Section Four: Imaging of the Athlete’s Heart
- The LV wall thickness is rarely greater than 13 mm in healthy athletes
- The LV relative wall thickness (RWT) and the LV mass to volume ratio are helpful in distinguishing hypertrophic cardiomyopathy (HCM) and athlete’s heart
- The origins of the right and left coronary arteries are often seen on transthoracic echocardiography in young athletes, which may suggest anomalous coronaries
- Wall and chamber measurements with cardiac magnetic resonance imaging (CMR) have been shown to be more accurate than with echocardiography
- Late gadolinium enhancement (LGE) on CMR is believed to represent dense replacement fibrosis and its pattern may help narrow the diagnosis. It is seen in approximately 50% of patients with HCM
- LV aneurysm, increased trabeculation of the LV, abnormal LV segmental wall motion or longitudinal strain, impaired LV diastolic function and/or systolic anterior motion of the mitral valve support the diagnosis of HCM or a myopathic process. The presence of right ventricular aneurysms or disproportionate dysfunction also suggest the possibility of arrhythmogenic right ventricular cardiomyopathy
Imaging is essential to the diagnostic algorithm when clues from an athlete’s history, an abnormal ECG or pre-participation evaluation suggest the possibility of structural heart disease. Appropriate test selection, optimal imaging protocols, and accurate interpretation are essential to distinguish between the “athlete heart” and cardiac pathology with potential clinical consequences.
The European Association of Cardiovascular Imaging (EACVI) published an expert consensus statement on multimodality cardiac imaging approach to the Athlete’s Heart in 20151 and the American Society of Echocardiography (ASE) in collaboration with the Society of Cardiovascular Computed Tomography (SCCT) and the Society of Cardiovascular Magnetic Resonance (SCMR) published guidelines on the use of multimodality cardiovascular imaging in young adult competitive athletes in 2020 2. Table 1 compares the imaging techniques we will describe in the following parts.
Table 1. Comparison of Imaging Modalities of the Athlete’s Heart described below
|Imaging Modality||Advantages||Disadvantages||Cardiac Diseases|
|Echocardiography||– Readily available
– Readily portable
– No radiation
|– Dependent on imaging windows and technician
– Limited visualization of proximal coronaries,and ascending aorta. LV trabeculations may be challenging to visualize.
|– Valvular heart disease
– Hypertrophic Cardiomyopathy
– Congenital heart disease
|Cardiac CT||– Gold standard for noninvasive coronary artery assessment
– Excellent at detecting calcification
– Risk of contrast-induced nephropathy
|– Coronary artery disease
– Coronary calcium
– Structural heart and EP procedure planning
|Cardiac MRI||– Gold standard for cardiac structure and myocardial tissue
– Can assess the pattern and amount of myocardial fibrosis
– No radiation
– Incompatibility with implanted metal
|– Hypertrophic Cardiomyopathy
– Valvular heart disease
– Congenital heart disease
Part 1. Exercise-induced Cardiac Remodeling
Exercise training can lead to cardiac remodeling, resulting in structural or functional changes that fall outside the limits of reference of non-athletes3. Athletic remodeling can be best described as proportional; LV mass often increases proportionally to left ventricular end-diastolic volume, left atrial volume often increases proportionally to stroke volume and the right heart often increases proportionally to left heart enlargement. In endurance athletes, right heart enlargement may be more prominent. Typically, LV systolic and diastolic function is preserved in elite athletes. However, endurance athletes, particularly if LV chamber dilation exists, may have a resting LV ejection fraction at the lower limits of normal or mildly reduced (LVEF 45-50%)4. Diastolic function is preserved in endurance athletes5. Just as the LV can dilate in response to endurance training, so too can the RV and atria6. In fact, endurance athletes can have RV chamber dimensions that exceed “normal” values and meet criteria for ARVC7. Isolated RV dilation (not accompanied by LV dilation) or RV regional abnormalities should raise suspicion for pathology.
Left ventricular (LV) adaptation or remodeling to prolonged exercise training was initially explained by the concept of the ‘Morganroth hypothesis’ (Figure 1)8. Using non-guided M-mode echocardiography, Morganroth et al. (1975) observed that endurance athletes (swimmers, long-distance runners) possessed increased LV end-diastolic volume (LVEDV), normal LV wall thickness and increased LV mass compared to sedentary subjects. In contrast, resistance-trained athletes (wrestlers) exhibited increased LV wall thickness and LV mass with no change in LVEDV compared to sedentary controls. These divergent patterns were later described as ‘eccentric’ and ‘concentric’ left ventricular hypertrophy, respectively, and resulted from episodic elevations in preload during endurance exercise and afterload during resistance exercise.
