The Athlete’s Heart: Cardiovascular Disease in the Athlete

  • Jodi L. Zilinski
  • Aaron L. BaggishEmail author


With the rising popularity of recreational and competitive athletics, clinicians will benefit from an understanding of the unique physiology, clinical presentations, and management of highly trained athletes. Cardiac enlargement in athletes has been documented since the late 1800s and our understanding of the “athlete’s heart” continues to advance as cardiovascular diagnostic technology improves. The term exercise-induced cardiac remodeling has been used to describe the significant changes in myocardial structure and function that result from repeated exposure to vigorous physical exercise. In clinical practice, these adaptations can be encountered during the physical examination and are clearly manifest on the electrocardiogram and during echocardiography of trained athletes. The approach to the athlete with symptoms including chest pain, syncope, or palpitation, all common in this population, requires a careful medical history with thorough assessment of athlete-specific topics including training regimen, competition history, and inquiry about performance-enhancing agents. This review provides an up-to-date summary of the science of cardiac remodeling in athletes as well as an overview of common clinical issues that are encountered in the cardiovascular care of the athlete.


Athletes Exercise-induced cardiac remodeling Syncope Chest pain Palpitations 


Vigorous exercise can transform an athlete’s entire body including the heart. Cardiac adaptations in athletes have fascinated clinicians and scientists for over a century. Our understanding of the “athlete’s heart” and the key clinical issues relevant to the care of the athletic patient have paralleled advances in cardiovascular diagnostic technology since initial descriptions of cardiac enlargement in trained skiers in the late 1800s. Contemporary concepts of the athletic heart include numerous distinct morphologic, functional, and electrophysiologic changes that occur in response to training. While exercise promotes good health, athletes and physically active patients are not immune to cardiovascular disease. With the increasing popularity of both recreational exercise and competitive athletics, the need for specialized cardiovascular care for athletes has become increasingly recognized.

Historical Overview

Since the late nineteenth century, there have been multiple descriptions of cardiac enlargement in athletes. The “father of modern medicine,” Sir William Osler, observed that individuals who underwent training had “a gradual increase in the capability of the heart … the large heart of athletes may be due to the prolonged use of their muscles, but no man becomes a great runner or oarsman who has not naturally a capable if not large heart” [1]. Many physicians in the late nineteenth and early twentieth centuries harbored the belief that athletic activity had deleterious effects on the heart based on calculations by a German cardiologist, Beneke, in 1879 describing disproportionate growth of the left ventricle relative to the ascending aortic diameter in pediatric athletes [2]. Early reports describing the enlarged cardiac dimensions of athletes based on detailed physical examination were conducted in 1899 as Eugene Darling studied Harvard rowers [3] and Henschen compared Nordic skiers to sedentary individuals [4]. Both of these early investigators speculated that cardiac enlargement in athletes may reflect acquired pathology, not benign or beneficial adaptation. Importantly, early outcomes data in athletes published in 1927 by Felix Deutsch and Emil Kauf at the Vienna Heart Station appeared to refute this notion [5]. These investigators used roentgenographic orthodiagraphy to demonstrate that although the transverse diameter of the heart was enlarged in male and female athletes compared to the normal population, clinical follow-up of these athletes revealed no serious complications [5]. The introduction of newer technologies including electrocardiography (ECG), echocardiography, and magnetic resonance imaging have enhanced the ability of scientists and clinicians to assess the structural and functional adaptations to exercise.

Overview of Exercise Physiology

Successful performance of vigorous exercise requires the integrated coordination of multiple organ systems including the following: (1) uptake of oxygen in the lungs and pulmonary vasculature, (2) transport of oxygen and energy substrate by heart and systemic vasculature, and (3) oxygen utilization and force generation by skeletal muscle. The interplay of these systems in exercise physiology has been reviewed previously, so this discussion will be limited to the key aspects of exercise physiology relevant to cardiac remodeling [6, 7, 8].

As exercise intensity increases, oxygen demand increases in both the myocardium and skeletal muscle. The ability to sustain muscular work primarily depends on the cardiovascular system supplying oxygen to exercising muscle, or cardiac output. The Fick equation (cardiac output = oxygen consumption/arteriovenous oxygen difference) quantifies the direct relationship between cardiac output and oxygen consumption, with both central and peripheral mechanisms involved. During strenuous exercise, cardiac output, the product of heart rate and stroke volume, can be amplified fivefold over resting levels.

While cardiac output determines the peak exercise level an athlete can attain, five factors detailed by Astrand and Rodahl [9] (Table 20.1) also influence cardiac work efficiency and thus impact athletic performance. Cardiac work becomes more efficient as chamber size increases (within limits) for three reasons: initiation of contraction at larger volume requires minimal myocardial shortening to eject a given stroke volume, less energy is lost in form of friction and tension in a dilated heart wall, and a stretched muscle fiber can provide higher tension than an unstretched one. This increased efficiency is tempered by another factor (LaPlace’s law) because a higher myocardial fiber tension is needed to sustain intraventricular pressure in an enlarged cardiac chamber. LaPlace’s law (wall tension = [intraventricular pressure × ventricle radius]/wall thickness) demonstrates that increases in chamber size can be modulated by concomitant increases in wall thickness. The last factor impacting work efficiency is that larger energy losses occur with rapid contraction, i.e., higher heart rate. Taken together these cardinal features theoretically predict an athlete would benefit most from a heart capable of producing a large stroke volume with a hypertrophied ventricular wall operating at a slow heart rate. The mechanical advantage a heart gains by remodeling to optimize work efficiency during stress of exercise training is the foundation of exercise-induced cardiac remodeling.
Table 20.1

Factors affecting cardiac work efficiency

Five factors modulating cardiac work efficiency

Effect at maximum workloads

Given stroke volume ejects with minimum myocardial shortening if contraction starts at larger volume


Dilated hearts lose less energy in heart wall friction and tension


Stretched muscle fiber can provide higher tension than unstretched


Loss of energy when rapid contraction, i.e., higher heart rate


Greater heart volume higher myocardial fiber tension needed to sustain intraventricular pressure (LaPlace’s law)


Exercise-Induced Cardiac Remodeling

As discussed above, to meet the demands of cardiovascular hemodynamics during exercise, the heart remodels to maximize cardiac output. As heart rate, one of the primary determinants of cardiac output, is variable, decreases with age, and cannot be raised with exercise training [10, 11], changes in stroke volume account for the augmentation of cardiac output during demands of strenuous exercise. With exercise the left ventricular (LV) end-diastolic volume can increase and the LV end-systolic volume can decrease resulting in an amplification of stroke volume. Sympathetic nervous stimulation mediates a reduction in LV end-systolic volume (especially in upright exercise), and multiple factors (heart rate, intrinsic myocardial relaxation, ventricular compliance, ventricular filling pressures, atrial contraction, and extracardiac factors) determine diastolic filling and thus LV end-diastolic volume [6, 12].

Left ventricular remodeling in response to exercise training has been well studied, from the increased voltage observed on ECG [13] to the left ventricular hypertrophy and LV dilation seen on echocardiography [14]. Due to an extensive pre-participation screening program, many of the published reference values for LV remodeling have been established in Italian athletes. Pelliccia et al. [15] studied 1,309 athletes from 38 different sports and found left ventricular end-diastolic diameter (LVEDD) ranged from 38 to 66 mm in women and 43–70 mm in men. Markedly dilated LV chambers (>60 mm) were observed in 14 % of the cohort and were more common in endurance athletes with nearly half the athletes having an LVEDD above the upper limit of normal. In addition, Pelliccia et al. [16] studied LV wall thickness in 947 elite athletes, but only a small percentage (1.7 %) had LV wall thickness ≥13 mm (and all athletes had concomitant LV dilation). Similar percentages have been seen in other studies of athletes and the most marked LV hypertrophy is seen more commonly in athletes at highest levels of exercise training, large body size, and Afro-Caribbean descent [17]. An LV wall thickness greater than 13 mm, which is rare even in athletes, should prompt further assessment to delineate adaptive from pathologic hypertrophy with consideration given to training status, body size, and ethnicity.

