CHEST CONDITIONS
Making Prudent Recommendations for
Return-to-Play in Adult Athletes With
Cardiac Conditions
Leonardo P. J. Oliveira, MD1 and Christine E. Lawless, MD, MBA, FACSM2,3
Abstract
Clinicians who treat millions of adult athletes throughout the world may be
faced with participation or return-to-play decisions in individuals with
known or suspected cardiac conditions. Here we review existing published participation guidelines and analyze emerging data from ongoing
registries and population-based studies pertaining to return-to-play decisions for cardiac conditions specifically affecting adult athletes. Considerations related to return-to-play decisions will vary according to age of the
athlete, with inherited disorders being the main consideration in younger
adult athletes aged 18 to 40 yr, and coronary artery disease being the
main consideration in older adult athletes aged 40 yr and older. Although
this arbitrary division is based on the epidemiology of underlying heart
disease in these populations, the essential return-to-play decision process
for both age groups is quite similar. Among the most widely used guidelines to make return-to-play decisions in this group of athletes are the
36th Bethesda Conference Eligibility Recommendations for Competitive
Athletes with Cardiovascular Abnormalities. These have long been considered the ‘‘gold standard‘‘ for determining return-to-play decisions in
young athletes in the United States. Other guidelines are available for
unique purposes, including The European Society of Cardiology guidelines, and the American Heart Association published recommendations
regarding participation of young patients (younger than 40 yr) with genetic
cardiovascular diseases in recreational sports. The latter are consistent
with the 36th Bethesda guidelines and cover common genetically based
diseases such as inherited cardiomyopathies, channelopathy, and connective tissue disorders like Marfan’s syndrome. The consensus on masters athletes (older than 40 yr) provides return-to-play decisions for a wide
variety of conditioned states, from elite older athletes to walk-up athletes.
For any adult athlete with a cardiac condition, return-to-play decisions
following use of medications, ablation procedures, device implantation,
corrective surgery, or coronary intervention depend on whether the procedure has sufficiently altered the risk for sudden cardiac events, and whether
there is a potential for unfavorable interaction with cardiac performance.
Introduction
Health care providers who treat millions of athletes of all ages throughout
the world are faced with a variety of
participation decisions, such as returnto-play for athletes with a musculoskeletal condition, an acute infectious
process, or a concussion. On occasion,
such decisions are required for an adult
athlete with a known or suspected cardiac condition, with the main objective being prevention of sudden cardiac
events during sports participation, while
allowing all individuals to experience
the benefits of exercise and physical
activity (37). Here we review existing
published participation guidelines, as
well as analyze emerging data from ongoing registries and population-based
studies pertaining to cardiac conditions
in adult athletes. The considerations related to return-to-play decisions (RTPD)
will vary according to age of the athlete,
with inherited disorders being the main
consideration in younger adult athletes
(aged 18Y40 yr) and coronary artery
disease (CAD) being the main consideration in older adults (aged 40 yr and
older). Although this arbitrary division is
based on the epidemiology of underlying
heart disease in these populations, the
essential RTPD process for both age
groups is quite similar.
1
Cleveland Clinic Sports Health, Department of Orthopaedic Surgery, Cleveland Clinic, Cleveland, OH; 2Sports Cardiology Consultants, LLC, Chicago, IL;
and 3School of Medicine, University of Chicago, Chicago, IL
Address for correspondence: Christine E. Lawless, MD, MBA, FACSM, Sports Cardiology Consultants, LLC and School of Medicine, University of Chicago,
360 W. Illinois St. #7D, Chicago, IL 60654 (E-mail: christine.lawless@yahoo.com).
1537-890X/1002/65Y77
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65
Major Published Guidelines for the Adult Athlete
Athletes Aged 18 to 40 yr
Major guidelines for sports participation for athletes
with known cardiac conditions are listed in Table 1 and are
reviewed in greater detail elsewhere (37,38). In the young
adult U.S. athlete between the ages of 18 and approximately
40 yr of age, the prevalence of sudden cardiac death (SCD)
ranges from 0.61I100,000Y1 person-years to 2I100,000Y1
person-years (51,53), with men at higher risk than women,
and the top two cardiac causes being hypertrophic cardiomyopathy (HCM) and congenital anomalies of the coronary
arteries (16,25,52). Effective preparticipation examinations
(PPE) have focused on trying to effectively screen for underlying undetected HCM and valvular and arrythmogenic
diseases (16,25,52). There still is a huge debate as to the
ideal screening method, and comparisons between different countries methodologies have been discussed elsewhere
(6,46,54,63).
Among the most widely used guidelines to make RTPD
in this group of athletes are the 36th Bethesda Conference
(#36BC) Eligibility Recommendations for Competitive
Athletes with Cardiovascular Abnormalities (57). These
have long been considered the ‘‘gold standard’’ for making
RTPD in the young athlete in the United States. An extremely important precedent was established when these
guidelines were used in a mid-1990s court case to support
disqualification of a college athlete (55). Because of this,
providers should be prepared to defend any decisions they
make that deviate from the #36BC recommendations.
The European Society of Cardiology (ESC) guidelines
are similar to the #36BC guidelines but with some notable
differences between the two documents (64). Specific recommendation for any given athlete most likely will depend
on where such decisionmaking takes place and the country of residence of the athlete or health care providers.
Some suggest presenting both options to the athlete. See
Tables 2Y6 for RTPD recommendations according to disease state and source of participation guidelines, ESC versus #36BC.
The American Heart Association (AHA) published recommendations regarding participation of young patients
(e40 yr) with genetic cardiovascular diseases in recreational
sports, proposing a convenient grading system that ranks
common forms of exercise on a scale of 0 to 5. These
guidelines are consistent with the 36th Bethesda guidelines
and cover common genetically based diseases such as
inherited cardiomyopathies, channelopathy, and connective
tissue disorders like Marfan’s syndrome (56).