While LV dilation is common in endurance athletes2, critics of the Morganroth hypothesis point to mixed evidence in strength athletes1. Also, sports and exercise is often a combination of both types of training. More recent data using MRI and serial monitoring also challenge this widely held belief. Spence et al9 examined the effects of 6 months of endurance training (3 hours per week of walking/jogging/running, n = 10) or resistance training (3 hours per week of Olympic weightlifting and supplemental strength exercises, n = 13) followed by 6 weeks of detraining on LV morphology and function, aerobic fitness, muscle strength and body composition in younger males (mean age: 27 years). In both groups, the LV mass to volume ratio (0.85 on average) did not change significantly. Using 3D echocardiography, Caselli et al10 showed that the LV mass to volume ratio was close to one in 511 Olympic athletes, irrespective of the type of sport. In college athletes (pre-season assessment), Moneghetti et al11 further demonstrates that the LV mass to volume ratio did not significantly change according to sport type although it was higher in athletes of Black race and lower in females.
Figure 1. The Morganroth Hypothesis, a recently challenged concept
The Morganroth Hypothesis for the Cardiac remodeling of exercise training
Measuring wall thickness in echocardiography is central for evaluating LV concentric remodeling or hypertrophy. Several pitfalls should be avoided, such as the inclusion of the septal band or mitral apparatus chords in wall thickness measures. Consistency between long axis and short axis also increases reliability of measures. Using the area-length method in both diastole and systole to estimate LV mass by echocardiography can provide greater confidence in the estimates with a usual difference below 5% (Stanford athletic center). A particular attention during screening should be given to asymmetric hypertrophy (septal vs. lateral or apical vs. basal). Apical hypertrophy may be missed on routine screening and acquisition of focused apical views are helpful.
Part 2. Distinguishing HCM from Athlete’s Heart in the “Gray Zone”
LV measurements often fall within the “gray zone” between what is expected for a trained athlete’s heart and pathologic heart disease. Repeat imaging after de-training is one method to distinguish athlete’s heart from pathologic cardiac disease, as the athlete’s LV may normalize. However, de-training is seldomly embraced by the competitive athlete, their trainers or their coaches.
A study of healthy professional NBA basketball players using transthoracic echocardiography (TTE) showed that maximum LV wall thickness exceeded the upper limits of normal (10 mm) in more than half the athletes (but never exceeded 15 mm), the LV end-diastolic diameter exceeded the upper limits of normal (58 mm) in more than one third the athletes (but was often normal when indexed to body surface area), and the LV mass index exceeded the upper limits of normal (115 g/m2) in more than a quarter of the athletes12.
The purpose of a study by Caselli et al13 was to consider the ability of echocardiographic and clinical variables to distinguish HCM and athlete’s heart. Twenty-eight athletes free of cardiovascular disease were compared with 25 untrained patients with HCM, matched for LV wall thickness (13 to 15 mm), age, and gender. Athletes had larger LV cavities (60 ± 3 vs 45 ± 5 mm, p <0.001), aortic roots (34 ± 3 vs 30 ± 3 mm, p <0.001), and left atria (42 ± 4 vs 33 ± 5 mm, p <0.001) than patients with HCM. LV cavity <54 mm distinguished HCM from the athlete’s heart with the highest sensitivity and specificity. Left atrium >40 mm excluded HCM with sensitivity of 92% and specificity of 71% (p <0.001). They concluded that in athletes with LV hypertrophy in the “gray zone” with HCM, LV cavity size <54 mm was the most reliable criterion to differentiate HCM from athlete’s heart.
Concentric LVH is less common in athletes than eccentric or normal geometry but can occur in up to 12% and is often mild14. The process of making a diagnosis involves a comprehensive investigation that typically includes ECG, functional indices from echocardiography, and CMR. Some of the findings used to distinguish athlete’s heart from HCM are represented in Table 2.
