Cardiovascular Magnetic Resonance and Sport Cardiology: a Growing Role in Clinical Dilemmas

Abstract

Exercise training induces morphological and functional cardiovascular adaptation known as the "athlete's heart" with changes including dilatation, hypertrophy, and increased stroke volume. These changes may overlap with pathological appearances. Distinguishing athletic cardiac remodelling from cardiomyopathy is important and is a frequent medical dilemma. Cardiac magnetic resonance (CMR) has a role in clinical care as it can refine discrimination of health from a disease where ECG and echocardiography alone have left or generated uncertainty. CMR can more precisely assess cardiac structure and function as well as characterise the myocardium detecting key changes including myocardial scar and diffuse fibrosis. In this review, we will review the role of CMR in sports cardiology.

Keywords: Athlete’s heart; CMR; Sport cardiology.

Fig. 1

Biventricular chambers, size, function and mass by CMR. In the top panel, a short axis stack covers both ventricles from the atrioventricular valve plane to the apex, and planned on 4- and 2-chamber views. The short axis stack is then used to accurately calculate mass, volumes and function by contouring endocardial and epicardial borders. The bottom panel shows a transverse RV stack, an RV 2-chamber and outflow tract view used for RV regional wall motion and morphology

Fig. 2

CMR findings in the athlete’s heart and mimics. Images show (left to right) 1) an end-diastolic 4-chamber cine; 2) a 4-chamber T1 map; 3) a 4-chamber LGE; 4) a mid-ventricular short axis LGE; in the following conditions (top to bottom): a athlete: demonstrating enlarged cardiac chambers with normal wall thickness. Native T1 map and 4-chamber LGE view are normal. There is inferior RV insertion point LGE, a normal finding when it is just a gram or so, as here. b HCM: predominantly septal LVH. Patchy elevated native T1 with patchy mid-wall LGE seen in hypertrophied myocardium and (here) the papillary muscles. c DCM: LV dilatation with normal native T1 map and no LGE. d ARVC: biventricular ARVC. Elevated native T1 is appreciated within the RV wall as well as extensive biventricular LGE. e LVNC: non-compaction of the LV. Native T1 map is normal and there is subtle LGE seen in the 4-chamber image within the apical cap. This appearance has to be interpreted with context, particularly of ethnicity and athleticism

Fig. 3

Role of CMR in the grey zone. The figure shows the role of CMR in the grey zone between athlete’s heart and cardiomyopathy. For every scenario, CMR features are shown. ARVD: arrhythmogenic right ventricular cardiomyopathy; DCM: dilated cardiomyopathy; ECV: extracellular volume fraction; HCM: hypertrophic cardiomyopathy; LGE: late gadolinium ehancement; LV: left ventricle; LVH: left ventricle hypertrophy; LVNC: left ventricular non-compaction; RV: right ventricle; SV: stroke volume; RWMA: regional wall motion abnormalities

Fig. 4

Focal hypertrophy potentially missed by echocardiography. Two athletes presenting with focal hypertrophy limited to the apex (a, b). c Short axis view by CMR showing focal hypertrophy limited to the inferior septum with a maximum wall thickness (16 mm) measured at the RV insertion point in an athlete. d The corresponding short-axis view by echocardiography underestimated the hypertrophy (12 mm)

Fig. 5

Multiparametric CMR imaging comparing HCM with the athlete’s heart. End diastolic 4-chamber cine of a patient with HCM showing septal thickening. Two regions of interest are drawn within the myocardium on native T1 mapping with elevated native T1 values (1107–1137 ms, range 950–1060 ms on 1.5 T Siemens Aera) with corresponding LGE and elevated ECV (37.6–40.1%, range 24–28% on 1.5 T Siemens Aera). In comparison, an athlete’s heart demonstrates normal wall thickness on 4-chamber cine with normal native T1 values in the thickest region (basal septum; 977 ms), no LGE and low ECV (21.3%)