Athletes Older Than 40 yr
The most common cause of SCD in the athlete older
than 40 yr is CAD. The incidence of SCD is higher in masters athletes compared to younger athletes, with the annual
incidence of SCD in masters joggers and marathon participants estimated to be 1I15,000Y1 and 1I50,000Y1, respectively (78). Masters athletes are defined as those older than
40 yr at various levels of conditioning. Despite exercising
at high intensity, these individuals still should be evaluated
for traditional risk factors, such as hypertension (61), diabetes, cigarette use, and hereditary and acquired dyslipidemias. According to the published guidelines for the older
66
Volume 10 & Number 2 & March/April 2011
Table 1.
Guidelines for sports participation for athletes with known cardiac
conditions.
Guideline
AHA 2007 Update
Comment
& 12-element focused
examination as part of
preparticipation examination
& Can help to identify athletes
with preexisting conditions or
suspected cardiac disease
& Does NOT recommend routine
ECG screening
36th Bethesda Conference
Recommendations
& Gold standard for RTP in United
States
& Classifies sports by static and
dynamic components; 1A
sports are low static/low
dynamic
European Society of
Cardiology
& Similar to Bethesda Guidelines
& Some notable differences
AHA Consensus for Young & Includes grading system for
Patients with Genetic CVD exercise
& Consistent with Bethesda
Guidelines
& Useful for prescribing exercise
for athletes with high-risk
conditions
NASPE Policy Conference on & Favored by EP community
Arrhythmias and the Athlete
& Older, but similar to Bethesda
Guidelines
& One exception is postablation
RTP; this technique is now
more common and athletes can
RTP sooner than described by
NASPE guidelines
WHF, IFSM, AHA Consensus & Similar to Bethesda Guidelines
on Masters Athletes
& Athletes 940 yr of age
& Range of conditioning, from
elite athletes to walk-up
athletes
AHA = American Heart Association; CVD = cardiovascular disease;
ECG = electrocardiogram; NASPE = North American Society for Pacing
and Electrophysiology (now the Heart Rhythm Society); WHF = World
Heart Federation; IFSM = International Federation of Sports Medicine;
EP = electrophysiology; RTP = return-to-play.
(Borrowed from Lawless CE. Return-to-play decisions in athletes with
cardiac conditions: guidelines and considerations. In: Sports Cardiology
Essentials: Evaluation, Management and Case Studies. New York, NY:
Springer Science + Business Media; 2011. p. 387–401. Copyright * 2011
Springer Science + Business Media. Used with permission.)
Return-to-Play in the Adult
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Table 2.
Summary of guidelines for athletes with known or suspected hypertrophic cardiomyopathy.
Condition
ESC (62Y64)
#36BC (49)
Definitive diagnosis of HCM
No competitive sports, with possible
exception of low-dynamic, low-static
sports (1A) in low-risk patients
No competitive sports, with possible exception
of low-dynamic, low-static sports (1A) in
low-risk patients
Athletes who are genotype-positive,
phenotype-negative
Only recreational, noncompetitive sport
activities
No restrictions to sports activities
ECG changes with normal echo
Individualize recommendation
Should undergo CMR to evaluate for changes
not detected on echo
CMR = cardiac magnetic resonance; ESC = European Society of Cardiology; HCM = hypertrophic cardiomyopathy; #36BC = 36th Bethesda
Conference.
athlete (50), it is advised that the 12-lead electrocardiogram
(ECG) be used for preparticipation screening of all masters
athletes. Stress testing as screening for CAD only is advised
for men older than 40 to 45 yr and women older than 50
to 55 yr with moderate to high cardiovascular risk. However, it is recommended for physically active individuals
and professional athletes. The probability of an exerciseinduced cardiac event is greater in athletes with CAD and left
Table 3.
RTP recommendations for common supraventricular rhythm disturbances.
Condition
Symptoms
ECG
Diagnosis
Treatment Options
Competitive Athlete
Atrial premature
complexes
Palpitation
Often NL
Monitor
Reassurance, BB if
disabling symptoms
No restrictions
Atrial flutter
Palpitations
Often NL
Monitor
RFA
Without structural heart disease,
return to competitive sports allowed
2Y4 wk without recurrence, or in a
few days after repeat EPS confirms
noninducibility*
Atrial fibrillation
Palpitations
Often NL
Monitor
Rate control,
If warfarin is used for anticoagulation,
anticoagulation,
sports with bodily contact should
antiarrhythmics, RFA
be avoided
Return to competitive sports allowed
4Y6 wk without recurrence or after
repeat EPS confirms noninducibility*
AVNRT
Palpitations,
LH
NL
Monitor,
EPS
BB, digoxin, CCB, RFA After 3Y6 months of a symptom-free
period.
If an ablation has been performed,
may participate in all competitive
sports after 2Y4 wk without
recurrence, or in a few days after
repeat EPS confirms noninducibility*
WPW
Asymptomatic
Short PR interval, ECG, EPS
delta waves
No therapy, or RFA
In order to compete, athletes should
if rapid conduction
undergo an EPS to stratify risk
through bypass tract
of SCD
Palpitations,
LH, syncope
Short PR interval, ECG, EPS
delta waves
RFA, antiarrhythmics
After 1Y2 months of a symptom-free
period.
If an ablation has been performed, may
participate in all competitive sports
after 2Y4 wk without recurrence,
or in a few days after repeat EPS
confirms noninducibility*
AVNRT = atrioventricular reentrant tachycardia; BB = beta blocker; CCB = calcium channel blocker; ECG = electrocardiogram;
EPS = electrophysiological study; LH = lightheadedness; NL = normal; RFA = radiofrequency ablation; SCD = sudden cardiac death; WPW =
Wolff-Parkinson-White.
(Adapted from Link MS, Estes NA. J. Cardiovasc. Electrophysiol. 2010; 21:1184Y9. Copyright * 2010 J. Cardiovasc. Electrophysiol. Used with
permission.)
*Recommendations from Zipes et al. [81], p. 1357Y9.
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67
Table 4.
Comparison of ESC and #36BC regarding RTP for ventricular rhythm disturbances.
Condition
ESC (27)
#36BC (81)
Premature ventricular
contraction
All sports allowed if no CVD. If CVD is present,
no competitive sports. Light to moderate
leisure-time sports with the avoidance of
sudden bursts of activity.