Various sport disciplines produce different hemodynamic loading conditions and thus impact exercise-induced cardiac remodeling differently. By altering the requirements of cardiac output and change in peripheral vascular resistance (PVR), exercise can be broadly divided into two types [6, 12]. Isotonic exercise, or endurance activities (e.g., running, cycling, swimming), involves sustained elevations in cardiac output with normal or reduced PVR, which acts as a volume challenge on all chambers of the heart. Isometric exercise, or strength training activities (e.g., weight lifting, throwing events), primarily involves increased PVR and normal or only slightly elevated cardiac output. While brief, the increased PVR causes transient systolic hypertension and LV afterload. Many other sports, including soccer, basketball, and hockey, are a mixture of endurance and strength exercise. Figure 20.1 [12] depicts the major training-specific changes in LV hypertrophy, ejection fraction, diastolic function, and torsion that have been observed. In general, strength-trained athletes develop concentric hypertrophy, whereas endurance-trained athletes develop eccentric hypertrophy [18]. Enhanced early diastolic LV filling has been extensively evaluated using 2D and tissue Doppler echocardiography in endurance athletes [17, 19, 20, 21], while one study in strength athletes has suggested impaired LV relaxation in American football players [18]. Functional echocardiography has also been used to assess the mechanics of LV systolic function [22] demonstrating that endurance athletes have increased apical rotation, LV torsion, and peak early diastolic untwisting rate [23].
Fig. 20.1

Summary of ventricular remodeling during sustained exercise training highlighting the sport-specific nature of exercise-induced cardiac remodeling (Reprinted with permission from Prog Cardiovasc Dis 2012;54:382)

The adaptations to exercise seen in the left ventricle do not occur in isolation. As previously described, endurance exercise requires a larger volume of blood in both the left and right ventricle (RV), thus the RV must also remodel to accommodate the volume load experienced during endurance training. As compared to sedentary controls, larger RV cavities and a trend toward thicker RV walls have been observed in endurance athletes on echocardiogram [24, 25] and have been confirmed on MRI studies [26], which suggest that RV enlargement parallels LV enlargement. Strength training appears to minimally impact RV architecture. Multiple comparisons of RV parameters in endurance and strength athletes have demonstrated no significant RV dilation in strength athletes [18, 24]. The relative immunity from RV remodeling in strength-trained athletes may be explained by the mitral valve shielding the pulmonary circulation and right side of the heart from the stress of systemic hypertension during isometric exercise.

Left atrial remodeling has also been observed in several echocardiographic studies. The largest study, conducted in 1,777 Italian athletes, demonstrated left atrial enlargement (anterior/posterior diameter >40 mm) in 20 % of athletes [27]. D’Andrea et al. [28] confirmed a high prevalence of left atrial enlargement in endurance-trained athletes. Left atrial enlargement has also been associated with the cumulative lifetime exercise training hours [29]. The clinical implications of left atrial enlargement have been one mechanism postulated for the increased prevalence of atrial fibrillation observed in older endurance athletes.

Diagnosis and Management of Athlete-Specific Cardiovascular Issues

While trained athletes are traditionally viewed as the standard bearers of health, they are not fully protected from cardiovascular disease. Athletes typically present to medical attention either as asymptomatic individuals with structural or functional abnormalities or after development of symptoms suggestive of cardiovascular disease during sport participation. While general fundamentals of patient care should still apply to athletes, there exist unique aspects to the care of the athletic population.

Additional components to a standard medical history are critical to a complete history in an athlete. The athlete’s prior and current training history should be obtained including (1) characterization of prior athletic achievements that can be useful in assessing the athlete’s competitive caliber as well as current fitness level, (2) recent training regimen, and (3) plans for future competitions. The physiologic adaptations involved in the “athlete’s heart” do not occur immediately and require a certain degree of training frequency and intensity, thus an exercise training history is critical in evaluating whether the cardiovascular structural findings are adaptive or pathologic. If the athlete is presenting with new or recent symptoms, it is important to assess for any changes in the athlete’s training habits, diet, or substance use that may correlate with the development of symptoms.

With a recent heightened awareness of sudden cardiac death in athletes after several highly publicized events, athletes presenting for cardiology evaluation should be screened for diseases that increase the risk of sudden cardiac death. A family history of sudden cardiac death is a major risk factor, and a detailed family history is essential. Specific components of the family history include any sudden or unexplained accidents in family members especially at a young age, a history of syncope, and/or any family members with implanted devices (e.g., pacemaker or implantable cardioverter-defibrillator).

In modern competitive athletics, pressure from media, sponsors, and fans for record-breaking performances has resulted in need to push the boundaries of athletic performance. This has led to marked increases in the use of cutting edge pharmacology including the use of illicit substances. Thus, a comprehensive medical history in the athletic patient includes questions focused on drug or supplement use. As with all patients, athletes of all ages should be routinely questioned about use of illicit drugs including traditional drugs of abuse (marijuana, cocaine, alcohol, etc.) as well as use of any performance-enhancing agents (PEAs). In addition to intentional use of PEAs, it is also important to evaluate the ingredient list of any supplement an athlete may be consuming. There is a comprehensive list of medications and substances banned in athletes published by The World Anti-Doping Agency [30], and athletes may be unintentionally using a banned substance in a supplement or over-the-counter medication. Anabolic steroids are the most widely used PEAs and previously have been shown to have deleterious cardiovascular effects such as dyslipidemia, exaggerated blood pressure response, and myocardial dysfunction [31, 32, 33]. Sport-specific considerations regarding PEA use should also be considered, for example, power sports, such as weight lifting or bodybuilding, tend to have higher use of anabolic steroids or nonsteroidal muscle mass growth stimulators such as human growth hormone and creatine. Long-term effects of the nonsteroidal muscle mass growth stimulators have been less studied. Athletes in endurance sports such as cycling have a greater likelihood of using erythropoietic stimulants that have been linked to complications such as microvascular myocardial infarction from excessive red cell mass. Stimulant use from prescription medications, such as methylphenidate, as well as over-the-counter use of caffeine or herbal stimulants has been increasing in competitive athletes and should also be specifically questioned, especially in athletes presenting with complaints such as palpitations.

Chest Pain

Within the younger population (<35 years) of highly trained athletes, cardiac causes of chest pain are relatively uncommon (<6 %) but can be life-threatening when present [34]. Table 20.1 lists clinical features that should raise concern for a cardiac cause of chest pain, and Table 20.2 lists cardiac causes of chest pain in athletes. When evaluating a population of athletes over age 35, these cardiovascular causes should be at the forefront of consideration. While regular physical exertion has been linked to decreased incidence of athlerosclerotic coronary artery disease (CAD) [35, 36, 37], athletic individuals are still at risk of cardiac events. Indeed, CAD is a leading cause of exercise-related cardiac events in adults over age 30, with an absolute risk of sudden cardiac death associated with vigorous physical exertion of approximately 1 per 200,000–250,000 healthy young individuals [38, 39]. A recent review of cardiac arrests in long-distance runners demonstrated a low overall risk of cardiac arrest (incidence rate, 0.54 per 100,000 participants) with the highest risk group comprised of male marathon runners [38]. Optimal care of the athletic patient with CAD is still being defined primarily based upon extrapolation from guidelines for care of the general population [40, 41] as well as participation guidelines for athletes such as the thirty seventh Bethesda Conference [42].
Table 20.1

Concerning features in medical history for athlete presenting with chest pain

Concerning clinical features in athlete with chest pain

Syncope or near syncope with chest pain (especially in setting of exercise)

Family history of sudden cardiac death

Electrocardiographic abnormalities not consistent with exercise-induced cardiac remodeling

Murmur on exam consistent with aortic stenosis or hypertrophic cardiomyopathy

Personal or family history of congenital abnormalities such as anomalous coronary arteries

Table 20.2

Cardiac causes of exertional chest pain in athletes

Cardiac causes of chest pain in athletes

Coronary artery disorders


 Anomalous origin of coronary artery

 Coronary artery dissection

 Myocardial bridging

Valvular disorders

 Aortic stenosis

 Mitral stenosis

 Mitral valve prolapse

Myocardial disorders

 Hypertrophic cardiomyopathy


Aortic disorders

 Aortic dissection

Electrophysiologic disorders

 Supraventricular arrhythmias (atrial fibrillation, Wolff-Parkinson-White syndrome, AVNRT)

AVNRT atrioventricular reentrant nodal tachycardia

In general, the care of athletes presenting with symptoms of potential cardiac cause, such as chest discomfort, dyspnea, or decreased exercise tolerance, should be evaluated according to contemporary guidelines [40, 41]. As previously described, a thorough initial evaluation of athletes presenting with symptoms of chest pain should include a detailed history, especially a training history, family history of sudden death, medication, supplement, and/or PEA use history. It is important to note that athletes may minimize their symptoms to avoid being restricted from competition and that many athletes and medical personnel ignore exertion-related complaints such as chest discomfort or dyspnea within the first 5 min of exercise (“warm-up” angina), exertion-related heartburn, and backache. Other key components of the chest pain history include characterization, timing, relation to exertion, alleviating/exacerbating factors, and any associated symptoms.

