We read with interest the article by d’Angelo et al. about a 30yo male diagnosed with myocarditis 3d after the second dose of an mRNA-based SARS-CoV-2 vaccine upon sub-epicardial late gadolinium enhancement (LGE) on cardiac MRI [1]. Symptoms resolved upon acetyl-salicylic acid, bisoprolol, and steroids [1]. It was concluded that clinicians should remain vigilant and suspect myocarditis in patients with cardiopulmonary symptoms after recent SARS-CoV-2 vaccinations [1]. The study is appealing but raises concerns.

LGE is not only a feature of myocarditis but also a classical cMRI feature of left ventricular hypertrabeculation (LVHT), also known as left ventricular noncompaction (LVNC) [2]. In patients with LVHT, LGE can be found sub-endocardially mid-myocardially, or sub-epicardially [3]. LGE can be also a feature of myocardial fibrosis due to inherited or acquired cardiomyopathy [4]. Thus, we should know if LVHT and myocardial fibrosis were appropriately excluded in the index patient. From the provided cMRI slices it cannot be assessed if LVHT was present in the left-ventricular apex as no axial layers distal to the papillary muscles are shown. 

Since the patient complained about retrosternal pain on admission we should know if it was dependent on inspiration or expiration. Supposing it increased on inspiration, pericarditis or pleuritic is quite likely. An argument for pericarditis is that there was mild pericardial effusion on transthoracic echocardiography and that subepicardial enhancement on cMRI can represent concomitant affection of the myocardium. An argument in favour of myocarditis is the presence of myocardial edema, which was only mentioned in the discussion but not the case description. Thus, we should know if there was indeed transmural myocardial swelling or not. 

Missing are follow-up cMRI figures, demonstrating that the features described on hospital-day-3 completely resolved. Missing is the information on which hospital-day steroids were started and in which dosage. Knowing the time course/dosages of the applied drugs is crucial to assess if resolution of symptoms and decline of troponin, CK-MB, and CRP are truly attributable to the medication or simply reflect the spontaneous course. From bisoprolol alone it cannot be expected that it lowers troponin, CRP, and CK-MB. If steroids were started not earlier than on hospital-day-4, clinical improvement and decline of elevated blood parameters is rather attributable to spontaneous recovery.

A limitation is that no endo-myocardial biopsy was performed to confirm/exclude myocarditis upon histological investigation of the myocardium.

Overall, the report has several limitations which challenge the results and their interpretation. These limitations should be addressed to strengthen the conclusions.