If no structural abnormality, no restrictions.
If normal heart but symptomatic or
structurally abnormality present, can
participate in class IA competitive sports.
Ventricular tachycardia in a
structurally normal heart
All sports allowed if no recurrence within
6 wk to 3 months after ablation.
Allowed to resume sports activities 2Y4 wk
after ablation of VT in a structurally normal
heart. If VT controlled by medications,
3 months required of suppression and
exercise testing or EPS required before
return to activities.
Ventricular tachycardia in an
abnormal heart
Competitive sports are not allowed except those
with a low cardiovascular demand (1A).
Competitive sports are not allowed except
for class IA.
Ventricular flutter and
fibrillation
May return to sports after 3 months if ablation
of the accessory pathway. If ICD present,
no competitive sports, except when low
cardiovascular demand and no risk for patient
or others.
Class IA competitive sports after ICD
placement.
Catecholaminergic
polymorphic ventricular
tachycardia
No competitive sports allowed. Low-demand
leisure-time sports only if arrhythmia and
symptom-free under therapy. Avoid sudden
bursts of activity.
Symptomatic unless treated with an ICD and
asymptomatic patients have are restricted
from competitive sports with the possible
exception of minimal contact, class IA
activities.
Brugada syndrome
Only competitive sports with low cardiovascular
demand. Leisure-time sports with moderate
demand.
Restriction to participation in class IA sports
is recommended.
Brugada syndrome gene
carriers without the
phenotypea
All gene carriers should be restricted from
competitive sports.
No restrictions.
Class IA = billiards, bowling, cricket, curling, golf, riflery; CVD = cardiovascular disease; EPS = electrophysiological study; ESC = European Society
of Cardiology; ICD = implantable cardioverter defibrillator; VT = ventricular tachycardia; #36BC = 36th Bethesda Conference.
ventricular (LV) dysfunction. Therefore, masters athletes
should be discouraged from participation in high-intensity
sports if they have LV ejection fraction less than 50% or evidence of exercise-induced ischemia, ventricular arrhythmia,
or systolic hypotension (50).
The scope of this article is to provide evidence-based
guidelines on what level of physical activity and which
sports are safe to allow for participation of adult patients
with cardiac conditions. This review was prepared by
completing a Pubmed search in addition to reviewing the
published guidelines.
Participation Considerations for Specific
Cardiac Conditions
HCM
HCM is the most well known cardiomyopathy related
to exercise in young athletes. Its paucity of symptoms and
interpatient variability in physical exam findings make
awareness of the condition, together with a detailed history and physical examination, essential components to
make the diagnosis accurately. It is an autosomal dominant
condition for which 12 gene mutations already have been
isolated and more than 400 specific mutations. The prevalence varies according to the study, but the range is within
0.5% and 2% of the population, with annual mortality
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Volume 10 & Number 2 & March/April 2011
around 1% (45,62,63,79). The genetic penetrance is agedependent, and although the phenotype is not present at
times of earlier evaluation, it may develop in later years
(45). The treatment is varied according to the symptoms,
risk factors, and stages of the disease and have been discussed elsewhere (16,45,48). A recent meta-analysis comparing myomectomy with septal alcohol ablation showed
similar mortality and functional capacity scores based on
the New York Heart Association Functional Class (2).
Nonetheless, despite the improvement in medical and surgical interventions, these individuals still are at high risk
of SCD because of persistence of the arrhythmogenic substrate and should not return to competitive sports (49,57).
The recommendations described in Table 2 for HCM do
not vary according to age, gender, phenotypic appearance,
symptoms, LV outflow obstruction, previous treatment
with drugs, or major interventions with surgery and alcohol
septal ablation. The role of the implantable cardioverter
defibrillator and the automated external defibrillator at the
sidelines are to prevent or treat SCD, not to allow these
individuals to participate in sports.
Arrhythmias
Cardiac arrhythmias may be difficult to diagnose because
they can be temporary, only to recur years after an initial
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Table 5.
Comparison of ESC and #36BC regarding RTP with supraventricular rhythm disturbances.
Condition
ESC (28)
#36BC (81)
Sinus node dysfunction V bradycardia
Allowed to participate in all sports if
asymptomatic and no cardiac disease.
Symptomatic individuals have to be
symptom free for 93 months and off
therapy to return to full activities.
Normal or structurally abnormal heart in
whom the bradycardic rate is increased
appropriately by physical activity can
participate in all competitive sports
consistent with the limitations imposed
by the structural heart disease.
Sinus node dysfunction/tachybrady
syndrome or inappropriate tachycardia
If no recurrence for 1Y3 months,
competitive sports allowed. Ablation
recommended.
Can participate in all competitive sports
if no structural heart disease and
asymptomatic for 2Y3 months.
Premature atrial contraction
Athletes can participate in all competitive
sports.
Athletes can participate in all competitive
sports.
Atrial flutter without structural
heart disease
Catheter ablation recommended. May
participate in all sports if asymptomatic
for more than 3 months.
Needs to maintain ventricular rate that
increases and slows appropriately
comparable to that of a normal sinus
response in relation to the level of
activity, while receiving no therapy or
therapy with AV nodal blocking drugs,
can participate in class IA competitive
sports with the warning that rapid
1:1 conduction still may occur. Full
participation in all competitive sports
should not be allowed unless the
athlete has been without atrial flutter
for 2Y3 months with or without drug
treatment.
Atrial flutter with structural
heart disease
Catheter ablation recommended.
Treatment of underlying condition
recommended.
Athletes with structural heart disease
who have atrial flutter can participate in
class IA competitive sports only after
2Y4 wk have elapsed without an
episode of atrial flutter.
Atrial flutter postablation
May participate in all sports if
asymptomatic for 93 months.
Athletes without structural heart disease
who have elimination of the atrial flutter
by an ablation technique or surgery
can participate in all competitive sports
after 2Y4 wk without a recurrence, or in
several days after an electrophysiologic
study showing noninducibility of the
atrial flutter in the presence of
bidirectional isthmus block.
Asymptomatic genotype positive
phenotype negative normal QTc
Discouraged from competitive sports
activity.