Table 2. Findings in the Patterns of Training and Hypertrophic Cardiomyopathy
(distance runners, wide receivers, backs, basketball)
(wrestlers, linemen, gymnasts)
|LVEDV (end diastolic volume)||Increased||Normal||Normal – Reduced*
(LVEDD < 54 mm)
|LVWT (wall thickness)||Normal
|RWT (relative wall thickness)**||<0.42||<0.42||>0.42#|
|Mass/Volume ratio||< 1.0||< 1.0||> 1.0 males
* In “burned-out HCM”, the LV becomes dilated and LV systolic function reduced
** RWT = 2 * posterior LV wall thickness/LV end-diastolic diameter
# In the paper by Caselli et al10, RWT was defined as the ratio of the septal and free wall thickness normalized to LV end-diastolic diameter
Part 3. Selecting the Appropriate Cardiac Imaging Modality in Athletes Without Known Cardiac Disease
Cardiac imaging is not routinely incorporated as a component of pre-participation screening for cardiac disease in athletes. The decision to pursue cardiac imaging is primarily driven by suspicious findings from the medical history (e.g. exertional chest pain or syncope), physical exam (e.g. murmur), or EKG (e.g. LBBB, frequent PVCs, pathologic Q-waves, ST-segment depression, T-wave inversion) that increase the athlete’s likelihood of cardiac disease. When cardiac pathology is suspected, TTE is often the initial cardiac imaging modality of choice, since it is widely accessible and comprehensively evaluates the structure and function of the heart without any risks to the athlete2.
However, TTE may be insufficient in diagnosing certain cardiac conditions due to image quality and/or its inherent limitations. Therefore, we propose a targeted imaging approach that depends on the cardiac pathology that is suspected (Figure 2). For example, master’s athletes who engage in higher intensity exercise and have a risk of coronary disease may be considered for cardiac imaging to evaluate for ischemia or electrical instability with maximal exercise testing, perfusion imaging, or coronary CT angiogram. The use of cardiac MRI has become an integral tool in many scenarios in the evaluation of the Athlete’s heart15. Cardiac CT also has an important role in imaging the athlete.
Athletes With Known Cardiac Disease
For any given cardiovascular condition, deciding which cardiac imaging test to pursue (if any) and when to test can be complex. There are multiple appropriate use criteria expert statements that give guidance on when a particular imaging modality is appropriate by modality (echocardiography16, cardiac CT17) and by disease (stable ischemic heart disease18, heart failure19, valvular heart disease20, structural non valvular heart disease21, and congenital heart disease22). There are also recent updated guidelines for hypertrophic cardiomyopathy23.
Part 4. Case Examples
CASE 1. A 20 year-old African American female basketball player presents to cardiology clinic for evaluation of chest pain and syncope during athletic activity. Two years ago she began experiencing fatigue during practice and games, but progressed to the point that she would develop these symptoms when she was ascending stairs. She also had a syncopal event during the middle of basketball practice without prodrome. She spontaneously regained consciousness. There was no family history of cardiac disease.
Physical exam was normal. EKG demonstrated normal sinus rhythm and T wave inversions in III and avF. TTE showed LVEF that grossly appeared low-normal with normal LV global longitudinal strain (-18.9%), severe LV diastolic dysfunction, and hypertrabeculation of the LV apex. Cardiac MRI demonstrated mildly dilated LV with increased trabeculation at the apex with non-compacted to compacted myocardial ratio of 2.5 in diastole with a calculated LVEF of 55%. There was absence of abnormal delayed myocardial enhancement to suggest scar or infiltrative disease.
Case 1 Figure 1. TTE 2 chamber view. Increased trabeculations in LV apex and anterolateral wall concerning for non-compaction. EF estimated at 35%
Case 1 Figure 2 and 3: Cardiac MRI 2 chamber and short-axis views of the left ventricle. Noncompacted to compacted myocardial ratio 2.5.
If LV hypertrabeculations with borderline LV ejection fraction are discovered on imaging in a competitive athlete, what is the strongest element that will distinguish true cardiomyopathy from physiologic changes in the athletic heart?
- A. Ratio of noncompacted to compacted myocardial layer thickness is >2.0 at end-systole by TTE
- B. Ratio of noncompacted to compacted myocardial layer thickness is >2.3 at end-diastolic by CMR
- C. Impaired systolic and/or diastolic function
- D. Positive family history of cardiomyopathy
- E. Presence of LGE on CMR
View the Correct Answer
Impaired systolic and/or diastolic function
Findings of borderline LV systolic function in conjunction with symptoms were concerning for a diagnosis of LV noncompaction. She completed an exercise treadmill test and there were no inducible arrhythmias. A 14-day event monitor demonstrated 1 run of ventricular tachycardia lasting 6 beats. She was referred for genetic evaluation, started on a low-dose beta blocker for suppression of her NSVT, and told to abstain from athletic activity in the short term with plans for serial reassessment with imaging and heart rate monitoring over time.
