The Role of Cardiovascular Magnetic Resonance Imaging in Athletic Individuals—A Narrative Review

Figures

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  Figure 1. Commonly adopted cardiac MRI sequences when evaluating athletes.

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  Figure 2. A mother presents to clinic for screening following the sudden death of her son who was a long-distance runner. Autopsy confirmed hypertrophic cardiomyopathy (HCM) secondary to a pathogenic TNNT2 variant. The victim’s uncle was also diagnosed with HCM in the interim and referred for transplantation. The mother was a carrier for the TNNT2 variant. The ECG was abnormal; echocardiography was normal. CMR identified mid-wall fibrosis in the lateral wall, despite the absence of left ventricular hypertrophy.

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  Figure 3. Caucasian male soccer player presenting with inferolateral T-wave inversion on ECG. SSFP cine imaging (A) showing apical hypertrophy, with evidence of apical fibrosis on post-contrast imaging (B,C).

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  Figure 4. A 21 year old male that presented with chest pain during a pre-participation evaluation to join the armed forces. ECG showing biphasic ST segments in leads V1-V3, with T-wave inversion in II/III/aVF. CT coronary angiogram ruled out epicardial coronary disease. A stress echocardiogram ruled out dynamic LVOT obstruction. Echocardiogram confirmed the presence of hypertrophic cardiomyopathy, secondary to a likely pathogenic MYBPC3 variant. Cardiac MRI (3T scanner) showing septal hypertrophy (arrow) (A), extensive replacement (arrow) (B), and interstitial fibrosis in the septal segments (arrow) (C) (T1 map using a MOLLI 5b(3b)3b [3T]). Perfusion imaging (D) also identifying an extensive perfusion defect (arrow) in the hypertrophied segments, confirming microvascular dysfunction.

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  Figure 5. A 21 year old Caucasian male found to have lateral T-wave inversion on pre-recruitment ECG to join the military. Echocardiography showed dilated left and right ventricles, a bicuspid aortic valve (AoV), and possibly an atrial septal defect (ASD). Cardiac MRI confirmed the presence of dilated ventricles (A) exceeding reference ranges for male athletes. A bicuspid AoV (Sievers Classification Type 0) was also confirmed (B), without regurgitation. Phase-contrast flow imaging confirmed the presence of an ASD (C). Post-contrast imaging showed no replacement fibrosis.

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  Figure 6. A 21 year old endurance athlete, referred for screening as her mother was diagnosed with arrhythmogenic cardiomyopathy secondary to a Desmoplakin pathogenic variant. The athlete was also gene-positive, with a normal ECG and echocardiogram. Cardiac MRI identified a ring-like subepicardial scar on post-contrast imaging (A), with a diffusely elevated T1 (B), resulting in a diagnosis of non-dilated left ventricular cardiomyopathy.

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  Figure 7. An 18 year old male Caucasian competitive swimmer who was seen because of a very long PR interval in the context of non-cardiogenic syncope. Echocardiography revealed a dilated LV. This was confirmed on CMR, though perfectly within normal athletic specific reference ranges. Post-contrast imaging showed posterior RV insertion-point fibrosis.

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  Figure 8. A 19 year old male soccer player who presented with dyspnoea, found to have increased LV trabeculation on echocardiogram. Cardiac MRI showed prominent apical hypertrabeculation, with preserved thickness of the non-compacted layer. There was preserved LV function, with a normal LV size and absence of regional wall motion abnormalities and fibrosis. The findings were attributed to athletic remodelling.

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  Figure 9. A 42 year old Caucasian male, engaging in power sport (recreational) for 20 years, presented with a profound drop in exercise tolerance. Murmur heard on physical examination. T-wave inversion in the inferior leads noted. Supraventricular arrhythmias during an exercise test. Mitral valve (MV) prolapse with moderate regurgitation noted on echocardiogram. Cardiac MRI showed a dilated LV, an LV ejection fraction of 58%, and mitral annular disjunction (arrow) (A). There was prolapse of the posterior MV leaflet with moderate regurgitation (B). Post-contrast imaging identified a subepicardial scar in the lateral wall (arrow) (C,D), consistent with a diagnosis of malignant MV prolapse. He was subsequently referred for MV surgery.

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  Figure 10. A 24 year old long-distance runner reported a drop in exercise tolerance. A murmur was heard at auscultation. Cardiac MRI showed a bicuspid aortic valve (Sievers Classification Type 0) (A), with eccentric closure and moderate regurgitation (B).

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  Figure 11. In a 34 year old Caucasian male soccer player, a routine screening echocardiogram identified a dilated proximal ascending aorta. He had a normal blood pressure; genetics was negative. A 3D aortogram on cardiac MRI confirmed the presence of a dilated aortic root and proximal ascending aorta, measuring 43 mm.

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  Figure 12. A 22 year old Caucasian male soccer player who presented for a routine screening echocardiogram. A dilated right ventricle (RV) led to a cardiac MRI. This confirmed a dilated RV (A), exceeding athletic reference ranges. MRI also identified a sinus venosus defect and anomalous pulmonary venous drainage (B), with a Qp:Qs > 1.5, reaching surgical thresholds.