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Images from Thiene G, Corrado D, Basso C. Orphanet J Rare Dis. 2007;2:45. [Open access.] PMID: 18001465, PMCID: PMC2222049. [Creative Commons Attribution License 2.0 Generic (CC by 2.0).]

Sudden Cardiac Death in Athletes

Moira Davenport, MD | July 12, 2022 | Contributor Information

Regular athletic activity can result in structural cardiac changes. These changes may be adaptive, or they may lead to cardiac complications.

Sudden cardiac death is an unexpected death caused by a change in heart rhythm and the loss of heart function,[1] and its occurrence in athletic populations is becoming increasingly common.[2-4] The estimated annual incidence of sudden cardiac death in athletes ranges from 1 in 50,000 to 1 in 200,000-300,000.[1,5,6] Cases have been reported among male and female athletes from all sports. Therefore, it is imperative that physicians be familiar with the risk factors for and common causes of sudden cardiac death in this population.

The above images are from a 17-year-old asymptomatic male athlete who died suddenly during a soccer game. Left images: (a) 12-Lead electrocardiogram (ECG) showing inverted T waves up to V4. (b) Isolated premature ventricular beats. Right images (cardiac cross-sections): The magnetic resonance image (MRI) (top) and gross specimen (bottom) show right ventricular dilatation with anterior and posterior aneurysms.

Image from Mursleen A, Hartlage G, Patel A, Harrison EE, Morales C. Case Rep Cardiol. 2016;2016:7685360. [Open access.] PMID: 27478651, PMCID: PMC4958473. [CC 4.0 International (CC by 4.0.)]

Sudden Cardiac Death in Athletes

Moira Davenport, MD | July 12, 2022 | Contributor Information

The above images are three-dimensional (3D) reconstructions of the coronary vessels and their corresponding images with the heart in a young adult male. The right coronary artery arises from the left coronary sinus, a cardiac anomaly associated with sudden cardiac death.[7]

Mechanism

Several ECG changes are associated with regular athletic activity, including bradycardia, premature ventricular or atrial complexes (PVCs, PACs), left ventricular hypertrophy (LVH), J-point elevation, and first-degree atrioventricular (AV) block.

Ventricular tachycardia leading to ventricular fibrillation is the most common presenting rhythm in, as well as the most common fatal rhythm among, athletes who suffer sudden cardiac death.[1,5,8,9] PVCs are often the initiating factor for ventricular tachycardias and ventricular fibrillation. It remains unclear whether the conduction abnormality itself is the triggering factor, or if inadequate output is the etiology for sudden cardiac death; these two factors may be interrelated.

Image from Wikimedia Commons/Bart.

Sudden Cardiac Death in Athletes

Moira Davenport, MD | July 12, 2022 | Contributor Information

Causes

Structural changes in the heart can be physiologic or pathologic, although overlap between the two etiologies is possible. Given that the heart is a muscle, it too can enlarge with regular exercise. Ventricle walls thicken and the cavities dilate, which can result in significantly increased cardiac parameters. The extent of the cardiac change is dependent on genetics, as well as on the particular sport(s) involved. Physiologic structural changes tend to decrease during periods of deconditioning.

Aerobic-based activities are prone to cause greater increases in ventricular cavity dimension, whereas power sports generally lead to increased ventricular wall thickness.[10-12] Asymmetrical enlargement of the ventricles can result in abnormal cardiac output, which can trigger arrhythmias, particularly ventricular fibrillation. An ECG can be a helpful screening tool, revealing LVH (shown), altered intervals (eg, QT), and signs of cardiac ischemia. However, the ECG can also be normal (as with some inherited channelopathies). Sarcomere mutations in eight genes (MYH7, MYBPC3, MYL2, MYL3, TPM1, ACTC1, TNNT2, and TNNI3) contribute to the development of hypertrophic cardiomyopathy (HCM),[13,14] but mutations in MYH7 and MYBPC3 are the most common.[14] Clinical testing for these mutations remains in the early developmental stage.

Image courtesy of Moira Davenport, MD.

Sudden Cardiac Death in Athletes

Moira Davenport, MD | July 12, 2022 | Contributor Information

This ECG is from a 25-year-old female elite marathon runner who presented with mild fatigue and a decreasing ability to keep up in her routine workouts. The ECG is somewhat typical for a distance runner, with the presence of bradycardia and LVH. However, the ST depressions in the inferior leads and the T-wave inversions in V3 and V6 are not associated with athletic activity and thus warranted further evaluation. Stress echocardiographic studies showed increased LV septal thickness and increased LV cavity dimensions, without other abnormalities. She was ultimately cleared to return to running and has remained asymptomatic.

Image from Wikimedia Commons/Blausen Medical Communications. [CC 3.0 Unported (CC by 3.0).]

Sudden Cardiac Death in Athletes

Moira Davenport, MD | July 12, 2022 | Contributor Information

Structural cardiac changes and abnormal ECGs may pose a challenge to physicians in differentiating between normal athletic remodeling ("athlete's heart") and pathologic cardiomyopathies (eg, HCM, dilated cardiomyopathy [DCM], arrhythmogenic right ventricular [RV] cardiomyopathy [ARVC]). Although left atrial enlargement is common in athlete's heart and HCM, other features may help in distinguishing between these conditions, including, respectively, the following[12]:

  • Absolute LV cavity diastolic dimension: 55 mm or larger versus smaller than 45 mm
  • LV diastolic filling: Normal versus altered
  • Family history of HCM: None versus positive
  • Maximal oxygen uptake (VO2): Normal or increased versus decreased
Images from Patrick J. Lynch (left) [CC 2.5 Generic (CC by 2.5)] and Agateller (right) [public domain], both via Wikimedia Commons.

