Excerpt

Cerny et al. provided an important investigation comparing cardiac CT (CCT) and delayed contrast-enhanced cardiac magnetic resonance (DE-CMR) in consecutive patients with dilated cardiomyopathy (DCM) [1]. At first glance, CCT may not be of particular advantage compared with CMR, since the limitation of low glomerular filtration rate is comparable for both techniques, and, moreover, CCT also involves a considerable radiation dosage. However, although the representational value of this comparative analysis may be limited because of the small number of DCM patients (n = 17), the high positive predictive value (100%) and the high specificity (100%) argue for a substantial value of CCT in reliably detecting myocardial scar in DCM. The lower reported sensitivity (50%) [1] may be attributable to further factors in addition to methodological differences between CCT and CMR. DE-CMR has been associated not only with interstitial fibrosis, but also with chronic intramyocardial inflammation in DCM, which is also linked to an adverse prognosis [2‐4]. The clinical spectrum of DCM comprises a heterogeneous pathogenesis, including myocarditis [5, 6]. The gold standard for detecting chronic intramyocardial inflammation in DCM and myocarditis, namely, inflammatory cardiomyopathy (DCMi), is the immunohistological evaluation targeting diverse phenotypes of infiltrates and the endothelial abundance of cell adhesion molecules in endomyocardial biopsies (EMB) [7, 8]. Considering the established high association between DE-CMR and the immunohistological detection of DCMi [9], we suggest that additional sources of DE-CMR may have been undetectable by CCT. Thus, the discrepancy regarding the sensitivity in the direct comparison between CCT and DE-CMR might not be due to a methodological shortcoming of CCT, but might hint toward a clear differentiation between inflammation and genuine scar without a substantial inflammatory component, the latter not being able to be differentiated by DE-CMR. A further issue that has not been sufficiently understood is the frequent localization in the anterolateral wall of the left ventricle and within the interventricular septum as reported with DE-CMR. However, the positivity frequency of DCMi and of viral genomes does not differ between right and left ventricular EMB [9]. Ultimately, this differentiation between scar and additional inflammation (that also always causes interstitial fibrosis), which is currently not possible by CMR, might be important for the guidance of immunomodulatory treatment strategies. …