CMR and the clinical diagnosis of myocarditis

CMR is a powerful diagnostic tool for the evaluation of myocarditis when clinically indicated. CMR is the only non-invasive imaging modality that can accurately measure myocardial function and provide tissue characterisation capable of detecting manifestations of myocarditis including necrosis/fibrosis/scar (using late gadolinium enhancement) and oedema/hyperaemia/capillary leak (using parametric mapping-derived T1 and T2 relaxation times).7 The European Society of Cardiology and the American Heart Association recommend a diagnostic algorithm for myocarditis predicated on both a clinical presentation suggestive of disease and concomitant abnormal diagnostic testing including data derived from CMR.8 9 Symptoms suggestive of myocarditis include acute/new-onset chest pain, dyspnoea, palpitations and syncope. Diagnostic criteria include ECG or rhythm abnormalities, elevated troponin, structural or functional abnormalities on cardiac imaging and abnormal tissue characterisation on CMR. Clinically suspected myocarditis is defined by the presence of ≥1 clinical symptom and ≥1 diagnostic criterion, or, in the absence of symptoms, ≥2 diagnostic criteria.8 Importantly, CMR-derived tissue characterisation abnormalities, in the absence of symptoms or other diagnostic abnormalities, do not fulfil the contemporary definition of clinical myocarditis.

CMR to screen for inflammatory heart disease

Effective screening tools are characterised by a balance between sensitivity and specificity that produces acceptable accuracy, manageable cost and adequate availability. To date, the use of CMR as a primary screening modality for inflammatory heart disease has not been rigorously studied. Theoretical consideration of CMR as a screening tool raises numerous concerns. There are inherent technical imaging challenges related to tissue characterisation and inconsistencies in clinical interpretation may arise from interpreter bias or inexperience. Specifically, techniques for parametric mapping, image acquisition and evaluation are vendor specific with heterogeneity across commercially available pulse sequences requiring imaging sites to derive their own normal reference ranges. Ideally, T1 and T2 times should be considered abnormal only when >2 SDs above the site-specific reference range. The degree to which these important technical details were considered in prior SARS-CoV-2 athlete studies is unclear and likely inadequate. Accurate CMR use is also highly dependent on acquisition and interpreter expertise. In small single-centre COVID-19 athlete studies, the prevalence of reported myocarditis ranged from 0% to 15%.3 10 Similarly, the prevalence of CMR-defined inflammatory heart disease in the Big Ten registry ranged from 0% to 7.6% among the participating 13 universities, with three sites reporting no myocarditis among 189 athletes.6 This marked heterogeneity is most likely not explained by underlying pathobiology but rather site-by-site technical and interpretation variability. The lack of a blinded core-laboratory review with healthy and appropriate case–controls also represents a significant limitation, and it must be emphasised that normative CMR data among young competitive athletes are sparse.6 Finally, CMR is expensive and frequently only available in tertiary care medical centres. Based on these considerations and the available evidence to date, devoting widespread CMR resources to screen athletes after SARS-CoV-2 infection is neither practical nor likely to improve clinical outcomes.

Adverse cardiac events following SARS-CoV-2 in athletes

The reported prevalence of SARS-CoV-2 cardiac injury among athletes ranges from 0.6% to 0.7% using a symptom-driven assessment followed by clinically indicated CMR,4 5 and 2.3%–3.0% when using CMR as the primary screening modality.4 6 Regardless, disease prevalence must always be coupled with disease relevance. It is noteworthy and highly reassuring that none of the large cohort studies in US collegiate and professional athletes, despite ongoing surveillance, have reported a confirmed SARS-CoV-2-associated adverse cardiac event. Accordingly, we recommend using CMR only when there is clinical suspicion of myocarditis, and we recommend against the use of CMR as a primary screening tool (table 1).

The French writer Jean-Baptiste Alphonse Karr coined the phrase ‘plus ça change, plus c’est la même chose’ (the more things change, the more they remain the same). Although many SARS-CoV-2 clinical uncertainties persist, the approach to cardiac testing following SARS-CoV-2 infection in athletes should rely on the clinical pretest probability of disease to determine the need for CMR. This approach is consistent with the proven strategy of using advanced diagnostic testing only when clinically indicated.