Among competitive athletes, especially those of African American ethnicity, hypertrabeculation of the LV and RV apex is more common. The hypothesized explanation is that a chronic increase in cardiac preload in the setting of isotonic physiology will produce enlargement of the intertrabecular recesses which may regress on detraining8. About 15% of those who meet the diagnostic cutpoints for pathologic noncompaction by TTE or CMR (ratio of noncompacted to compacted myocardial layer thickness is >2.0 at end-systole by TTE, and ratio of noncompacted to compacted myocardial layer thickness is >2.3 at end-diastole by CMR) will be overdiagnosed with LV noncompaction. In order to distinguish physiologic changes in the athletic heart from a true diagnosis of LV noncompaction, the strongest element to support the diagnosis of a myocardial disease is impaired systolic or diastolic function1. A cutoff of EF <50% has been suggested. In borderline cases where the EF is between 50-54%, a reduction in global longitudinal strain of < -15% may be suggestive of an underlying cardiomyopathy.
Other features that distinguish true noncompaction cardiomyopathy from physiologic changes in the competitive athlete include very thin compacted layer (<5 mm), marked impairment of LV systolic function, presence of LGE on CMR, and clinical findings suggestive of the diagnosis such as heart failure, tachyarrhythmias, and embolic events1.
CASE 2. A 40 year-old male long distance runner and mountain biker with paroxysmal atrial fibrillation presented with decreased exercise capacity during episodes of atrial fibrillation. His exercise regimen consists of 75-100 miles of mountain biking a week. He is taking propafenone, metoprolol succinate, and rivaroxaban, which were prescribed post-cardioversion, and in the past he had tried flecainide but did not maintain sinus rhythm. His family history is significant for coronary artery disease in two second degree relatives. There is no personal history of congenital heart disease.
Physical exam was normal. EKG demonstrated normal sinus rhythm and an incomplete RBBB. A 14-day event monitor demonstrated 0% atrial fibrillation burden and his CHADSVASC score was 0. TTE showed LVEF of 65%, normal LV diastolic function, a moderately enlarged RV with preserved systolic function, a mildly dilated LA with a size of 45 mL/m2, a severely dilated RA with a size of 38 mL/m2, trace tricuspid regurgitation, and normal pulmonary pressures. Cardiac MRI demonstrated right ventricular dilation and mild right ventricular hypertrophy without ARVC/D criteria, normal right ventricular function, mild dilation of the LV, and biatrial enlargement (Figure below). Both ventricles did not demonstrate anatomic abnormalities such as sacculations, aneurysms, or focal thinning.
The differential diagnosis for an athletic patient with RV dilation includes arrhythmogenic RV cardiomyopathy, toxic cardiomyopathies, primary and secondary pulmonary hypertension, and congenital heart diseases1. Ultimately because the RV did not demonstrate any structural or functional abnormalities, the majority of the patient’s findings were attributed to physiologic adaptations of the heart in an endurance athlete. The patient was told to continue to exercise without limitations, and was referred to electrophysiology for consideration of ablation in light of his recurrent need for cardioversions and insufficient treatment with different antiarrhythmic and rate control strategies.
Case 2 Figure. TTE 4 chamber view. Moderately enlarged RV, a mildly dilated LA with a size of 45 mL/m2, a severely dilated RA with a size of 37.7 mL/m2
What would be the next best step in management in this endurance athlete with paroxysmal atrial fibrillation?
- A. Continue current management
- B. Uptitration of beta blocker to a resting heart rate of 30
- C. Retrial of pill-in-the-pocket approach with a higher dose of flecainide
- D. Referral for ablation
- E. Recommendation for detraining
View the Correct Answer
Answer: D. Referral for ablation
Athletes have higher vagal tone resulting in resting sinus bradycardia. Rate control can have the effect of slowing the resting heart rate while also reducing performance during exercise by lowering the heart rate, producing unwanted side effects both during rest and during exercise. Therefore, a rhythm control strategy is often preferred8.
Antiarrhythmics such as flecainide and propafenone, when used alone, can organize atrial fibrillation into 1:1 atrial flutter due to slowing of atrial myocardial conduction without the use of an additional AV blocking drug. Therefore, AV nodal blockers are used in combination with flecainide and propafenone and are rarely tolerated in athletes,given the AV nodal blocker slowing of heart rate that can inhibit performance. A pill in the pocket approach with 200-300 mg of flecainide can be considered for athletes with low AF burden and absence of sinus node disease, but is not always effective, as in the case of this patient. Given the frequent intolerance or aversion to medications in athletes, ablation is often considered early. Success rates are similar for athletes and nonathletes, with 84% freedom from recurrence after 3 years following multiple procedures24.
