent).
Femoral pulse to exclude aortic coarctation.
Physical stigmata of Marfan syndrome.
Brachial artery BP (sitting position).
If CV 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 in the following text, although they are not routinely recommended by the AHA.
The 12-lead ECG is indicated in patients suspicious of serious CVD raised by the 14-element AHA screening history and physical examination. The ECG is a practical and cost-effective alternative to routine echocardiography. Table 25.2 lists examples of normal and abnormal findings in the ECG screen.
The ECG is abnormal in 75% to 95% of patients with HCM. Abnormalities may include LVH, ST-T changes, and abnormally deep Q waves (owing to septal hypertrophy) with diminished or absent R waves in V5 and V6. Occasionally, “giant” negative T waves are seen in V5 and V6. Cardiac arrhythmias and first-degree AV block may be seen occasionally.
Coronary artery abnormalities may show ST-T wave abnormalities or abnormal Q waves.
Long QT syndrome (QTc >0.46 sec), Brugada syndrome (RBBB with ST-segment elevation), and other inherited syndromes can be identified by the ECG.
The ECG may also raise suspicion of myocarditis (PVCs, ST-T changes) or arrhythmogenic RV cardiomyopathy (by T-wave inversion in leads V1 through V3, tall P waves, decreased RV potentials).
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 (1) increased R- or S-wave voltages, (2) Q-wave and repolarization abnormalities, and (3) frequent or complex ventricular tachyarrhythmias on Holter ECG monitors.
On the other hand, normal ECG does not necessarily rule out significant cardiac abnormalities.