Aside from atherosclerotic coronary disease, the differential diagnosis of chest pain in an athlete includes other coronary artery pathologies as listed in Table 20.2. It is important to have a high index of suspicion for congenital coronary artery anomalies because, although rare in the general population (detected in <1 % of individuals at coronary angiography) [43], they have been shown to account for 15–20 % of sudden death events in athletes [44, 45, 46]. There are multiple other potential etiologies aside from coronary pathology for chest pain in an athlete, and it is important to consider other organ systems as well as the athlete’s particular sport during the evaluation. Common noncardiac causes of chest pain include musculoskeletal disease, trauma, infectious/inflammatory processes, and gastroesophageal reflux disease (GERD) [34, 47]. Table 20.3 details clinical features and specific athletes at risk for noncardiac causes of chest pain. Other miscellaneous and infrequent causes include sickle cell disease with chest pain resulting from decreased carrying capacity of erythrocytes in high-output states, pregnancy in the female athlete with new onset chest pain and exercise intolerance, use of drugs of abuse (cocaine, anabolic steroids, and stimulants) [47], and eating disorders involving purging that can cause conditions such as esophagitis and Mallory-Weiss tears.
Table 20.3

Noncardiac causes of chest pain



Physical exam



Athletes at risk

Return to competition


Rib fracture

Direct blunt trauma, pleuritic pain

Splinting, tenderness to palpation, bony crepitus, muscle spasm, ecchymosis

CXR to assess for associated injury (PTX, hemothorax, liver laceration), rib detail radiograph

Pain control, intercostal nerve blocks acutely, incentive spirometry

Contact sports (e.g., football, boxing, hockey)

When pain controlled, contact sports should wear flak jacket for 4–6 weeks

Rib stress fracture

Vague chest wall pain progresses to point tenderness

Splinting, tenderness to palpation

Bone scan more sensitive than CXR

Rest and analgesia, encourage deep breaths to avoid atelectasis

Rowers (incidence 12 %), throwing sports, weight lifting

When pain controlled


Rib pain 2–5 at junction of rib and sternum, provoked by movement

Reproducible pain with direct pressure over costochondral junction

History and exam

Reassurance, NSAIDs

Any, usually younger

When pain controlled

Rib subluxation

Increased mobility of posterior articulation, rib may slip off transverse process, pleuritic posterior pain

Posterior pain, radiates along rib, tender over affected area

History and exam, may consider rib films

Rest and analgesia, may require physical manipulation

Rowers, butterfly swimmers, gymnasts

When rib no longer subluxed and pain adequately controlled

Slipping rib syndrome

Pain from increased mobility of anterior ribs 8–10, irritation of intercostal nerve, refers to abdomen or ant chest wall

Sharp pain for seconds, followed by aching pain for days

“Hooking maneuver” – fingers are hooked under the ribs at the costal margin and the ribs are gently pulled forward

Rest and analgesia

Women > men, mean age 40

When pain controlled



Exertional chest tightness, shortness of breath, cough, wheezing, start minutes after exercise or in recovery

Prolonged expiratory phase, +/− wheezing

Clinical history, negative cardiac workup, spirometry (possibly pre and post exercise) +/− bronchodilator trial

Inhaled bronchodilator

Cold environment sports (ice hockey, figure skating), endurance athletes

After negative cardiac workup, after inhaled bronchodilator prophylactic trial


Spontaneous (tall, thin body habitus, + family hx) or post trauma

Decreased or absent breath sounds, hyperresonance to percussion (tension PTX = absent breath sounds, elevated JVP, hypotension)

Clinical history, exam, AP inspiratory film, expiratory film if not seen

Small apical can be observed or catheter aspiration. Moderate to large require chest tube or those causing symptoms or increasing size

Weight lifting, running, scuba. Risk factors: smoking, substance abuse

Suggested time frame 4–6 weeks prior to contact sports, some case series football players returned within 2 weeks [48]

Pulmonary embolus

Acute chest pain, new wheeze, pleuritic pain, hemoptysis, dyspnea,

Wheeze, evidence of DVT on exam, tachycardia, tachypnea

Contrast chest CT, ventilation perfusion scan

Anticoagulation, consider fibrinolysis if hemodynamically significant

Athletes at risk for thrombosis – recent surgery or injury (leg trauma), family clotting history, women on OCPs

No specific guidelines, contact sports usually prohibited while on anticoagulation



Heartburn, chest/epigastric pain, belching, nausea, vomiting (50 % during heavy exercise, 90 % of fed runners during and postexercise)

Symptoms may only occur with exercise

History, can consider endoscopy or exercise test with pH probe to demonstrate reflux with exertion

Changes in training or diet habits. Avoid exercise after meals. Avoid high-calorie meals 3 h prior to exercise. Protein supplements decrease gastric emptying and caffeine lowers LES tone, may need to avoid. Trial of anti-reflux medication (PPI)

Runners, jumpers, weight lifters. NSAIDs can worsen

No restrictions but may need alteration in training method


Pulmonary contusion

Blunt injury to thorax. Dyspnea, hemoptysis in 50 %

Tachypnea, tachycardia, cyanosis, chest wall bruising, rales, decreased breath sounds

CXR findings variable: patchy infiltrates to consolidation 4–6 h post injury, CT more sensitive at early phase

Assess for associated morbidity, hospitalize, pulmonary toilet, pain management, may need mechanical ventilation (mortality 5–15 %)

Usually great force causing injury, fall from height or high velocity (cycling, motor sports)

No specific guidelines, consider when symptoms and imaging demonstrate resolution. Symptom guided return to activity

Cardiac contusion

Blunt chest trauma. Assoc complications: arrhythmia, CHF, shock, hemopericardium, tamponade. May be asymptomatic

Sinus tachycardia (70 %), hypotension. Varied presentation

ECG shows sinus tachycardia, PAC or PVC, AF, NSVT, RBBB, LBBB, IVCD. Cardiac biomarkers, echocardiography and radionuclide studies not helpful

Admit symptomatic patients and those with ECG changes for monitoring (arrhythmia within 12 h post injury)

Contact sports, any significant blunt trauma (fall/accident while cycling, motor sports)

Sport-specific guidelines do not exist. Depend on extent of cardiac injury

CXR chest radiograph, PTX pneumothorax, NSAIDs Nonsteroidal anti-inflammatory drugs, JVP jugular venous pressure, DVT deep vein thrombosis, CT computed tomography, OCPs oral contraceptive pills, LES lower esophageal sphincter, PPI proton pump inhibitor, ECG electrocardiograph, PAC premature atrial contraction, PVC premature ventricular contraction, AF atrial fibrillation, NSVT nonsustained ventricular tachycardia, RBBB right bundle-branch block, LBBB left bundle-branch block, IVCD intraventricular conduction delay

As part of the initial diagnostic evaluation in athletes presenting with chest pain, an electrocardiogram (ECG) should be obtained. It is important to note that athletes, especially endurance-trained athletes, may demonstrate more ECG abnormalities than are observed in more sedentary individuals. These features include resting sinus bradycardia, mild enlargement of cardiac chambers, early repolarization pattern (presence of a “J wave” at the junction of the QRS and ST segment [49] that has been associated with increased prevalence after intense physical training) [50], or increased voltage suggestive of left ventricular hypertrophy (LVH) [51, 52]. Further workup based on history and physical may include exercise testing, especially if exertional symptoms are described. As some of the characteristic ECG findings in athletes (e.g., LVH) can lead to false-positive results during exercise ECG testing, the addition of an imaging modality such as echocardiography or nuclear scintigraphy may be required [40]. Exercise stress testing in athletes should be performed to maximal exercise capacity and not terminated prematurely due to heart rate. While the Bruce protocol is easily performed and well tolerated by most athletes, athletes who experience symptoms only during their particular activity may need specialized exercise testing designed to simulate their primary sporting activity. Further diagnostic evaluation of suspected CAD after initial history, examination, ECG, and exercise testing may require definition of coronary anatomy by cardiac computed tomography (CT) or coronary angiography. Detection of coronary anomalies and determination of their physiologic relevance requires the use of coronary imaging studies including cardiac CT, cardiac magnetic resonance (CMR), or conventional coronary angiography coupled with exercise stress testing.

The diagnosis of atherosclerotic CAD is defined as follows: (1) history of myocardial infarction (MI); (2) history suggesting angina pectoris, with objective evidence of inducible ischemia; or (3) coronary atherosclerosis demonstrated on imaging (coronary angiogram, CMR, cardiac CT) [42]. Once an athlete has been diagnosed with CAD, management consists of aggressive risk factor modification and risk stratification to guide exercise advice. Secondary prevention of an athlerosclerotic event involves antiplatelet therapy, antihypertensive therapy, and lipid-lowering therapy [42, 43, 53]. As with the general population, the mainstay of antiplatelet therapy is aspirin with addition of thienopyridines in patients who have experienced an acute coronary syndrome (ACS) or coronary revascularization [54, 55, 56]. In athletes participating in contact sports, the potential risk of hemorrhage on dual antiplatelet therapy should be discussed but is not an absolute contraindication to participation in certain types of sports [53]. For antihypertensive therapy in athletes, vasodilators including angiotensin-converting enzyme inhibitors (ACE-I) and calcium channel blockers are the primary initial medications as they are usually well tolerated. Adjunctive diuretic therapy may be useful but should be administered with caution in endurance athletes prone to exertional dehydration. While β (beta)-blockers have been shown to reduce recurrent events in patients with CAD (especially in setting of reduced left ventricular [LV] ejection fraction [EF]), they are less effective antihypertensive agents and may decrease athletic performance in endurance athletes. However, in athletes with impaired left ventricular function, β (beta)-blockers may be a reasonable strategy [54]. For all patients following ACS, guidelines recommend β (beta)-blockers [57], but for athletes with preserved EF, the negative performance effects may result in decreased adherence. Thus, use of β (beta)-blockers should be tailored on an individualized basis [53]. Lipid-lowering therapy is another core tenant of risk factor modification and primarily involves the use of statins. Recommendations for goal LDL levels in athletic populations are the same as the general population (LDL <70 mg/dL following ACS or 25 % reduction from baseline) [54]. It must be noted that statins commonly cause myalgias, with an increased prevalence in physically active individuals [58] and athletes [59, 60], potentially resulting from augmentation of exercise-related muscle injury. Thus, statin use as a maintenance medication in athletes may be difficult requiring multiple trials, different potency statins, or alternative dosing regimens. Reducing the lipid content of atherosclerotic plaques may help stabilize lipid-rich plaques at risk for exercise-induced rupture. A demonstrated benefit has been shown for early aggressive statin treatment following an ACS event even if statin therapy later needs to be discontinued [61], which has resulted in some experts recommending restriction from aggressive training and competition for 2 years following an ACS event with reduction of LDL to lowest level tolerated [53].

