Summary
Myocardial late enhancement, an imaging technique acquired after gadolinium administration, has become an integral part of cardiovascular magnetic resonance imaging over the past decade. Initially principally utilized for imaging myocardial infarction, more recently it has also become an invaluable tool for identifying myocardial scarring in other cardiomyopathic processes. Our experience using this technique has led us to identify several manifestations of late gadolinium enhancement imaging that can confound interpretation of pathology and potentially lead to misinterpretation and subsequently misdiagnosis for the patient. The purpose of this article is to review and illustrate typical and atypical myocardial late enhancement in the most common myocardial diseases seen in routine clinical practice.
Résumé
Les séquences de rehaussement tardifs, acquis après injection de produit de contraste sont devenues une part clé de l’IRM cardiaque. Initialement utilisée dans l’imagerie de l’infarctus du myocarde, ces séquences sont devenues un outil indispensable d’identification de cicatrice myocardique dans un grand nombre de cardiomyopathies. Notre expérience dans ce domaine nous a conduit à identifier des rehaussements tardifs typiques mais également atypiques pouvant potentiellement conduire à des diagnostics erronés. Le but de cette revue est d’identifier et d’illustrer des rehaussements tardifs typique et atypiques dans quatre principales cardiomypathies (infarctus aigu du myocarde, myocardite, cardiopathie dilatée et cardiopathie hypertrophique).
Technical aspects of late gadolinium enhancement
A myocardial LGE study is performed 10 to 20 minutes after injection of an extracellular contrast agent that distributes in extracellular water but cannot cross the intact myocyte cell membrane. LGE imaging utilizes inversion-recovery gradient echo sequences with the inversion time set to null viable myocardium.
The technique for LGE imaging has been shown to be effective in identifying the presence and extent of myocardial scarring. Compared with normal myocardium, the wash out of gadolinium in a myocardial scar is delayed. In the acute stage (i.e. necrosis), leaky cell membranes allow gadolinium to enter the cells, thereby increasing the volume of distribution of gadolinium, resulting in a bright signal intensity of suitable inversion-recovery (‘LGE’) images . In the chronic setting, fibrous tissue replaces necrotic tissue and is associated with a significant expansion of the interstitial space and a subsequent increase in the volume of distribution of gadolinium . The enhancement is not disease specific and can be caused by ischaemic necrosis, inflammatory or infectious pathology, ischaemic and non-ischaemic scars and tumorous lesions.
Different patterns of LGE have been described, primarily segmented into ischaemic and non-ischaemic patterns. Ischaemic necrosis expands from the subendocardium to the epicardium with increasing coronary occlusion time . Infarct-related areas of bright signal in LGE images are typically subendocardial with an increasing degree of transmural extension, depending on the extent of the infarct. The circumferential extent is related to the size of the perfusion bed and the location of the coronary artery occlusion. Conversely, in the non-ischaemic pattern, the subendocardium typically is spared, with the high-signal areas localized in the midwall and subepicardium, appearing patchy or more diffuse.
For a number of ischaemic and non-ischaemic disease processes, LGE has a well-defined typical pattern. However, LGE can appear atypical and can be challenging for the reader. The purpose of this article is to review and describe typical and atypical myocardial LGE in common myocardial diseases.
Clinical setting of acute myocardial infarction
LGE imaging facilitates establishing the diagnosis and quantitative assessment of MI. Hyperintense areas of LGE accurately depict the location and extent of irreversibly injured myocardium. Typically, LGE in acute MI almost always involves the subendocardial layer, with increasing degrees of transmurality depending on the total occlusion time, while the subendocardial extent of infarct depends on the localization of the occlusion (proximal versus distal) and the size of the perfusion bed dependent on the occluded coronary artery. An acute reperfused MI can be associated with MVO . The presence and absolute amount of MVO are associated with adverse left ventricular remodelling and prognosis . In LGE and other postcontrast images, MVO typically appears as a low-signal area within the bright infarcted zone, lacking significant uptake of gadolinium unlike the enhanced surrounding infarct tissue ( Fig. 1 ). Atypically, MVO may involve the subendocardium predominantly, which can be challenging for the clinician, mimicking a ‘normal myocardium’ and suggesting a non-ischaemic pattern or a left ventricular thrombus. Careful examination of short-axis and long-axis views enables differentiation between thrombus, normal myocardium and MVO ( Fig. 2 ).
In the clinical setting of acute MI, CMR imaging is indicated for accurate assessment of right and left ventricular function, identifying the presence of thrombus, assessing the amount of salvaged myocardium and guiding prognosis by the presence of MVO.
Clinical setting of acute myocarditis
Acute myocarditis is an inflammatory disease of the myocardium associated with oedema, cellular infiltration and myocyte necrosis . The clinical manifestations of myocarditis vary and are frequently insidious and non-specific. CMR is the non-invasive diagnostic tool of choice for assessing myocarditis and is recommended in symptomatic patients with suspected myocarditis . Recently, standard diagnostic CMR criteria for myocarditis have been proposed based on oedema, hyperaemia/capillary leakage and irreversible injury (necrosis/fibrosis) detected in T2-weighted and T1-weighted images before and after contrast administration . If two or more of the three criteria are positive, the diagnostic accuracy is 78%, while LGE imaging alone has a diagnostic accuracy of 68% with limited sensitivity.
In acute myocarditis, areas of LGE represent irreversibly injured myocardial tissue related to increased volume of distribution as a result of myocardial necrosis . Typically, LGE is located in the lateral, inferolateral or inferior wall with a midwall to subepicardial distribution; in young male patients a ‘pearl necklace’ is observed frequently ( Fig. 3 ). These regional distribution patterns are distinct from the more uniform patterns found in MI, which consistently includes the subendocardium. Importantly, however, atypical cases of myocarditis may present with transmural ( Fig. 4 ) or diffuse enhancement ( Fig. 5 ).
