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 return-to-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 18-40 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.

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 0.61·100,000^-1 person-years to 2·100,000^-1 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 2-6 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 (≤40 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 1·15,000^-1 and 1·50,000^-1, 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 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 exercise-induced cardiac event is greater in athletes with CAD and left 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 around 1% (^45,62,63,79). The genetic penetrance is age-dependent, 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 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 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 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 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 real-time telemetry) because of excessive sweating, contact with opponents, or the fact that sport is practiced under water. 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 0.43·100^-1 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 common 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: 44.4±13.0 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 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 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 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, ≥70%, and detected by maximal stress testing. This vulnerable plaque has been precisely more defined: thin cap <100(μ), a large lipid core (>40% 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.

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 absence of significant coronary artery stenosis (>50%) are classified as low risk (¹⁷). These characteristics correspond to a SCORE of <5% 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 (V˙O_2max), 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 V˙O₂max 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 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.

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).

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 real-time functional and anatomical information, and assessing risk. Once the physiology of the heart is understood in a 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.