For the athletic patient with CAD as previously defined, comprehensive risk stratification should be performed prior to returning to training or competition. Patients are determined to be at mildly increased risk if they demonstrate the following: (1) preserved LV EF, (2) normal exercise tolerance for age, (3) absence of exercise-induced ischemia or complex ventricular arrhythmia, (4) absence of hemodynamically significant stenosis (>50 % luminal narrowing), and (5) successful revascularization [42]. Such patients can participate in most sports at a moderate to high-intensity level. In contrast, patients with high-risk features may require restriction to low dynamic and low/moderate static competitive sports and should be counseled to avoid intensely competitive situations. Patients at substantially increased risk (those with impaired LV EF, evidence of exercise-induced ischemia or complex ventricular arrhythmia, or hemodynamically significant stenosis [luminal narrowing >50 %]) should be restricted to low-intensity competitive sports [42]. Athletes with a coronary anomaly and inducible myocardial ischemia should be restricted from activity until surgical correction [43].


Palpitations, the awareness of forceful, rapid, or irregular heartbeats, are common among trained athletes. Palpitations and benign arrhythmias can be found in younger (school-age) athletic populations and when noted are unlikely to require restriction from activity [62]. In contrast, the complaint of palpitations in older and highly trained athletes is more common [63]. While the majority of palpitations are considered benign, certain conditions such as high premature ventricular contraction (PVC) burden (>2,000 PVCs in 24 h), atrial fibrillation, and exercise-induced palpitations may reflect underlying heart disease or an arrhythmia/conduction abnormality and should be evaluated [64]. The differential diagnosis of possible medical conditions contributing to palpitations and arrhythmias in athletes (Table 20.4) is broad, and diagnosis usually relies on ECG documentation of arrhythmia via either long-term ambulatory monitoring or exercise testing. Diagnosis can be complicated by the fact that both bradyarrhythmias and tachyarrhythmias have been documented in trained athletes.
Table 20.4

Medical conditions contributing to arrhythmias

Medical conditions contributing to arrhythmia

Coronary artery disease

Valvular heart disease

Cardiomyopathy (including HCM, ARVC)


Long QT syndrome

Brugada syndrome


Electrolyte abnormalities


Thyroid abnormalities

Hypo- or hyperglycemia


Pulmonary disease (contributes to multifocal atrial tachycardia)

Autonomic neuropathies (e.g., postural orthostatic tachycardia syndrome)

HCM hypertrophic cardiomyopathy, ARVC arrhythmogenic right ventricular cardiomyopathy

Athletes often demonstrate bradyarrhythmias, including resting sinus bradycardia (which may reflect cardiovascular fitness), junctional bradycardia, first-degree atrioventricular (AV) block, and Mobitz type I AV block. Resting heart rates (HRs) during sleep may demonstrate profound bradycardia, which reflects heightened parasympathetic activity or increased vagal tone and are not considered pathologic. It has also been suggested that intrinsic sinoatrial slowing may be a result of repeated exercise training [65, 66] and former endurance athletes may demonstrate intrinsic sinus node disease years after their peak training performances.

Tachyarrhythmias, particularly atrial fibrillation, can be the source of arrhythmia-related complaints in athletes. In one study of Italian elite athletes with a history of palpitations, atrial fibrillation was the cause in 40 % of patients [67]. Multiple studies have suggested that athletes, especially older endurance sport athletes, are at increased risk of developing atrial fibrillation both during their periods of active training as well as years after their high-intensity training [67, 68, 69, 70, 71]. Multiple potential mechanisms have been postulated to account for the observed increased frequency of atrial fibrillation in athletes including the following: exercise-induced LA remodeling [27, 72], systemic inflammation [70, 73], augmentation of vagal tone which shortens atrial refractory period facilitating reentry [70], and increased sympathetic activity during exercise. Other supraventricular arrhythmias such as AV nodal reentrant tachycardia, AV reciprocating tachycardia, and atrial tachycardias are not more common in athletes.

Premature atrial contractions (PACs) and PVCs as well as nonsustained ventricular tachycardia (NSVT), a burst of ventricular activity less than 30 s with spontaneous return to sinus rhythm, have all been observed in trained athletes. Premature beats are another common reason for athletes to present with palpitations. As athletes are usually lean and felt to be “in tune” with their bodies, they may have a heightened sensitivity to premature beats. It is important to assess the frequency of PVCs on Holter monitor as well as exclude structural heart disease and evaluate the impact of exercise. The presence of structural heart disease or frequent complex ventricular arrhythmias during exercise in structurally normal hearts may require further testing to exclude conditions such as CAD, arrhythmogenic right ventricular cardiomyopathy (ARVC), or catecholaminergic polymorphic ventricular tachycardia (CPVT) [74]. However, most patients with PVCs have a benign prognosis. In one study of trained Italian athletes, 30 % of the athletes noted to have more than 2,000 PVCs in 24 h were found to have underlying heart disease [63]. In athletes without structural heart disease, especially those with PVCs suppressed by exercise, premature beats have not been related to sudden cardiac death. The frequency of PVCs in both the population of athletes with and without structural heart disease has decreased after deconditioning, which may be useful in treating symptomatic athletes [75]. Reassuring data have also been published regarding the benign nature of NSVT in athletes without structural heart disease [66]. US guidelines recommend no restriction on activity in athletes without structural heart disease or symptoms [74].

While no specific recommendations for the evaluation and management of palpitations in an athlete exist, guidelines have focused on recommendations for specific arrhythmias [74, 76]. Athletes presenting with palpitations should have a thorough history and physical focused on timing of palpitations, relation to exertion, associated symptoms, family history of sudden death, and dietary/supplement intake (e.g., caffeine). Table 20.5 lists the drugs and medications that can contribute to palpitations and/or arrhythmias in athletes. Further diagnostic evaluation of the athlete with symptomatic palpitations, tachyarrhythmias, or frequent PVCs should include an assessment for structural and valvular heart disease as well as exclusion of metabolic causes such as hyperthyroidism or hypoglycemia. With frequent or easily reproducible symptoms, a Holter monitor during the athlete’s specific exercise may be useful in diagnosis. Exercise testing may need to be adapted to the athlete’s specific activity in order to simulate the conditions in which the arrhythmia is experienced, for instance, mode of activity or rate of workload intensity may need to be altered from conventional exercise testing.
Table 20.5

Drugs contributing to arrhythmias

Drugs contributing to arrhythmia

QT prolonging agents (antipsychotics, antibiotics, etc.)



Over-the-counter drugs (e.g., pseudoephedrine)

Supplements with stimulants (ephedra, bitter orange, guarana)

Anabolic steroids

Illicit drugs (e.g., cocaine)

Management of athletes with arrhythmias depends on the underlying etiology of the arrhythmia and whether it occurs in fast heart rate conditions (i.e., exercise) or slow heart rate conditions (i.e., sleep, exercise recovery). The management of bradyarrhythmias in the athlete primarily consists of reassurance and documentation of an adequate chronotropic response to exercise. Higher-grade AV block such as Mobitz II or complete heart block is unusual in athletes and should be considered pathologic, likely requiring a pacemaker [74, 77].

