Athlete heart syndrome

Last revised by Patrick J Rock on 2 Aug 2021

Athlete heart syndrome refers to adaptations in both cardiac structure and function seen in people engaged in high-performance and endurance physical exercise.

The prevalence of the condition has increased due to the increased popularity of recreational exercise, approx 3.6/100,000 young athletes die per year 1.

Patients are commonly asymptomatic or have rhythm disturbances (e.g. sinus bradycardia), syncope, palpitations, and/or chest pain. They will have a history of regular physical exercise, often more than an hour per day.

Common electrocardiographic patterns in patients with athlete heart syndrome include:

  • benign early repolarization
  • high left ventricular voltage (HLVV)
  • diffuse T-wave inversion
  • narrow, deep Q waves

Athletic heart syndrome is due to adaptations in the cardiovascular system in order to be able to meet the physiological demands required during physical exercise. Hypertrophy and dilatation of the ventricles as a response to exercise causes enlargement of the ventricles. A larger stroke volume due to enlargement of the ventricles makes the cardiac function more efficient and demands can be met with a lower heart rate, often resulting in bradycardia.

An inexpensive and widely available modality at the point-of-care, transthoracic echocardiography has established value in screening for structural heart disease and may also allow initial differentiation between extreme physiologic adaptation to exercise and potential pathologic mimics, such as

Salient sonographic features of the "athlete's heart" include 12:

  • biventricular hypertrophy and dilation
    • enlarged LV end-diastolic diameter (>55mm), contrasting the decreased LVIDd (<45 mm) in HCM12.  
      LV wall thickening attributable to exercise-induced cardiac remodeling, regardless of whether it occurs in an eccentric or concentric morphology, rarely leads to measurements that exceed 12-13 mm; a LV wall thickness >15 mm should raise suspicion for pathology and should stimulate further testing to exclude or confirm an explanatory cardiomyopathy15.
    • preservation of LV:RV size ratio and LV volume:LV mass ratio
      • global right ventricular enlargement, allowing differentiation from ARVC, which preferentially affects the RVOT 
      • with increased ventricular trabeculation, predominantly in the mid-left ventricle
  • atrial dilatation
    • biatrial enlargement
      • symmetric increase in right and left atrial volumes without concomitant elevations in pressure
        • the measured E/e' should be, therefore, within normal limits (correlate of left atrial pressure)
      • expected left atrial volume parameters (i.e. upper limits) should be adjusted in male athletes
  • aortic root dilation

Spectral Doppler derived diastolic function parameters, as well as newer modalities including speckle tracking, allow further differentiation from pathological ventricular hypertrophy and/or dilation, as those with the "athlete's heart" demonstrate the following:

  • normal to slightly decreased left ventricular systolic function
    • with rapid exercise-induced normalization of the latter
    • absence of regional wall motion abnormalities
  • enhanced diastolic function
    • rapid septal and lateral mitral annular e' velocities
    • vigorous relaxation may mimic restrictive physiology when one uses mitral filling indices or pulmonary venous Doppler
      • supranormal lusitropic function results in an increased gradient for early diastolic left ventricular filling, with an E/A ratio often > 2
        • exaggerated by a decreased active atrial contribution to LV filling in athletes 
      • this abnormally strong negative pressure gradient results in reversal of the pulmonary venous S/D ratio, with predominant antegrade PV flow in diastole
  • supernormal (or normal) radial and circumferential strain
    • with normal left ventricular global longitudinal strain (GLS)
  • enhanced right ventricular systolic function
    • lower RV peak global longitudinal strain (GLS)

Cardiac MRI is superior to echocardiography with a sensitivity and specificity of 80 and 90% respectively 2. It is also useful to differentiate the normal adaptation of the heart to exercise from pathological conditions and to discard acute myocarditis (seen in 5–22% of athletes’ sudden cardiac attack) 1.

The condition requires no treatment. There is no proven association between athlete heart syndrome and an increased risk of sudden cardiac death.

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Cases and figures

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