No restrictions to sports activity except
LQT1 mutation (competitive swimming).
Borderline QTc and negative genotyping
Allowed to participate but with
surveillance.
No restrictions.
Short QT syndrome
Only competitive sports and leisure-time
sports with low static/dynamic
demand. Sports with risk for patient
or others due to (pre)syncope are
relatively contraindicated for phenotype
positive patients and phenotype
positive genotype negative.
Not addressed in the document.
AV = atrioventricular; ESC = European Society of Cardiology; QTc = corrected QT interval; #36BC = 36th Bethesda Conference.
a
No symptoms and no ventricular tachycardia in electrophysiological study.
event. If the rhythm abnormality occurs during exercise,
there is an increased yield of causing symptoms but may be
unnoticed if happening at rest (43). Depending on the sports
activity, an individual might develop symptoms secondary
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to the arrhythmia. Individuals who have near syncope,
syncopal, or seizure events warrant further evaluation.
Approximately 50% of the cases of syncope can have a
cause identified, by history and exam alone in several of the
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Table 6.
RTP recommendations in athletes with CAD.
Condition
Stable angina
ESC (17)
#36BC (74)
Individuals with SA and high probability for
exercise induced events are not eligible for
competitive sports.
Low risk Y preserved LV function, normal
exercise tolerance for agea, absence of
ischemia and significant stenosis, and
successful revascularization.
SA and a low probability of exercise-induced
events are eligible for competitive sports with
low-moderate static and low dynamic sports.
Increased Risk Y Abnormal LV Function,
Exercise Ischemia, Hemodynamic ally
significant stenosis or greater than 50%.
Low risk Y normal exercise capacity for age and
sex, as well as for intended activity, absence
of exercise-induced ischemia during stress
testing, EF 950%, absence of complex
ventricular arrhythmias at rest and during 24-h
Holter monitor.
Mildly increased risk group can participate in
low dynamic and low/moderate static
competitive sports (IA/IIA) but avoid intensely
competitive situations.
Substantially increased high risk are restricted
to low-intensity competitive sports (IA).
CAD after PCI
If no evidence of myocardial ischemia is found
after completion of outpatient cardiac rehab
(usually 3Y4 months), patients may resume
individually tailored activity.
Should avoid vigorous exercise training for
competition for approximately 4 wk.
CAD after CABG
If no evidence of myocardial ischemia is found
after completion of outpatient cardiac rehab
(usually 3Y4 months), patients may resume
individually tailored activity.
Following coronary bypass surgery, patients
should avoid vigorous training until their
incisions can tolerate vigorous activity,
around 4Y6 wk.
CAD in transplant patients
Not addressed.
If no coronary luminal narrowing and
exercise-induced ischemia in the setting of
normal exercise tolerance for age, athlete
can participate in all competitive sports as
appropriate.
Myocardial bridging
Evaluate patient for CAD with stress test and
also for HCM.
Athletes with surgical resection of the
myocardial bridge should be restricted to
low-intensity sports for at least 6 months after
the procedure. Athletes who remain
asymptomatic after the procedure should
undergo exercise testing. If exercise tolerance
is normal for age and gender and without
evidence of ischemia, athlete may participate
in all competitive sports.
Coronary artery vasospasm
Not addressed.
Athletes with coronary vasospasm documented
at rest or with exercise and angiographically
normal coronary arteries or without evidence
of arterial plaquing should be restricted to
low-intensity competitive sports (class IA).
CAD = coronary artery disease; CABG = coronary artery bypass graft surgery; Class IA = billiards, bowling, cricket, curling, golf, riflery; Class IIA =
archery, auto racing, diving, equestrian, motorcycling.
EF = ejection fraction; ESC = European Society of Cardiology; HCM = hypertrophic cardiomyopathy; LV = left ventricle; PCI = percutaneous
coronary intervention; SA = stable angina; #36BC = 36th Bethesda Conference.
Greater than 10 metabolic equivalents (METS), or greater than 35 mL O2Ikg-minj1 if younger than 50 yr; greater than 9 METS, or greater than
31 mL O2Ikg-minj1 for 50 to 59 yr old; greater than 8 METS, or greater than 28 mL O2Ikg-minj1, if 60 to 69 yr old; and greater than 7 METS, or
greater than 24 mL O2Ikg-minj1, if greater than or equal to 70 yr old.
a
cases. Both the #36BC and the ESC recommend a careful
cardiac examination, a 12-lead ECG, echocardiogram, exercise stress test, and according to each individual case,
appropriate 24-h ambulatory ECG monitoring (81). The
choice of monitoring will depend on the frequency the
rhythm disturbance is occurring. For instance, if it occurs
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Volume 10 & Number 2 & March/April 2011
daily, then 24-h monitoring is adequate; however, if it occurs once every 3 wk, prolonged ambulatory monitoring
will be required. Certain sports may preclude prolonged
external ambulatory monitoring (event monitors or realtime telemetry) because of excessive sweating, contact with
opponents, or the fact that sport is practiced under water.
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In this case, clinicians can consider implantable loop
recorders.
In a review of 690 deaths in athletes documented to be
caused by cardiovascular conditions, 6% were attributed
to channelopathies and Wolff-Parkinson-White combined
(51). Therefore, family history obtained at the time of the
PPE and during an evaluation of a syncopal event is a key
component in order to screen for possible hereditary rhythm
disturbances.