The management of tachyarrhythmias in athletes varies with specific etiology and encompasses education, medication, and invasive treatment (catheter ablation). Athletes should be educated on avoidance of drugs that can precipitate tachyarrhythmias (e.g., cocaine, pseudoephedrine). In athletes with supraventricular arrhythmias such as atrial fibrillation, management with nodal agents such as β (beta)-blockers (BB) and calcium channel blockers (CCB) may minimize symptoms but does not affect the frequency of atrial fibrillation episodes. As these agents affect the heart rate both at rest and during exercise, they may reduce exercise capacity in some individuals. In some competitive athletes, it should be noted that agents such as BB may be banned [30]. Class Ic antiarrhythmic agents, such as flecainide or propafenone, may be effective methods of maintaining sinus rhythm. These agents increase AV conduction, thus they usually require a nodal agent to counteract potential accelerated ventricular response in setting of atrial flutter. A “pill in the pocket” strategy using either flecainide or propafenone to abort an episode of symptomatic atrial fibrillation may be an attractive option for athletes who do not wish to take a medication daily [64]. Catheter ablation of some arrhythmias may be preferable to drug treatment in some athletes, although this has only been studied in small populations of athletes with atrial fibrillation [73, 78, 79]. In the setting of Wolff-Parkinson-White (WPW) syndrome, if the conduction through the accessory pathway is very rapid (able to conduct at heart rates greater than 240), patients are felt to be at risk of sudden death and curative ablation is recommended [80, 81]. In some cases, athletes whose arrhythmia has been successfully ablated can return to athletics within days if an easily inducible arrhythmia prior to ablation is unable to be induced post-ablation during isoproterenol administration. Consensus opinions regarding return to play for various arrhythmias have been established [74].


In both the athletic and general population, syncope is a common complaint. Syncope is defined as the transient loss of consciousness accompanied by loss of postural tone with spontaneous recovery. Whereas “benign” forms of syncope, including neurally mediated syncope (NMS), often require no evaluation in the general population, syncope in an athlete should always raise concern, especially when syncope occurs during exertion. Determining the specific cause of syncope is not possible in up to ~35 % of cases [82]. Thus, the most important aspect of evaluating a syncopal episode in an athlete is to rule out underlying cardiac etiologies that can cause sudden cardiac death, and athletes may need to be withheld from athletic participation until cardiac pathology has been excluded [74, 76].

The majority of syncope in athletes is unrelated to exercise or occurs postexercise. As seen in one cohort of 7,568 athletes undergoing pre-participation screening, 6.2 % of patients reported a syncopal episode within the last 5 years. In this series, most episodes were not related to exertion, 12 % occurred post-exertion, and 1.3 % were during exercise [83]. The most common cause of syncope in athletes is NMS, and the vast majority of post-exertional syncope is neurally mediated. In normal physiology, venous pooling (from standing, exercise, etc.) causes decreased venous return to the right ventricle, and the body compensates by increasing heart rate, contractility, and peripheral vascular resistance to augment cardiac output, thereby increasing preload and venous return [84, 85]. During exercise, increased sympathetic stimulation raises heart rate and diastolic blood pressure increasing cardiac output, which is distributed to skeletal muscle. This preload-dependent increase in cardiac output is maintained by peripheral muscle activity returning volume to the heart, functioning in effect as a “muscle pump.” With abrupt cessation of exercise, the muscle pump ceases and the resulting sudden fall in venous return produces a vigorous contraction in a relatively empty right ventricle stimulating mechanoreceptors that trigger a cardiac depressor reflex resulting in bradycardia and hypotension [80]. Reductions in heart rate and blood pressure combined with decreased venous return ultimately cause decreased cerebral perfusion and syncope.

The history and physical examination are the most essential part of the syncope evaluation and can identify the etiology in about 45 % of cases in which a cause is found [82]. Syncope during exertion has many potential causes (Table 20.6). History taking in syncope can be difficult because the patient often has some degree of amnesia for the event. In athletes this may be even more challenging as symptoms may be withheld due to fear of being removed from competition. Thus, it is important to question bystanders and witnesses and/or obtain any medical records from emergency personnel. The salient historical features of a syncopal episode include the following: any prodrome, inciting factors and the activity being undertaken prior to the episode, duration of syncope, any muscular movements during LOC and their initiation, and post-syncope symptoms such as confusion or bowel/bladder incontinence [86, 87, 88, 89, 90]. In addition to a detailed description of the event, a thorough patient history should also be obtained with particular attention to any prior history of syncope, any personal or family history of cardiac problems or sudden death, risk factors for cardiac disease, and a detailed medication list including any over-the-counter supplements, illicit drugs, or PEAs. Important factors in the physical examination of the athlete with syncope include complete vital signs, including orthostatic vital signs as well as blood pressure in both upper extremities and one lower extremity [76]. Careful vascular and neurologic exams may reveal findings suggestive of particular causes of syncope. Cardiac auscultation should include positional maneuvers such as standing, squatting, postexercise, and Valsalva to elicit dynamic changes seen in cardiomyopathies such as hypertrophic cardiomyopathy (HCM) or valve disease such as aortic stenosis or mitral stenosis. Table 20.7 describes clinical features that may suggest a specific etiology.
Table 20.6

Differential diagnosis of exertional syncope

Potential causes of exercise-induced syncope

Aortic stenosis

Hypertrophic cardiomyopathy

Mitral stenosis

Pulmonary hypertension

Ischemia from coronary artery disease

Ischemia from anomalous coronary artery disease


Brugada syndrome

Cardiac dilatation or depressed cardiac function

Catecholamine-dependent polymorphic ventricular tachycardia

Commotio cordis


Eating disorders


Sick sinus syndrome

Ventricular tachycardia/ventricular fibrillation

Ventricular preexcitation (Wolff-Parkinson-White)

Vasodepressor reflex

Table 20.7

Clinical features suggestive of etiology of syncope

Finding on history or exam

Suggested diagnoses

Occurs with micturition, defecation, cough, deglutition, playing brass instrument, weight lifting

Neurally mediated syncope/situational syncope

Associated with throat or facial pain (glossopharyngeal or trigeminal neuralgia)

Neurally mediated syncope/neuralgia

Occurs within an hour after eating

Neurally mediated syncope/postprandial hypotension

Occurred with prolonged standing

Neurally mediated syncope/vasovagal syncope

Associated with pain, fear, and unpleasant sight, smell, or sound

Neurally mediated syncope/vasovagal syncope

Occur in warm or crowded environment

Neurally mediated syncope/vasovagal syncope

Well-trained athlete with structurally normal heart after exertion

Neurally mediated syncope/vasovagal syncope

Tonic-clonic movements short (<15 s) and occur after loss of consciousness

Neurally mediated syncope/vasovagal syncope

Tonic-clonic movements prolonged and initiates during or prior to loss of consciousness


Syncope associated with tongue biting, aching muscles, and prolonged confusion


Occurs upon standing

Orthostatic hypotension

Taking one or more antihypertensive medications (especially polypharmacy in elderly)

Drug-induced syncope

Multiple medications prolonging QT or causing bradycardia

Drug-induced syncope

Associated with vertigo, dysarthria, diplopia

TIA, stroke, vertebrobasilar insufficiency

Blood pressure difference between arms

Subclavian steal or aortic dissection

Syncope during arm exercise (e.g., painting a fence)

Subclavian steal

Occurs with change in position (upright to supine, bending over) +/− murmur that also varies with position

Atrial myxoma, thrombus

Family history of sudden cardiac death

Long QT, Brugada, HCM

Deaf patient who experiences syncope after effort or strong emotion

Long QT syndrome

Triggered by laughter or strong emotions with normal cardiac evaluation


Child <5 years old after frustrating episode or injury

Breath holding spell

Diabetic who skipped meals


TIA transient ischemic attack, HCM hypertrophic cardiomyopathy

The initial evaluation of athletes with syncope always includes an ECG to exclude arrhythmias and cardiomyopathy. Careful examination of the ECG in an athletic patient (Table 20.8) is important because several ECG findings can be suggestive of a cardiac cause. Many features that could be considered abnormal in the general population are commonly observed in highly trained athletes and should not be considered as a cause of syncope [50, 91, 92].
Table 20.8

Athlete ECG abnormalities and relation to syncope

Observed in trained athletes/related to training

Suggestive of arrhythmogenic syncope

Unrelated to training

Suggestive of arrhythmogenic syncope

Sinus bradycardia

Rare cause in athlete

Second (Mobitz II) or third-degree AV block


First-degree AV block


T-wave inversion


Incomplete right bundle-branch block


Pathological Q waves


Early repolarization


Left atrial enlargement


Isolated LVH criteria by QRS voltage


Left-axis deviation/left anterior hemiblock



Right-axis deviation/left posterior hemiblock



Right ventricular hypertrophy



Preexcitation (i.e., WPW syndrome)



Complete left bundle-branch block or right bundle-branch block



Abnormal QT interval



Brugada pattern



T-wave inversion V1–V3, epsilon waves, and ventricular late potentials (i.e., ARVC)


AV atrioventricular, LVH left ventricular hypertrophy, WPW Wolff-Parkinson-White, ARVC arrhythmogenic right ventricular cardiomyopathy

After the initial evaluation of history, physical, and ECG, there should be a low threshold for obtaining an echocardiogram and in the case of exertional syncope, an exercise test (after echocardiography) [76]. The leading causes of death in American athletes under age 35 include conditions that may present with syncope such as HCM, anomalous coronary arteries, myocarditis, and ARVC. An echocardiogram may be useful in detecting these conditions or other structural cardiac problems [44, 45, 93]. A detailed assessment including left ventricular and right ventricular size and function, wall thickness, valve lesions, aortic root dilation, elevated right ventricular systolic pressure, and coronary ostia should be conducted. As discussed previously, exercise testing protocols should simulate athlete’s training conditions to maximize likelihood of eliciting symptoms [80, 94].

