Dilated cardiomyopathy (DCM) represents the final common morphofunctional pathway of various pathological conditions in which a combination of myocyte injury and necrosis associated with tissue fibrosis results in impaired mechanical function. Recognition of the underlying aetiology of disease and accurate disease monitoring may be crucial to individually optimize therapeutic strategies and stratify patient’s prognosis. In this regard, CMR has emerged as a new reference gold standard providing important information for differential diagnosis and new insight about individual risk stratification. The present review article will focus on the role of CMR in the evaluation of present condition, analysing respective strengths and limitations in the light of current literature and technological developments. 1. Introduction The main hallmark of primary dilated cardiomyopathy (DCM) is the presence of a left or biventricular dilatation with severely impaired systolic function in the absence of abnormal loading conditions (i.e., hypertension, valve disease, etc.) or ischaemic heart disease sufficient to cause global systolic impairment [1–5]. Primary forms of disease are diagnosed in approximately 30–40% of the cases and include a series of genetic, acquired, or mixed conditions in which the pathological involvement is predominantly limited to the myocardium and associated with a strong genetic inheritance in idiopathic cases (≈30% of patients). In secondary DCM conversely, ventricular dilation occurs as the final stage of extensive myocardial damage which can be associated with an extremely heterogeneous group of systemic affections from autoimmune, cytotoxic or metabolic diseases [1, 6–13]. Recognition and differentiation of the underlying pathological substrate leading to ventricular dilatation may be crucial not only to specifically the target patient’s therapy (e.g., treatment of heart failure symptoms versus revascularization versus immunosuppressive and/or antiviral) but also for better individual risk stratification because of the extremely variable prognostic implications associated with the different forms of disease [14–17]. Postischemic DCM, for example, is the consequence of postischemic ventricular remodelling leading to chronic heart failure which is usually associated with a worse prognosis [18–20] and may benefit from revascularization and/or secondary preventive pharmacotherapy with statins and aspirin; among nonischemic forms, the worst prognosis had been associated with infiltrative myocardial disease (including amyloidosis, sarcoidosis, or
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