Long QT Syndrome (LQTS)
This abnormality of the QT interval can predispose
patients to SCD by triggering Torsades de Pointes polymorphic ventricular tachycardia and ventricular fibrillation
(67). In the general population, LQTS is estimated to affect
one in every 2500 people, whereas in elite athletes it is
present in 0.4% (31). So far, 12 susceptibility genes have
been discovered. Mutations in the sodium and potassium
channels are responsible for 95% of the identifiable long
QT syndrome. Although Schwartz and colleagues developed a score to evaluate the likelihood of an individual
having long QT syndrome (69), it has been criticized due
to lack of sensitivity (68). The ESC has a lower corrected
QT interval (QTc) threshold to withhold from sports participation in comparison with the #36BC (i.e., males: ESC
0.44 s vs #36BC 0.47 s; women: ESC 0.46 s vs #36BC
0.48 s). In athletes with QTc interval lengthening above
these limits, genetic testing is recommended to increase the
likelihood of definitive diagnosis. Upon detection of a prolonged QT interval, genetic testing is recommended by both
societies. When the LQTS diagnosis is confirmed, the recommendation is for exclusion of the athlete from all competitive sports. However, while asymptomatic genotype
positive and phenotype negative should be restricted from all
competitive sports according to the ESC, the #36BC believes
that there are no data to preclude these patients from competing. The #36BC indicates that serious arrhythmias are
uncommon in QTc intervals less than 0.5 s. LQT1 mutation
is the only exception, with regards to competitive water
activities, because of the link of cardiac events with this
sport (64).
Acquired Prolonged QT
Prolonged QT interval can occur from other factors, such
as side effects of medications (e.g., quinidine, dofetilide,
sotalol, and erythromycin) and medication interactions. In
individuals who exercise and have been found to have a
prolonged QT interval, it is paramount to know the prescription medications in addition to any over-the-counter
medications, including nonprescription remedies and herbal
supplements.
Atrial Fibrillation
Atrial fibrillation (AF) is more common in athletes than
in the general population, around 0.43I100Y1 each year in
marathon runners (72). Individuals who practice regular
physical activity have a twofold higher risk of developing AF
(11). However, vigorous exercise only was associated with
AF in a subgroup analyses in men younger than 50 yr and
joggers (3). It seems that years of endurance training are
necessary to develop atrial fibrillation (34). The most comwww.acsm-csmr.org
mon presentation is lone atrial fibrillation (LAF) secondary
to vagal mediation. The pathophysiology is thought to be
secondary to a shortened refractory period or slowed conduction, which reduces the excitation wavelength and facilitates the reentry mechanism (72). Newer reports add that
overtraining could lead to the release of proinflammatory
mediators, which have been associated with AF, although not
confirmed in athletes (34,72). Every individual who develops
AF should have an appropriate metabolic, pharmacological,
and structural evaluation of the heart in order to evaluate for
conditions such as valvular diseases and structural abnormalities that could lead to the arrhythmia. Left atrial
enlargement, which is commonly seen in athletes, is not
associated with higher rates of LAF (72).
Atrial fibrillation also can occur in younger adult athletes, such as football and basketball players. Some of these
rhythms are ablatable, especially those arising from the
pulmonary veins, tricuspid valve, or those that begin as
paroxysmal supraventricular tachycardia and deteriorate to
atrial fibrillation. Younger athletes usually do not have the
risk factors requiring anticoagulation such as age greater
than 75, hypertension, diabetes mellitus, prior history of
stroke, or congestive heart failure, which are referred as
CHADS2 score. Therefore, athletes generally only require
anticoagulation with aspirin in addition to rate control
(43). Rate control, especially in athletes, should be guided
by stress testing, since only 51% of patients with adequate
heart rate at rest had adequate control at moderate exercise (30). In master athletes, the clinical scenario might
be different due to the presence of risk factors mentioned
previously, and an athlete with a CHADS2 score equal
or greater than 1 will need appropriate anticoagulation
according to age, clinical risk factors, risk of bleeding
complications, patient’s ability to safely adapt to chronic
anticoagulation, and patient’s preference (22). The current
options are coumadin, or aspirin added to clopidrogrel in
patients who can’t tolerate vitamin K antagonists (76).
Pharmacological treatment with flecanide is recommended in vagally mediated LAF without structural heart
disease (72). Amiodarone is used commonly in the general
population; however, it has multiple side effects, with the
most serious involving the pulmonary and hepatic systems.
Because anticoagulation with vitamin K antagonists will
preclude athletes from participating in contact sports (43),
several will choose radiofrequency catheter ablation (RFA)
as a definitive therapy. RFA has been shown in recent years
to be an effective therapy in the general population, and a
recent study by Furlanello reported it to be useful for drug
refractory AF in 20 male athletes (mean age: 44.4T13.0
standard deviation [SD] yr). Some athletes required up to
three procedures, but 6 months after, none had recurrence
of the arrhythmia, and all were considered eligible for participation according to the Italian eligibility guidelines for
continuing sports participation (21). Long-term studies to
evaluate effects in sports participation are necessary.
Supraventricular Arrhythmias
Table 3 illustrates RTP recommendations for common
supraventricular rhythm disturbances, including atrial fibrillation. This information was adapted from the Electrophysiology (EP) literature and the #36BC, and it is important
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71
to note that there may be some minor differences between the
#36BC guidelines and the EP publications because of publication at different times.
Ventricular Arrhythmias
Those athletes with idiopathic ventricular arrhythmias
arising from the right ventricle outflow tract, or fascicle,
with evidence of normal LV function, can RTP after successful ablation, provided absence of any recurrent symptoms during a 6-wk to 3-month period postintervention and
no evidence of underlying structural disease. However, close
early follow-up is warranted (every 3 months for the first
year and immediately after recurrence of symptoms) and
also later (at least yearly), since some may have underlying,
slowly progressive cardiac disease that will only manifest
over time. Athletes with underlying structural heart disease
or LV dysfunction are at high risk for a ventricular rhythm
disturbance. For them, RTP is not advised, even with an
implanted defibrillator (43,81). Further recommendations
of eligibility for common ventricular arrhythmias are addressed in Table 4.
Other Structural Abnormalities
Patent foramen ovale. Since diving and climbing are growing
in popularity world-wide, the effects and risks of exercise on
the physiology of patent foramen ovale (PFO) merits mentioning here. PFO, a remnant of the fetal circulation, is the
communication between the LA and the right atrium (RA)
due to incomplete fusion of the septum primum against
septum secundum in an oblique, slit-like defect. The remainder flap acts as a valve-like structure (33). It has been
associated with multiple conditions such as paradoxical
embolism, venous-to-arterial gas embolism, and cardiac
events under the condition of environmental extremes,
increased risk of decompression sickness in divers, and
hypoxic vasoconstriction and high altitude pulmonary edema
(33,66). The prevalence of this condition in athletes has not
been evaluated, but in the general population, autopsy data
suggest an incidence of 27.3% to 29%.