If exercise testing does not reveal any symptoms or reproduce syncope, long-term ambulatory ECG monitoring may be needed. For patients with frequent and easily reproducible symptoms, a Holter monitor worn for 24–48 h may be useful in capturing the episode. However, Holter monitoring is generally low yield when symptoms are intermittent and either an external event monitor or implantable loop recorder (ILR) is recommended. Noncompliance can be an issue with external monitors, especially in athletes in whom the electrodes and monitor may interfere with a training regimen [76]. Therefore, in athletes the placement of an ILR, which is a subcutaneous monitor that automatically records arrhythmias, may be advantageous [80].

Additional diagnostic testing modalities such as tilt-table testing, electrophysiologic (EP) study, and advanced imaging have limited roles in the evaluation of unexplained syncope in athletes due to poor sensitivity and specificity as well as potential for identifying abnormalities unrelated to presenting symptoms. Athletes have a high rate of positive tilt tests, and the reproducibility of tilt tests has been markedly variable [80, 87] such that widespread use is not recommended. The diagnostic utility of EP studies for evaluation of bradyarrhythmias is limited in athletes due to their high vagal tone. In tachyarrhythmias, the role of EP studies is for the confirmation and treatment (via catheter ablation) of specific suspected etiologies [81]. The role of advanced imaging in syncope should likewise be limited to evaluation of specific suspected etiologies, such as cardiac CT to evaluate for anomalous origin of the coronary arteries or aortic pathologies [80] or CMR for enhanced definition of cardiomyopathies, such as HCM or ARVC [95].

Management of syncope should be tailored to the specific etiology found on diagnostic testing. The focus of treatment in NMS involves recognition of pre-syncopal symptoms, avoidance of triggers, and instruction on counterpressure maneuvers (e.g., squatting, arm tensing, leg crossing) to abort orthostatic intolerance [81, 94, 96, 97]. In athletes with structurally normal hearts and NMS, volume and/or salt loading coupled with lower-extremity compression stockings is recommended. The role of pharmacologic therapy in NMS is limited; the best data from randomized controlled trials supports the use of midodrine [96]. Due to the potential for devastating consequences of even benign etiologies of syncope, such as NMS, in athletes participating in high-risk activities (e.g., diving, cycling) or those with minimal prodrome, these athletes may require more intense therapies or restriction from play. According to the thirty sixth Bethesda Conference, athletes with syncope attributed to arrhythmias may return to competition after they have been asymptomatic for 2–3 months following treatment and evaluation by a physician [74]. In patients with ventricular arrhythmia where ablation is not curative or an ICD is placed, moderate- and high-intensity sports as well as contact sports are not recommended [74]. However, there is variation in practice and some cardiologists allow sports participation for athletes with ICDs [98], and a large registry is currently following athletes with implantable devices [99]. Athletes with potentially life-threatening etiologies of syncope should be restricted from play. While the safe return to physical activity is paramount, it is important to consider the emotional, social, and/or financial ramifications from activity restriction in athletes.

Key Points

  • Athlete heart – distinct structural entity with sport-type/training-type specific changes:
    • Need to differentiate from pathologic causes of cardiac enlargement

  • Historical features:
    • Need to discuss training regimen and/or changes in athlete presenting with new symptoms

    • Need to routinely inquire about performance-enhancing agents

  • Chest pain, palpitations, or syncope with exertion are common in athletes and should be evaluated to exclude underlying cardiac disease.

  • Athletes should be restricted from training and competition during evaluation until the cardiac diseases associated with increased risk of sudden death are ruled out.

  • Management of cardiac conditions in athletes may require individualized treatment regimens as core medical therapies (e.g., statin or β (beta)-blockers) may have negative effects on performance resulting in decreased adherence.