Sudden Cardiac Death in Athletes

Moira Davenport, MD | July 12, 2022 | Contributor Information

Commotio cordis is the R-on-T phenomenon that arises when the precordial region (left) sustains direct blunt trauma, usually from a projectile (eg, hockey pucks, pitched baseballs) or bodily contact (eg, karate blow, colliding athletes).[12] The transmission of forces from the chest wall to the heart can result in cardiac dysrhythmia, particularly ventricular tachycardia that leads to ventricular fibrillation.

Commotio cordis is most likely to be triggered when an impact to the chest wall occurs 15-30 milliseconds before the T-wave peak during repolarization (right). Young athletes are at increased risk for commotio cordis because of the increased compliance of their chest walls. Unfortunately, chest protectors have not been shown to reduce an athlete's risk of commotio cordis.[12]

Cardiac MRI from Thiene G, Corrado D, Basso C. Orphanet J Rare Dis. 2007;2:45. [Open access.] PMID: 18001465, PMCID: PMC2222049. [CC by 2.0.]

Sudden Cardiac Death in Athletes

Moira Davenport, MD | July 12, 2022 | Contributor Information

ARVC is characterized by RV fatty infiltration (shown), resulting in RV hypertrophy and the potential for fatal cardiac dysrhythmias from this hypertrophy. Abnormalities in the ryanodine calcium channel receptor have also been reported.[15,16] Individuals with ARVC may be advised to avoid competitive sports.

Image from Thiene G, Corrado D, Basso C. Orphanet J Rare Dis. 2007 Nov 14;2:45. [Open access.] PMID: 18001465, PMCID: PMC2222049. [CC by 2.0.]

Sudden Cardiac Death in Athletes

Moira Davenport, MD | July 12, 2022 | Contributor Information

ARVC is common in individuals (and their descendants) from the Veneto region of northern Italy.[12] Transmission is believed to be autosomal dominant. The initial presentation of this condition is sudden cardiac death; therefore, screening family members of affected individuals is key to identifying new cases.

A major diagnostic criterion for ARVC is the ECG presence of epsilon waves following QRS complexes (arrows).[17] These waves may be present in up to 30% of patients with ARVC.[17]

Image from Wikimedia Commons/Sponge. [CC ShareAlike 3.0 Unported (CC by-SA 3.0).]

Sudden Cardiac Death in Athletes

Moira Davenport, MD | July 12, 2022 | Contributor Information

Methylphenidate (Ritalin), a stimulant used to treat attention-deficit/hyperactivity disorder and other conditions, is shown.

Role of Stimulants

Stimulant use is extremely common among athletes at all levels of competition, and they have been implicated in sudden cardiac death in athletes.[12] The most commonly used substances include caffeine, pseudoephedrine, and ephedra. These products can increase heart rate and blood pressure above the increases associated with exercise, thereby placing the athlete at risk for cardiac complications.

Images from David Richfield (left) [CC by-SA 3.0] and Psychonaught (right) [public domain], both via Wikimedia Commons.

Sudden Cardiac Death in Athletes

Moira Davenport, MD | July 12, 2022 | Contributor Information

Role of Performance-Enhancing Drugs

Use of performance-enhancing drugs (PEDs) is also common in sports and may impact cardiac function. Multiple studies have shown that regular use of PEDs, particularly anabolic steroids, can increase levels of total cholesterol, very low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and triglycerides,[18] while potentially impacting inflammatory markers.[19] Abnormal lipid profiles can raise the athlete's risk of coronary artery disease to that of the general population.

Image from Kim DJ, Cho KI, Cho EA, et al. Clin Hypertens. 2015;21:24. [Open access.] PMID: 26893934, PMCID: PMC4750792. [CC by 4.0.]

Sudden Cardiac Death in Athletes

Moira Davenport, MD | July 12, 2022 | Contributor Information

This image depicts echocardiographic assessments of epicardial fat tissue (EFT) in the parasternal long-axis view. Increased EFT thickness appears to predispose to sudden death in individuals with coronary artery atherosclerosis.[20]

Preparticipation Cardiac Screening

To date, no standard cardiac screening protocol has been established for the athletic patient. The American Heart Association (AHA) recommends a screening ECG in any athlete aged 40 years or older who is starting a new exercise program.[21] The European Society of Cardiology and European Association of Cardiovascular Prevention and Rehabilitation recommend a screening ECG in athletes of any age.[22-24] If any abnormalities are detected on an ECG, further evaluation and testing should be performed, with transthoracic echocardiographic studies recommended as the first-line study.[21,22,25]

The screening of high school athletes remains somewhat controversial.[26] Current guidelines recommend a focused review of the AHA 14-point screening questionnaire combined with a thorough cardiac examination, including the auscultation of possible murmurs in various positions.[27,28] However, the efficacy of the AHA 14-point screening evaluation has been questioned.[29]

Image from Science Source/Chassenet.

Sudden Cardiac Death in Athletes

Moira Davenport, MD | July 12, 2022 | Contributor Information

In 2015, the American College of Cardiology (ACC) and AHA recommended that athletes with coronary artery disease undergo exercise tolerance testing prior to starting an exercise program[30]; LV function should be evaluated as well.[31] The ACC and AHA also recommended that risk factor reduction therapy be in place prior to starting an exercise program. Furthermore, exercise participation is reasonable if the LV ejection fraction is over 50% and there is no inducible ischemia.[31] Athletes should wait at least 3 months after a myocardial infarction or a revascularization procedure to start an exercise program.[31]

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