It is thought that diving-related phenomena could increase RA pressure, leading to increasing right to left shunting in people with PFO (9). A study by Blatteau showed no
difference in intracardiac shunting from divers with and
without a PFO (9) Individuals with large PFO are more
susceptible to acute hypoxic pulmonary vasoconstriction of
high altitudes, which can lead to a vicious cycle of worsening hypoxemia and pulmonary hypertension as the final
product (66). However, at this time further studies are necessary to determine the best strategy in evaluating divers or
athletes going to high altitudes. One option being used for
patients with congenital heart disease classified as functional
class 1 in the New York Heart Association is to obtain a
transthoracic echocardiogram and exercise stress with oxygen concentration at 12% and measure the pressure difference from right ventricle to right atrium. A difference of
more than 40 mmHg or worsening right ventricular function discourages these individuals from going to high
altitudes (66). These findings correlate to potential development of pulmonary hypertension at high altitudes increasing
substantially the risk of high altitude pulmonary edema.
Such individuals may be considered for PFO closures, and
72
Volume 10 & Number 2 & March/April 2011
successful closure may allow full return to competitive
activity (42). This topic is not addressed in the #36BC, but
there is information on the web at the Divers Alert Network
(www.diversalertnetwork.org). Further research is necessary
to decide whether prophylactic PFO closure for athletes
going to high altitudes is beneficial and what parameters
would predict a favorable outcome.
Coronary Arteries and Athletes
Coronary anomalies. The coronary arteries play a substantial role in sudden cardiac events and SCD in athletes.
In individuals younger than 35 yr, anomaly of the coronary
arteries is responsible for 17% of SCD in competitive athletes (51). There are several subtypes, and not all of them
subject the athletes to same risk of SCD. There can be a
change in the origin of the vessel, or in its course, or both.
The most common abnormality leading to SCD is origin
of the left main coronary artery from the right sinus of
valsalva (5,20). It is believed that the mechanism leading
to death is lack of blood flow from changes in the vessel
orientation or compression of the vessel between the great
vessels. The diagnosis is hard to make because of lack of
abnormalities on resting ECG and variable sensitivity of
stress testing. The diagnosis was made in the past by coronary angiography but with the advancements in transthoracic imaging, transthoracic echocardiogram has been
the proposed method of screening. Recent studies propose
electrocardiography gated multidetector coronary computerized tomography (CT) angiography as the best test for
evaluation of the coronary anomalies (73). Individuals who
have their coronary anomalies surgically corrected are able
to return to full competitive activity. A study in the pediatric
population by Brothers and colleagues demonstrated mild
chronotropic impairment in maximal exercise but no change
in maximal oxygen consumption and anaerobic threshold
(12). The RTP decision following corrective surgery depends
on whether the procedure has sufficiently reduced the risk
for SCD. For example, surgical myectomy or alcohol septal
ablation in a patient with HCM can reduce outflow tract
obstruction and relieve symptoms; however, the underlying
arrhythmogenic substrate remains largely unchanged. Conversely, surgical correction of an anomalous coronary artery
results in anatomical correction of the underlying problem and likely reduces or eliminates risks of ischemia and
malignant ventricular arrhythmias. According to the #36BC,
sports participation is allowed 3 months after surgical correction, so long as there is no evidence of exercise-induced
LV dysfunction, arrhythmia, or ischemia.
CAD. There are several unique considerations with regards
to CAD in the athlete and exercising individual. These
include the effects of exercise on the development of CAD,
modification of risk factors in the exercising individual, the
role of subclinical atherosclerosis and the vulnerable plaque on risk of cardiac events, detection of subclinical disease, the indications for 12-lead ECG and stress testing
when conducting preparticipation screening, physiology of
the physical activity and its oxygen requirement, and the
effects of medications, residual ischemia, and revascularization and cardiac performance. Because the population
is aging and the number of exercising individuals at risk
for CAD keeps increasing, we will devote considerable
Return-to-Play in the Adult
Copyright © 2011 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
discussion to the adult athlete with known, suspected, or
undetected CAD.
CAD is the most common cause of death in athletes older
than age 30 (74) and is responsible for 35% of the deaths in
the United States population (4). As the prevalence of the
major risk factors such as hypertension, diabetes, hyperlipidemia, and obesity increases, so does the risk of CAD,
stroke, and myocardial infarction. In professional athletes,
the exact prevalence of CAD is unknown but is estimated
around 13.7% to 16% (14,47). The mechanism leading to
SCD is occlusion of the coronary arteries due to plaque
rupture or erosion, which leads to a sequence of events,
including cytokine release by the inflammatory cascade and
platelet aggregation. This will culminate into ventricular
tachycardia, which degenerates into ventricular fibrillation
and later on asystole (1).
At the same time that exercise causes benefits in the
metabolic, circulatory, and nervous systems contributing
to primary and secondary prevention of CAD (5,32,41), it
also is a trigger for plaque rupture because of increase in
intraluminal pressure, promotion of thrombus formation
and activation of the coagulation cascade (18).
Vulnerable plaque and risk stratification. Atherosclerosis
is a continuous process that starts around age 20 in the
form of fatty streaks and plaques. It is known that plaques with large lipid cores, thin fibrous caps, numerous
macrophages, and few smooth muscle cells are more
likely to rupture. Autopsies have revealed that plaque
ruptures can be clinically silent and the healed ruptures
contribute to the expansion of the atherosclerotic disease. Plaque burden is the ideal risk factor for CAD, and
several diagnostic modalities have attempted to quantify it
(75). In individuals who have documented CAD by coronary
angiography, it has been shown that plaques that originate
cardiac events often have around 50% to 70% diameter
narrowing. This complicates the treatment of CAD, which
commonly is focused on the high grade narrowing, Q70%,
and detected by maximal stress testing. This vulnerable plaque has been precisely more defined: thin cap G100(K), a
large lipid core (940% of the plaque’s volume), endothelial
denudation with superficial platelet aggregation, and a fissured cap. The fissured cap is a sign of recent rupture or
severe stenosis, which makes the plaque more prone to shear
stress (4,19).