  1. 1.
    Osler W. The principles and practice of medicine. New York: Appleton and Company; 1892.Google Scholar
  2. 2.
    Karpovich PV. Textbook fallacies regarding child’s heart. Res Quart. 1937;8:33.Google Scholar
  3. 3.
    Darling E. The effects of training: a study of the Harvard University crews. Boston Med Surg J. 1899;161:229–33.CrossRefGoogle Scholar
  4. 4.
    Henschen S. Skilauf und Skiwettlauf. Eine medizinische Sportstudie. Mitt Med Klinik Upsala. 1899;2:15–8.Google Scholar
  5. 5.
    Deutsch F, Kauf E. Heart and athletics. St. Louis: CV Mosby Company; 1927.Google Scholar
  6. 6.
    Baggish AL, Wood MJ. Athlete’s heart and cardiovascular care of the athlete: scientific and clinical update. Circulation. 2011;123:2723–35.PubMedCrossRefGoogle Scholar
  7. 7.
    Thompson PD, editor. Exercise and sports cardiology. New York: McGraw-Hill; 2001.Google Scholar
  8. 8.
    Thompson PD. Exercise prescription and proscription for patients with coronary artery disease. Circulation. 2005;112:2354–63.PubMedCrossRefGoogle Scholar
  9. 9.
    Astrand P, Rodahl K. Textbook of work physiology. New York: McGraw-Hill Book Company; 1977.Google Scholar
  10. 10.
    Jose AD, Collison D. The normal range and determinants of the intrinsic heart rate in man. Cardiovasc Res. 1970;4:160–7.PubMedCrossRefGoogle Scholar
  11. 11.
    Uusitalo AL, Uusitalo AJ, Rusko HK. Exhaustive endurance training for 6–9 weeks did not induce changes in intrinsic heart rate and cardiac autonomic modulation in female athletes. Int J Sports Med. 1998;19:532–40.PubMedCrossRefGoogle Scholar
  12. 12.
    Weiner RB, Baggish AL. Exercise-induced cardiac remodeling. Prog Cardiovasc Dis. 2012;54:380–6.PubMedCrossRefGoogle Scholar
  13. 13.
    Venerando A, Rulli V. Frequency morphology and meaning of the electrocardiographic anomalies found in Olympic marathon runners and walkers. J Sports Med Phys Fitness. 1964;50:135–41.PubMedGoogle Scholar
  14. 14.
    Roeske WR, O’Rourke RA, Klein A, Leopold G, Karliner JS. Noninvasive evaluation of ventricular hypertrophy in professional athletes. Circulation. 1976;53:286–91.PubMedCrossRefGoogle Scholar
  15. 15.
    Pelliccia A, Culasso F, Di Paolo FM, Maron BJ. Physiologic left ventricular cavity dilatation in elite athletes. Ann Intern Med. 1999;130:23–31.PubMedCrossRefGoogle Scholar
  16. 16.
    Pelliccia A, Maron BJ, Spataro A, Proschan MA, Spirito P. The upper limit of physiologic cardiac hypertrophy in highly trained elite athletes. N Engl J Med. 1991;324:295–301.PubMedCrossRefGoogle Scholar
  17. 17.
    Baggish AL, Yared K, Weiner RB, et al. Differences in cardiac parameters among elite rowers and subelite rowers. Med Sci Sports Exerc. 2010;42:1215–20.PubMedGoogle Scholar
  18. 18.
    Baggish AL, Wang F, Weiner RB, et al. Training-specific changes in cardiac structure and function: a prospective and longitudinal assessment of competitive athletes. J Appl Physiol. 2008;104:1121–8.PubMedCrossRefGoogle Scholar
  19. 19.
    Caso P, D’Andrea A, Galderisi M, et al. Pulsed Doppler tissue imaging in endurance athletes: relation between left ventricular preload and myocardial regional diastolic function. Am J Cardiol. 2000;85:1131–6.PubMedCrossRefGoogle Scholar
  20. 20.
    D’Andrea A, Cocchia R, Riegler L, et al. Left ventricular myocardial velocities and deformation indexes in top-level athletes. J Am Soc Echocardiogr. 2010;23:1281–8.PubMedCrossRefGoogle Scholar
  21. 21.
    Prasad A, Popovic ZB, Arbab-Zadeh A, et al. The effects of aging and physical activity on Doppler measures of diastolic function. Am J Cardiol. 2007;99:1629–36.PubMedCrossRefGoogle Scholar
  22. 22.
    Baggish AL, Yared K, Wang F, et al. The impact of endurance exercise training on left ventricular systolic mechanics. Am J Physiol Heart Circ Physiol. 2008;295:H1109–16.PubMedCrossRefGoogle Scholar
  23. 23.
    Weiner RB, Hutter Jr AM, Wang F, et al. The impact of endurance exercise training on left ventricular torsion. JACC Cardiovasc Imaging. 2010;3:1001–9.PubMedCrossRefGoogle Scholar
  24. 24.
    D’Andrea A, Riegler L, Golia E, et al. Range of right heart measurements in top-level athletes: the training impact. Int J Cardiol. 2013;164(1):48–57.PubMedCrossRefGoogle Scholar
  25. 25.
    Oxborough D, Sharma S, Shave R, et al. The right ventricle of the endurance athlete: the relationship between morphology and deformation. J Am Soc Echocardiogr. 2012;25:263–71.PubMedCrossRefGoogle Scholar
  26. 26.
    Scharhag J, Schneider G, Urhausen A, Rochette V, Kramann B, Kindermann W. Athlete’s heart: right and left ventricular mass and function in male endurance athletes and untrained individuals determined by magnetic resonance imaging. J Am Coll Cardiol. 2002;40:1856–63.PubMedCrossRefGoogle Scholar
  27. 27.
    Pelliccia A, Maron BJ, Di Paolo FM, et al. Prevalence and clinical significance of left atrial remodeling in competitive athletes. J Am Coll Cardiol. 2005;46:690–6.PubMedCrossRefGoogle Scholar
  28. 28.
    D’Andrea A, Riegler L, Cocchia R, et al. Left atrial volume index in highly trained athletes. Am Heart J. 2010;159:1155–61.PubMedCrossRefGoogle Scholar
  29. 29.
    Wilhelm M, Roten L, Tanner H, Wilhelm I, Schmid JP, Saner H. Atrial remodeling, autonomic tone, and lifetime training hours in nonelite athletes. Am J Cardiol. 2011;108:580–5.PubMedCrossRefGoogle Scholar
  30. 30.
    World Anti-doping agency. The World Anti-Doping Code: The 2013 Prohibited List. 2013; (accessed October 9, 2013).
  31. 31.
    Kiraly CL. Androgenic-anabolic steroid effects on serum and skin surface lipids, on red cells, and on liver enzymes. Int J Sports Med. 1988;9:249–52.PubMedCrossRefGoogle Scholar
  32. 32.
    Riebe D, Fernhall B, Thompson PD. The blood pressure response to exercise in anabolic steroid users. Med Sci Sports Exerc. 1992;24:633–7.PubMedCrossRefGoogle Scholar
  33. 33.
    Baggish AL, Weiner RB, Kanayama G, et al. Long-term anabolic-androgenic steroid use is associated with left ventricular dysfunction. Circ Heart Fail. 2010;3:472–6.PubMedCrossRefGoogle Scholar
  34. 34.
    Perron AD. Chest pain in athletes. Clin Sports Med. 2003;22:37–50.PubMedCrossRefGoogle Scholar
  35. 35.
    Leon AS, Connett J, Jacobs Jr DR, Rauramaa R. Leisure-time physical activity levels and risk of coronary heart disease and death. The multiple risk factor intervention trial. JAMA. 1987;258:2388–95.PubMedCrossRefGoogle Scholar
  36. 36.
    Blair SN, Kohl 3rd HW, Paffenbarger Jr RS, Clark DG, Cooper KH, Gibbons LW. Physical fitness and all-cause mortality. A prospective study of healthy men and women. JAMA. 1989;262:2395–401.PubMedCrossRefGoogle Scholar
  37. 37.
    Kannel WB, Wilson P, Blair SN. Epidemiological assessment of the role of physical activity and fitness in development of cardiovascular disease. Am Heart J. 1985;109:876–85.PubMedCrossRefGoogle Scholar
  38. 38.
    Kim JH, Malhotra R, Chiampas G, et al. Cardiac arrest during long-distance running races. N Engl J Med. 2012;366:130–40.PubMedCrossRefGoogle Scholar
  39. 39.
    Engelstein ED, Zipes DP. Sudden cardiac death. In: Alexander RW, Schlant RC, Fuster V, editors. The heart, arteries, and veins. New York: McGraw-Hill; 1998. p. 1081–112.Google Scholar
  40. 40.
    Gibbons RJ, Balady GJ, Bricker JT, et al. ACC/AHA 2002 guideline update for exercise testing: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to update the 1997 exercise testing guidelines). Circulation. 2002;106:1883–92.PubMedCrossRefGoogle Scholar
  41. 41.
    Medicine. ACoS. Guidelines for exercise testing and prescription. 7th ed. Baltimore: Lippincott Williams & Wilkins; 2005.Google Scholar
  42. 42.
    Thompson PD, Balady GJ, Chaitman BR, Clark LT, Levine BD, Myerburg RJ. Task force 6: coronary artery disease. J Am Coll Cardiol. 2005;45:1348–53.PubMedCrossRefGoogle Scholar
  43. 43.
    Baggish AL, Thompson PD. The Athlete’s heart 2007: diseases of the coronary circulation. Cardiol Clin. 2007;25:431–40, vi.PubMedCrossRefGoogle Scholar
  44. 44.
    Maron BJ, Epstein SE, Roberts WC. Causes of sudden death in competitive athletes. J Am Coll Cardiol. 1986;7:204–14.PubMedCrossRefGoogle Scholar
  45. 45.
    Maron BJ, Shirani J, Poliac LC, Mathenge R, Roberts WC, Mueller FO. Sudden death in young competitive athletes. Clinical, demographic, and pathological profiles. JAMA. 1996;276:199–204.PubMedCrossRefGoogle Scholar
  46. 46.
    Corrado D, Thiene G, Nava A, Rossi L, Pennelli N. Sudden death in young competitive athletes: clinicopathologic correlations in 22 cases. Am J Med. 1990;89:588–96.PubMedCrossRefGoogle Scholar
  47. 47.
    Singh AM, McGregor RS. Differential diagnosis of chest symptoms in the athlete. Clin Rev Allergy Immunol. 2005;29:87–96.PubMedCrossRefGoogle Scholar
  48. 48.
    Levy AS, Bassett F, Lintner S, Speer K. Pulmonary barotrauma: diagnosis in American football players. Three cases in three years. Am J Sports Med. 1996;24:227–9.PubMedCrossRefGoogle Scholar
  49. 49.
    Wellens HJ. Early repolarization revisited. N Engl J Med. 2008;358:2063–5.PubMedCrossRefGoogle Scholar
  50. 50.
    Noseworthy PA, Weiner R, Kim J, et al. Early repolarization pattern in competitive athletes: clinical correlates and the effects of exercise training. Circ Arrhythm Electrophysiol. 2011;4:432–40.PubMedCrossRefGoogle Scholar
  51. 51.
    Hanne-Paparo N, Drory Y, Schoenfeld Y, Shapira Y, Kellermann JJ. Common ECG changes in athletes. Cardiology. 1976;61:267–78.PubMedCrossRefGoogle Scholar
  52. 52.
    Huston TP, Puffer JC, Rodney WM. The athletic heart syndrome. N Engl J Med. 1985;313:24–32.PubMedCrossRefGoogle Scholar
  53. 53.
