Role of cardiac magnetic resonance in the evaluation of dilated cardiomyopathy: diagnostic contribution and prognostic significance

Abstract

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.

Figure 1

Idiopathic dilated cardiomiopathy in a 27-year-old asymptomatic patient occasionally identified during a routinary clinical screening. T1-weighted turbo spin echo 4-chamber image (a) shows a hugely dilated left ventricular chamber (end-diastolic volume 296 mL; ejection fraction 26%). Late gadolinium enhancement image acquired on the same orientation plane (b) shows absence of pathological enhancement within both ventricular chambers. There is also concomitant significant amount of pericardial effusion (arrow) located within the midbasal left ventricular lateral free wall which was initially interpreted as expression of a post pericardiomyocarditis form.

Figure 2

Postischemic dilated cardiomyopathy in a 69-year-old patient with severe dyspnea and symptoms of systemic heart failure. Cine-SSFP short-axis images displayed on end-diastolic (a) and end-systolic (b) phases show a markedly dilated left ventricular chamber (EDV: 287 mL) with severely compromised ejection fraction (11%). LGE image (c) depicts extensive ischemic scarring within the anterior and antero-septal and lateral walls of the left ventricle with typical subendocardial distribution of myocardial enhancement. Minimal right ventricular involvement is also present and observed as a linear hyperintense rim at the level of the right interventricular septum. Selective coronary angiography confirmed the presence of a severe 3-vessel disease which was only treated with medical therapy.

Figure 3

A specific midwall late enhancement stria in a 71-year-old patient with chronic dilated CMP. LGE image (a) acquired in a 4-chamber plane shows a linear post-Gd hyperintensity located within the midlateral wall of the left ventricle without corresponding to T2-STIR (b) signal abnormality. The present finding likely represents the expression of a postmyocarditic form of disease (inconfirmed in this patient).

Figure 4

Cardiac magnetic resonance (CMR) exam performed in a 45-year-old patient with acute (5th day) myocarditis presenting a cardiomyopathic onset of disease. T2 short-tau inversion recovery image (T2-STIR) acquired on mid-ventricular short axis (a) shows subepicardial edematous imbibition of the anterior and inferolateral segment of the left ventricular myocardium (arrows) with corresponding late gadolinium enhancement with the same nonischemic pattern of distribution ((b)-(c)). Left ventricle appears moderately dilated (EDV: 203 mL); systolic function was depressed (EF: 32%).

Figure 5

Anthracyclines induced dilated cardiomyopathy assessed with cardiac magnetic resonance at symptoms onset ((a), (b)) and eight months after drug suspension ((c), (d)). At clinical presentation, end-diastolic and end-systolic cine steady-state free-precession images show increased left ventricular volumes (EDV: 166 mL; ESV: 106 mL) with a reduced ejection fraction of 36% and a regional wall motion abnormality mostly involving apical segments. After contrast administration (b), patchy subtle areas of inhomogeneous late enhancement predominantly subepicardially distributed are depicted mostly involving the inferior and inferolateral wall of the left ventricle (arrows) and likely representing foci of replacement fibrosis related to the active inflammation associated with the drug's exposure. At follow-up ((c), (d)) after drug suspension, cine-MR shows significant recovery in global LV function (EDV 151.4 mL; ESV: 77 mL; EF: 49%) with reduced wall thickness (midseptal wall thickness from 13 mm to 10 mm). At late enhancement imaging (d), regional hyperintensity is no longer observed highly suggesting the healing of the process.