Screening for CAD. While the ECG might be useful for
arrhythmias and to evaluate for HCM, and the stress test
useful to detect high grade narrowings, detection of subclinical CAD can be difficult, especially in athletes. In
physically active individuals there is a higher likelihood
of a negative stress test. Cardiac stress testing performed
with concurrent imaging increases the diagnostic accuracy
(36,70), but the test only has good sensitivity and specificity
in the setting of a high pretest probability. In physically
active individuals who have a reduced number of risk factors, the pretest likelihood will be low (65). Despite controversies, the guidelines recommend to stress test competitive
masters athletes for risk stratification (17,74). In addition,
if the athlete has had CAD documented by coronary angiography, prior history of myocardial, inducible ischemia, or
coronary artery calcium score (CAC) score greater than 100,
the LV function must be evaluated.
www.acsm-csmr.org
The Marathon Study (59) was developed to evaluate subclinical CAD and its risk factors in master male marathon
runners. The results showed that late gadolinium enhancement in cardiac magnetic resonance imaging (CMR), which
has a high diagnostic accuracy for myocardial infarction, was
correlated with CAC scores, and there was no difference
between the marathon runners and an age-matched control
group. This is in contrast to Framingham risk scores, which
were significantly higher in the latter group. Moreover, CAC
greater than 100 had a significant prognostic value (44,58).
In athletes with a paucity of symptoms and negative stress
tests, CMR seems to be a promising, noninvasive tool
allowing visualization of the vessel lumen and wall without
using ionized radiation (7).
At this time we recommend that every athlete above
age 45 who plans on participating in vigorous exercise
activity (competitive included) be considered for stress
testing. Imaging modalities commonly have been added in
order to increase the diagnostic capabilities for evaluation
of CAD. Stress echocardiogram and nuclear testing are
the most utilized and would be our initial choices. Both
options are noninvasive and have substantial supporting
evidence (24). Stress echocardiography does not involve
radiation, which is important, especially in females. Nonetheless, the test is operator-dependent and can be cumbersome to interpret in the setting of baseline wall motion
abnormalities and rhythm disturbances (i.e., left bundle
branch block, paced rhythms), and prognostic power is
not as robust as nuclear stress testing (8). These limitations
need to be taken into account upon recommending the
patient for stress testing. Traditional cardiovascular risk
factors need to be treated and medications individualized
(61). Routine CT angiography or CMR angiography may
detect the vulnerable plaque, but at this time there are no
guidelines to support routine application of this approach.
Clinicians ought to have high index of suspicion in athletes
with multiple risk factors, or positive CAC, and they may
wish to investigate further in individual cases.
Treatment of CAD and RTP considerations in adult athletes
with CAD. The choices for treatment of chronic CAD are
optimal medical therapy, and revascularization with percutaneous coronary interventions (PCI) and coronary artery
bypass graft surgery (CABG). RTPD will be based on numerous factors, including matching the ability of the athlete
to meet the oxygen requirements of the sport (determined
by assessing the MVO2 of the athlete and matching it with
known demands of sport identified by the literature), the
effects of medications on cardiac performance, known efficacy of medications in the physically active adult, residual
ischemia, and success of revascularization (PCI and CABG).
The main determinants of RTPD are whether the treatment has sufficiently altered the risk for sudden cardiac
events, and whether there is a potential impact on cardiac
performance.
When evaluating athletes with CAD, it is key to assess
their risk of cardiac events because this information will
guide which sports they may be able to play. Individuals
who younger than 55 yr, with fewer than two controlled
risk factors (e.g., HTN, DM, HPL), normal ejection fraction
(EF), absence of ventricular arrhythmias at rest and with
exercise, and no exercise-induced ischemia in addition to
Current Sports Medicine Reports
Copyright © 2011 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
73
absence of significant coronary artery stenosis (950%) are
classified as low risk (17). These characteristics correspond
to a SCORE of G5% risk (15). These athletes should then
have a maximal aerobic exercise test in order to obtain their
ventilatory threshold. They should participate in exercise
activities up to 60% to 75% of the maximal aerobic
capacity (V̇O2max), which will correspond to around 70%
to 85% of the maximal heart rate or 10 beats below the
heart rate obtained at the time of ischemic threshold. The
exercise physiology literature has extensive information
on the O2 requirements of the physical activity or sport.
Activities at more than 80% of V̇O2max produce more
harm than benefits (26). Patients who have undergone
PCI or CABG may only resume low dynamic or low to
medium static competitive sports (Table 7) after a 12-month
symptom- and event-free period, according to the ESC.
In contrast, the #36BC allows low-risk PCI athletes to go
back to vigorous exercise activity 4 wk after the procedure,
and post-CABG patients are restricted until the surgical
scars have healed. This is provided normal ejection fraction
(EF), absence of ventricular arrhythmias at rest, and with
exercise and no exercise-induced ischemia. Both groups
recommend yearly follow-up (17,74). Guiducci with the
Italian Organizing Committee for Cardiac Fitness for Sport,
COCIS, believes that young individuals with optimal medical
treatment and global risk assessment might be able to participate in moderate to high dynamic sports, as long as they
have semester follow-ups (26). In the real world, Guducci’s
statement is probably what is diffusely practiced, although
there is a lack of evidence to support this treatment plan.
Optimized medical treatment versus revascularization.
Some patients with CAD may be treated medically without revascularization and do quite well. The COURAGE
trial showed no difference in outcomes when individuals
on optimized medical therapy were compared with the
combination of optimized medical therapy with PCI. (10).
However, a second article from the same major study
addressing quality of life and angina scores demonstrated
a transient improvement from 3 to 24 months. This difference fades away after 36 months of follow-up (77). However, the study was conducted in individuals who had at
least 70% in one major epicardial vessel or 80% in one of
the coronaries in addition to classic angina without provocative testing. This may not apply to the athlete with
CAD, as the study’s hypothesis has not been tested in this
population. In addition, treatments such as beta blockade,
when given in doses adequate to treat angina, may result
in chronotropic incompetence and reduced cardiac performance. Moreover, according to our present guidelines
from the ESC and #36BC, athletes within these criteria
would necessarily have PCI or CABG before returning to
competitive activity.