    Parker MW, Thompson PD. Assessment and management of atherosclerosis in the athletic patient. Prog Cardiovasc Dis. 2012;54:416–22.PubMedCrossRefGoogle Scholar
  54. 54.
    Kushner FG, Hand M, Smith Jr SC, et al. Focused updates: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction (updating the 2004 guideline and 2007 focused update) and ACC/AHA/SCAI guidelines on percutaneous coronary intervention (updating the 2005 guideline and 2007 focused update): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2009;2009(120):2271–306.CrossRefGoogle Scholar
  55. 55.
    Wright RS, Anderson JL, Adams CD, et al. ACCF/AHA focused update of the guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction (updating the 2007 guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2011;2011(123):2022–60.Google Scholar
  56. 56.
    Gibbons RJ, Abrams J, Chatterjee K, et al. ACC/AHA 2002 guideline update for the management of patients with chronic stable angina – summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (committee on the management of patients with chronic stable angina). Circulation. 2003;107:149–58.PubMedCrossRefGoogle Scholar
  57. 57.
    Smith Jr SC, Benjamin EJ, Bonow RO, et al. AHA/ACCF secondary prevention and risk reduction therapy for patients with coronary and other atherosclerotic vascular disease: 2011 update: a guideline from the American Heart Association and American College of Cardiology Foundation. Circulation. 2011;124:2458–73.PubMedCrossRefGoogle Scholar
  58. 58.
    Bruckert E, Hayem G, Dejager S, Yau C, Begaud B. Mild to moderate muscular symptoms with high-dosage statin therapy in hyperlipidemic patients – the PRIMO study. Cardiovasc Drugs Ther. 2005;19:403–14.PubMedCrossRefGoogle Scholar
  59. 59.
    Sinzinger H, O’Grady J. Professional athletes suffering from familial hypercholesterolaemia rarely tolerate statin treatment because of muscular problems. Br J Clin Pharmacol. 2004;57:525–8.PubMedCrossRefGoogle Scholar
  60. 60.
    Meador BM, Huey KA. Statin-associated myopathy and its exacerbation with exercise. Muscle Nerve. 2010;42:469–79.PubMedCrossRefGoogle Scholar
  61. 61.
    Ford I, Murray H, Packard CJ, Shepherd J, Macfarlane PW, Cobbe SM. Long-term follow-up of the West of Scotland coronary prevention study. N Engl J Med. 2007;357:1477–86.PubMedCrossRefGoogle Scholar
  62. 62.
    Fuller CM, McNulty CM, Spring DA, et al. Prospective screening of 5,615 high school athletes for risk of sudden cardiac death. Med Sci Sports Exerc. 1997;29:1131–8.PubMedCrossRefGoogle Scholar
  63. 63.
    Biffi A, Pelliccia A, Verdile L, et al. Long-term clinical significance of frequent and complex ventricular tachyarrhythmias in trained athletes. J Am Coll Cardiol. 2002;40:446–52.PubMedCrossRefGoogle Scholar
  64. 64.
    Lawless CE, Briner W. Palpitations in athletes. Sports Med. 2008;38:687–702.PubMedCrossRefGoogle Scholar
  65. 65.
    Stein R, Medeiros CM, Rosito GA, Zimerman LI, Ribeiro JP. Intrinsic sinus and atrioventricular node electrophysiologic adaptations in endurance athletes. J Am Coll Cardiol. 2002;39:1033–8.PubMedCrossRefGoogle Scholar
  66. 66.
    Baldesberger S, Bauersfeld U, Candinas R, et al. Sinus node disease and arrhythmias in the long-term follow-up of former professional cyclists. Eur Heart J. 2008;29:71–8.PubMedCrossRefGoogle Scholar
  67. 67.
    Furlanello F, Bertoldi A, Dallago M, et al. Atrial fibrillation in elite athletes. J Cardiovasc Electrophysiol. 1998;9:S63–8.PubMedGoogle Scholar
  68. 68.
    Abdulla J, Nielsen JR. Is the risk of atrial fibrillation higher in athletes than in the general population? A systematic review and meta-analysis. Europace. 2009;11:1156–9.PubMedCrossRefGoogle Scholar
  69. 69.
    Molina L, Mont L, Marrugat J, et al. Long-term endurance sport practice increases the incidence of lone atrial fibrillation in men: a follow-up study. Europace. 2008;10:618–23.PubMedCrossRefGoogle Scholar
  70. 70.
    Sorokin AV, Araujo CG, Zweibel S, Thompson PD. Atrial fibrillation in endurance-trained athletes. Br J Sports Med. 2011;45:185–8.PubMedCrossRefGoogle Scholar
  71. 71.
    Mont L, Elosua R, Brugada J. Endurance sport practice as a risk factor for atrial fibrillation and atrial flutter. Europace. 2009;11:11–7.PubMedCrossRefGoogle Scholar
  72. 72.
    Wilhelm M, Roten L, Tanner H, Schmid JP, Wilhelm I, Saner H. Long-term cardiac remodeling and arrhythmias in nonelite marathon runners. Am J Cardiol. 2012;110:129–35.PubMedCrossRefGoogle Scholar
  73. 73.
    Turagam MK, Velagapudi P, Kocheril AG. Atrial fibrillation in athletes. Am J Cardiol. 2012;109:296–302.PubMedCrossRefGoogle Scholar
  74. 74.
    Zipes DP, Ackerman MJ, Estes 3rd NA, Grant AO, Myerburg RJ, Van Hare G. Task force 7: arrhythmias. J Am Coll Cardiol. 2005;45:1354–63.PubMedCrossRefGoogle Scholar
  75. 75.
    Biffi A, Maron BJ, Verdile L, et al. Impact of physical deconditioning on ventricular tachyarrhythmias in trained athletes. J Am Coll Cardiol. 2004;44:1053–8.PubMedCrossRefGoogle Scholar
  76. 76.
    Brignole M, Alboni P, Benditt DG, et al. Guidelines on management (diagnosis and treatment) of syncope – update 2004. Europace. 2004;6:467–537.PubMedCrossRefGoogle Scholar
  77. 77.
    Barold SS, Padeletti L. Mobitz type II second-degree atrioventricular block in athletes: true or false? Br J Sports Med. 2011;45:687–90.PubMedCrossRefGoogle Scholar
  78. 78.
    Koopman P, Nuyens D, Garweg C, et al. Efficacy of radiofrequency catheter ablation in athletes with atrial fibrillation. Europace. 2011;13:1386–93.PubMedCrossRefGoogle Scholar
  79. 79.
    Kelly J, Kenny D, Martin RP, Stuart AG. Diagnosis and management of elite young athletes undergoing arrhythmia intervention. Arch Dis Child. 2011;96:21–4.PubMedCrossRefGoogle Scholar
  80. 80.
    Hastings JL, Levine BD. Syncope in the athletic patient. Prog Cardiovasc Dis. 2012;54:438–44.PubMedCrossRefGoogle Scholar
  81. 81.
    Link MS, Estes 3rd NA. How to manage athletes with syncope. Cardiol Clin. 2007;25:457–66, vii.PubMedCrossRefGoogle Scholar
  82. 82.
    Linzer M, Yang EH, Estes 3rd NA, Wang P, Vorperian VR, Kapoor WN. Diagnosing syncope. Part 1: value of history, physical examination, and electrocardiography. Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med. 1997;126:989–96.PubMedCrossRefGoogle Scholar
  83. 83.
    Colivicchi F, Ammirati F, Santini M. Epidemiology and prognostic implications of syncope in young competing athletes. Eur Heart J. 2004;25:1749–53.PubMedCrossRefGoogle Scholar
  84. 84.
    Freeman R. Clinical practice. Neurogenic orthostatic hypotension. N Engl J Med. 2008;358:615–24.PubMedCrossRefGoogle Scholar
  85. 85.
    Goldschlager N, Epstein AE, Grubb BP, et al. Etiologic considerations in the patient with syncope and an apparently normal heart. Arch Intern Med. 2003;163:151–62.PubMedCrossRefGoogle Scholar
  86. 86.
    Benditt DG, Remole S, Milstein S, Bailin S. Syncope: causes, clinical evaluation, and current therapy. Annu Rev Med. 1992;43:283–300.PubMedCrossRefGoogle Scholar
  87. 87.
    Calkins H, Seifert M, Morady F. Clinical presentation and long-term follow-up of athletes with exercise-induced vasodepressor syncope. Am Heart J. 1995;129:1159–64.PubMedCrossRefGoogle Scholar
  88. 88.
    Calkins H, Shyr Y, Frumin H, Schork A, Morady F. The value of the clinical history in the differentiation of syncope due to ventricular tachycardia, atrioventricular block, and neurocardiogenic syncope. Am J Med. 1995;98:365–73.PubMedCrossRefGoogle Scholar
  89. 89.
    Kapoor WN. Current evaluation and management of syncope. Circulation. 2002;106:1606–9.PubMedCrossRefGoogle Scholar
  90. 90.
    Sheldon R, Rose S, Ritchie D, et al. Historical criteria that distinguish syncope from seizures. J Am Coll Cardiol. 2002;40:142–8.PubMedCrossRefGoogle Scholar
  91. 91.
    Pelliccia A, Maron BJ, Culasso F, et al. Clinical significance of abnormal electrocardiographic patterns in trained athletes. Circulation. 2000;102:278–84.PubMedCrossRefGoogle Scholar
  92. 92.
    Lawless CE, Best TM. Electrocardiograms in athletes: interpretation and diagnostic accuracy. Med Sci Sports Exerc. 2008;40:787–98.PubMedCrossRefGoogle Scholar
  93. 93.
    Maron BJ, Doerer JJ, Haas TS, Tierney DM, Mueller FO. Sudden deaths in young competitive athletes: analysis of 1866 deaths in the United States, 1980–2006. Circulation. 2009;119:1085–92.PubMedCrossRefGoogle Scholar
  94. 94.
    Verma S, Hackel JG, Torrisi DJ, Nguyen T. Syncope in athletes: a guide to getting them back on their feet. J Fam Pract. 2007;56:545–50.PubMedGoogle Scholar
  95. 95.
    Prakken NH, Velthuis BK, Cramer MJ, Mosterd A. Advances in cardiac imaging: the role of magnetic resonance imaging and computed tomography in identifying athletes at risk. Br J Sports Med. 2009;43:677–84.PubMedCrossRefGoogle Scholar
  96. 96.
    Romme JJ, Reitsma JB, Black CN, et al. Drugs and pacemakers for vasovagal, carotid sinus and situational syncope. Cochrane Database Syst Rev. 2011:CD004194.Google Scholar
  97. 97.
    Benditt DG, Nguyen JT. Syncope: therapeutic approaches. J Am Coll Cardiol. 2009;53:1741–51.PubMedCrossRefGoogle Scholar
  98. 98.
    Heidbuchel H. Implantable cardioverter defibrillator therapy in athletes. Cardiol Clin. 2007;25:467–82, vii.PubMedCrossRefGoogle Scholar
  99. 99.
    Lampert R, Olshansky B, Heidbuchel H, et al. Safety of sports for athletes with implantable cardioverter-defibrillators: results of a prospective, multinational registry. Circulation. 2013;127:2021–2030.Google Scholar

Copyright information

© Springer-Verlag London 2014

Authors and Affiliations

  1. 1.Department of CardiologyMassachusetts General HospitalBostonUSA

Personalised recommendations