Follow-up assessment of myocardial calcification secondary to fulminant myocarditis with computed tomography

A 16-year-old man underwent venoarterial extracorporeal membrane oxygenation (VA-ECMO) therapy due to hemodynamic collapse caused by viral fulminant myocarditis. Supplementary Figure 1 presents the time course of treatment. High-density areas wtihin the myocardium were initially detected by computed tomography (CT) 10 days after admission which was not observed on admission (Fig. 1A). The CT tissue attenuation value reached 106 Hounsfield Unit (HU) in these areas 40 days after admission (Fig. 1B), with changes in the left lateral wall being more evident than other areas. The patient's hemodynamic condition gradually improved and he was discharged 2 months after admission with cardiac function meeting New York Heart Association class II criteria. The patient's myocardial calcification and cardiac function were followed periodically with CT and echocardiography, respectively. As shown in Supplementary Figure 2, Supplementary Figure 3, the cardiac function remained stable after discharge and the density of calcification reached its peak (CT value of 142 HU) seven months after admission, followed by a subtle decline (Fig. 1C). Furthermore, the right ventricular calcification almost disappeared at 1-year follow-up (Fig. 1D), while the left ventricular calcification just regressed slightly 3 years after admission (Fig. 1E). Dystrophic myocardial calcification is a rare but possibly life-threatening complication of viral myocarditis. Dystrophic calcification is the pathological calcification observed in the ischemic and injured areas. As in our case, the calcium salts accumulated in the myocardium as result from damage from inflammatory cytokines released from Epstein–Barr (EB) virus. Additionally, previous reports pointed out that the use of VA-ECMO support and high-dose exogenous glucocorticoids could lead to an imbalance in calcium-phosphate homeostasis.1Kapandji N. Redheuil A. Fouret P. et al.Extensive myocardial calcification in critically ill patients.Crit Care Med. 2018; 46: e702-e706Crossref PubMed Scopus (10) Google Scholar,2Sato A.Y. Peacock M. Bellido T. Glucocorticoid excess in bone and muscle.Clin Rev Bone Miner Metabol. 2018; 16: 33-47Crossref PubMed Scopus (31) Google Scholar However, serum calcium levels of the patient were always normal or decreased slightly, and the exact mechanisms are still unclear. In our case, repeated CT scans revealed a detailed progression of calcium deposition during follow-up. Remarkably, cardiac magnetic resonance (CMR) and echocardiography during follow-up suggested normal left ventricular function although there was massive ventricular calcification, which was different from several prior reports.3Nance Jr., J.W. Crane G.M. Halushka M.K. Fishman E.K. Zimmerman S.L. Myocardial calcifications: pathophysiology, etiologies, differential diagnoses, and imaging findings.J Cardiovasc Comput Tomogr. 2015; 9: 58-67Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar,4Lippolis A. Buzzi M.P. Romano I.J. Dadone V. Gentile F. Stone heart: an unusual case of heart failure with preserved ejection fraction due to massive myocardial calcification.J Cardiol Cases. 2021; 23: 145-148Abstract Full Text Full Text PDF PubMed Scopus (2) Google Scholar Perhaps, these observations were linked to a timely and effective comprehensive treatment regimen. The exact mechanisms still need further investigation. In conclusion, myocardial calcification can progress over time and is probably not a marker of a pathologic process that influences cardiac function. Our report underlines the importance of early intervention, efficient management, and the utility of CT which plays a key role in thoroughly managing and evaluating the prognosis of patients with myocardial calcification secondary to viral myocarditis. This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.