Although statins probably are necessary whether one
has medical therapy or revascularization, there are some
unique considerations in athletes. In addition to lowering
the cholesterol, statins have a wide variety of effects such as
improving endothelial function, preserving coronary perfusion, decreasing oxidative stress, reducing platelet aggregation and thrombosis, stabilizing plaque, and possibly
promoting angiogenesis (29,82). However, there is no evidence at this time that statins improve athletic performance.
A small study of 12 individuals, average age of 66 yr, did
not show any change in aerobic capacity or skeletal muscle
function. On the other hand, 22 professional athletes with
history of familial hypercholestolerolemia taking statins
had to stop taking the cholesterol-lowering medication
because of muscle pain (71). This may not be obvious with
routine activities of daily life, but it may be unmasked by
vigorous exercise. The strategy here is to prescribe the least
amount of the most powerful statin (a little goes a long way)
to achieve lipid goals. This usually is successful.
Table 6 summarizes the current eligibility recommendations for conditions involving the coronaries established by
the ESC and #36BC.
Special Considerations for Athletes Older Than 18 yr
Sports Participation After Exertion and
Postexertional Syncope
When evaluating athletes who have collapsed during
exercise activity or a near syncopal event, it is very important to quickly assess the patient’s condition and intervene.
Exercise-associated collapse (EAC) commonly is related to
Table 7.
Classification of Sports (17,26).
A. Low Dynamic
(G40% max O2)
B. Moderate Dynamic
(40Y70 max O2)
Table tennis, tennis (doubles),
volleyball, baseball
C. High Dynamic
(970% max O2)
I. Low static (G20% MVC)
Archery, bowling, cricket,
golf, rifle shooting
Badminton, walking, running
(marathon), cross-country
skiing (classic)
II. Moderate static
(20%Y50% MVC)
Auto racing, diving,
Fencing, field events (jumping),
equestrian,motorcycling,
figure skating, lacrosse,
gymnastics, karate/judo,
running (sprint)
sailing
Basketball, biathlon, ice hockey,
field hockey, football, soccer,
cross-country skiing, running
(mid/long), squash, tennis (singles),
team handball
III. High static (950% MVC)
Bobsledding, field events
Bodybuilding, downhill skiing,
(throwing), rock climbing, wrestling
luge, waterskiing, weight
lifting, windsurfing
Boxing, canoeing, kayaking,
cycling, decathlon, rowing,
speed skating
Max O2 = maximal aerobic capacity; MVC = maximal voluntary contraction.
74
Volume 10 & Number 2 & March/April 2011
Return-to-Play in the Adult
Copyright © 2011 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
the acute interruption of exercise activity preventing the
return of blood that had been retained in the venous system
to the heart. Commonly, it is affected by dehydration and
excessive heat as well. EAC usually is a benign condition
without long-term sequelae (13).
Exercise-related syncope, on the contrary, warrants caution because of a broad range of differential diagnoses, in
addition to the fact that it involves transient loss of consciousness, which may lead to an unresponsive athlete in
the sidelines. In these situations, the patient should be evaluated for rhythm disturbances (i.e., bradycardia, supraventricular tachycardias, and ventricular tachycardias), valvular
diseases (i.e., aortic stenosis), disorders of the myocardium
(i.e., HCM, arrythmogenic right ventricular dysplasia), illicit
and licit drugs, and disorders related to the intravascular
volume (i.e., dehydration, hemorrhage).
The establishment of the diagnosis with history, physical
examination, and laboratory testing as indicated will direct
toward the appropriate conduct pertaining to permission to
play (60). The symptom of syncope alone must not be used
in RTPD. It is necessary to determine cause of underlying
syncope and use guidelines to make your decision.
given adult athlete, the appropriate set of guidelines is applied for RTPD. Further studies are required to determine
whether participation is safe for individuals with moderate
or high risk, even after intervention to the coronary arteries.
Despite having fewer risk factors than the general population, treatment of traditional risk factors for CAD must not
be forgotten in the evaluation of a noncompetitive or competitive athlete.
Implanted Defibrillators and Pacemakers
Although implanted cardiac defibrillators (ICD) generally are effective in preventing SCD in nonathletes with
diagnoses such as HCM, it cannot be assumed that ICD
will reliably defibrillate under the conditions of sport, because the fluid shifts, electrolyte abnormalities, and catecholamine excess that occur during vigorous activity may
alter defibrillation thresholds. According to the #36BC,
athletes with high-risk conditions such as HCM should not
participate in vigorous sports, even when an ICD is present
(81). Despite this recommendation, clinical practice often
differs from this recommendation. Surveys of implanting
physicians and team physicians in the United States suggest
that as many as 70% of athletes with ICD and underlying
cardiac conditions continue to participate in sports (35,40).
Similarly, a recent survey of the Pediatric and Congenital
Electrophysiology Society (PACES) found a wide variation
in physician recommendations for sports participation for
patients with pacemakers (23). Level of contact, level of
competition, and adequacy of escape rhythm had the largest
influence on recommendations.
The Sports ICD Registry was created in 2006 to address
issues surrounding the safety of ICD in athletic and actively
exercising individuals (39,80).
8. Blankstein R, Devore AD. Selecting a noninvasive imaging study after
an inconclusive exercise test. Circulation. 2010; 122:1514Y8.
Conclusion
In summary, we have discussed the main cardiovascular
topics that will play significant roles in the return of athletes
with cardiac conditions. It is very important to obtain a detailed history of their symptoms regardless of the situation:
PPE, general follow-up, or post-syncope. Monitoring the
heart rate and performance with exercise testing is key as
the athlete returns to full competitive activities. Resources
such as maximal aerobic capacity testing, echocardiography,
nuclear stress testing, CMR, CAC, and CT angiography are
valuable tools that can assist the physician in getting realtime functional and anatomical information, and assessing
risk. Once the physiology of the heart is understood in a
www.acsm-csmr.org
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