Detraining is effective at reducing AF in an athlete, but significant deescalation of athletic regimen is not desirable for many athletes and often is not recommended until all other options are exhausted24.
In our particular case, the patient was deemed to have echo findings consistent with endurance athlete changes and not a cardiomyopathy. He was told to continue to exercise without limitations, and was referred to electrophysiology for consideration of ablation in light of his recurrent need for cardioversions and insufficient treatment with different antiarrhythmic and rate control strategies.
CASE 3. A 40 year-old woman competitive bodybuilder was referred to cardiology for a systolic murmur and transthoracic echocardiogram showing LVH. She had prior syncope associated with blood draw and with stress while taking a hot shower. In addition to competitive weightlifting, she also does high intensity interval training (HIIT) and exercises in total about 3 hours 6 days per week. Her family history is significant for HCM in her cousin, who underwent myectomy and primary prevention ICD. Continuous rhythm monitoring showed no ventricular arrhythmia. Her TTE demonstrated asymmetric septal hypertrophy with LV septal thickness of 20 mm, systolic anterior motion of the mitral valve with an LVOT gradient of 48 mmHg with Valsalva and these findings were consistent with HOCM. Cardiac MRI showed 5-10% LGE in the LV septum without evidence of aneurysm.
Parasternal long and short images, which demonstrate asymmetric septal hypertrophy with a thickness of ~ 20 mm.
Parasternal long and short images, which demonstrate asymmetric septal hypertrophy with a thickness of ~ 20 mm.
Apical 5 chamber view without color Doppler, which demonstrates systolic motion of the anterior mitral leaflet and flow acceleration through the left ventricular outflow tract.
Apical 5 chamber view with color Doppler, which demonstrates systolic motion of the anterior mitral leaflet and flow acceleration through the left ventricular outflow tract.
Peak LVOT gradients at rest, with Valsalva maneuver, and at peak exercise
T1-weighted cardiac magnetic resonsance image with gadolinium contrast showing the left ventricle in short axis. Within the left ventricular septum (dark), there is evidence of late gadolinium enhancement (bright), which constituted 5-10% of the left ventricular myocardium
Question 1 of 3: Which of the following cardiac imaging findings are NOT associated with increased risk of sudden cardiac death?
- A. LGE > 15% on cardiac MRI
- B. Presence of LV aneurysm
- C. Maximal LV wall thickness > 30 mm in any segment
- D. Mitral regurgitation
- E. LVEF < 50%
View the Correct Answer
Answer: D. Mitral regurgitation
Question 2 of 3: Should she undergo prophylactic ICD implantation?
- A. Yes
- B. No
View the Correct Answer
She has 0 “major” risk factors (sudden death in a first degree relative, LVH > 30 mm, recent unexplained syncope, LV aneurysm, and LVEF < 50%). Other risk factors that may aid in the decision-making, extensive LGE or CMR (>15% of LV mass) and NSVT, were also absent.
Question 3 of 3: How should she be counseled in regards to her exercise regimen?
- A. Refrain from all physical activity
- B. No exercise restrictions
- C. Shared discussion about participation in moderate or high-intensity sports
View the Correct Answer
After a discussion with this athlete, we decided that she avoid her weightlifting and high-intensity interval training. Previous guidelines recommended against moderate or high-intensity competitive sports in athletes with clinical expression of HCM. However, recent evidence of HCM patients showed a similar ventricular arrhythmia burden in competitive athletes versus non-athletes20. Current HCM guidelines21 suggest a shared discussion about participation in moderate or high-intensity competitive sports for individuals with HCM, recognizing that the risk of SCD may be increased.
* Imaging modalities that may supplement exercise testing include echocardiography, nuclear (PET or SPECT), and MRI
ARVC = arrhythmogenic right ventricular cardiomyopathy; BNP = basic natriuretic peptide; CAD = coronary artery disease; CTA = computed tomography angiography; CMR = cardiac magnetic resonance imaging; HCM = hypertrophic cardiomyopathy; IVCD = interventricular conduction delay; LBBB = left bundle branch block; LGE = late gadolinium enhancement; MRA = magnetic resonance angiography; PVC = premature ventricular tachycardia, SCD = sudden cardiac death; TEE = transesophageal echocardiogram; TTE = transthoracic echocardiogram;