Table 5 Differentiation from disease—key points

Hypertrophic Cardiomyopathy

Echo parameters to suggest pathological LVH in athletes:

  - LVH > 15mm

  - Asymmetrical LVH

  - Concentric LVH geometry

  - LVEDD < 54mm

  - GLS < 16%

  - Abnormal MV and subvalvular apparatus

  - LVOTO/SAM

  - LV crypts

Dilated Cardiomyopathy

The athlete with physiologic dilation of the LV should demonstrate normal or supra-normal indices of diastolic function.

An LV EF less than 40% and/or impaired indices of diastolic function, should raise concern for DCM.

Among endurance athletes with mildly reduced LV EF, assessment of LV systolic function during exercise to confirm normal augmentation is warranted.

Left Ventricular Hypertrabeculation

Left ventricular non-compaction is now no longer considered to be a cardiomyopathy and is identified as an isolated phenotypic trait or occurring in combination with systolic dysfunction and ventricular arrhythmias.

Athletes with LV hypertrabeculation in the absence of symptoms, family history of cardiomyopathy, abnormal ECG, impaired LV systolic function or complex ventricular arrhythmias can participate in sports of any intensity.

Athletes with LV hypertrabeculation and impaired LV systolic function that is consistent with exercise induced cardiac remodelling should follow the recommendations for athletes with dilated cardiomyopathy

Arrhythmogenic Cardiomyopathy

Most commonly RV enlargement and dysfunction, with regional wall motion abnormalities. LV or biventricular involvement is increasingly recognised.

Diagnosis of ACM is complex and requires integration of data from the ECG, ambulatory monitoring, imaging investigations, and genetics. Newer proposed diagnostic criteria have acknowledged LV involvement, and the utility of echocardiographic strain assessment.

Pathology should be suspected when there is profound remodelling exceeding thresholds in Figs. 6 and 7, remodelling which is disproportionate to the athlete’s demographic profile (Fig. 3), unbalanced remodelling, impaired long axis function (TDI or strain), or regional wall motional abnormalities in either ventricle.

Vigorous augmentation of cardiac function (including the RV) should be seen during exercise echocardiography in healthy athletes.

A period of detraining (at least 6 weeks) should result in partial or complete resolution of training-induced structural and function adaptations in the RV and/or LV.

Coronary Anomalies

Optimise athlete position to acquire standardised and non-standarised views.

PLAX view may give clues to low/high take off coronary arteries, intramural course.

Emphasis on modified SAX view at AV level; with angulation of probe above the AV and modified sweeping movements with gentle clockwise and anticlockwise rotation.

Focus on optimising the image (zoom, sector width, gain, cine/freeze function) to adequately comment on the (a) individual ostia of the coronary arteries from the ascending aorta; and (b) any potential abnormal course of the ostia or proximal segments of the artery.

Myocarditis (including COVID)

Myocarditis is an important cause of cardiac damage in athletes

TDI and Strain play an important role in the identification of regional abnormalities.

Athletes diagnosed with myocarditis required evaluation in expert sports cardiology centres.

Return to play protocols should be followed to avoid cardiac complications.

Aortic Root Disease and Bicuspid Aortic Valve

Increased intensity of sport correlates with larger aortic dimensions, but they rarely exceed normal limits even in endurance athletes.

Bicuspid aortic valve is the commonest congenital heart defect, present in 1-2% of the population, with one-third developing aortic stenosis, regurgitation, or aortic root dilation.

Risk of SCD is related to sudden aortic dissection, accounting for 0.8% of SCD in athletes

Mitral Valve Prolapse

Arrhythmic MVP is typically associated with myxomatous degeneration and prolapse of both leaflets with a degree of mitral annular disjunction (MAD).

An increase in LV end-diastolic or end-systolic dimensions/volumes or reduction in LVEF within a short time-frame and without a change in training type or volume are more the adverse remodelling effects of chronic significant MR in athletes with MVP.

Disproportionate dilatation of the LA is more likely related to the degree of MR in athletes with MVP.

ateral S’ that peaks in late systole (‘Pickelhaube sign’) and at a velocity > 16 cm/s has been proposed as a marker of greater arrhythmic risk in MVP and MAD.