Diagnostic and prognostic role of late gadolinium enhancement in cardiomyopathies

Abstract

Late gadolinium enhancement (LGE) is the most relevant tool of cardiac magnetic resonance for tissue characterization, and it plays a pivotal role for diagnostic and prognostic assessment of cardiomyopathies. The pattern of presentation of LGE allows differential diagnosis between ischaemic and non-ischaemic heart disease with high diagnostic accuracy, and among different cardiomyopathies, specific presentation of LGE may help to make a diagnosis. Late gadolinium enhancement may be caused by conditions that significantly increase the interstitial space or, less frequently, that slow down Gd exit, like myocardial fibrosis. In chronic myocardial infarction, hypertrophic cardiomyopathies (HCM), dilated cardiomyopathy, Fabry disease, and other conditions, LGE is a marker of myocardial fibrosis, but also in patients with acute myocarditis where LGE may be also explained by the increase of interstitial space caused by interstitial oedema or by tissue infiltration of inflammatory cells. In cardiac amyloidosis, LGE represents myocardial fibrosis but the interstitial overload of amyloid proteins should also be considered as a potential cause of LGE. The identification of the pattern of presentation of LGE is also very important. In the ischaemic pattern, LGE always involves the subendocardial layer with more or less transmural extent, it is confluent, and every single scar should be located in the territory of one coronary artery. In the non-ischaemic pattern, LGE does not fulfil the previous criteria, being midwall, subepicardial, or mixed, not necessarily confluent or confined to a territory of one coronary artery. For cardiomyopathies, the exact pattern of non-ischaemic LGE is important. Quantitative analysis of LGE is required in some specific conditions as in HCM. Magnetic resonance imaging with LGE technique should be performed in every patient with suspect of cardiomyopathy. The lack of standardization of pulse sequence and mostly of quantification methods is the main limitation of LGE technique.

Myocardial Tissue Characterization in Patients with Hypertensive Crisis, Positive Troponin, and Unobstructed Coronary Arteries: A Cardiovascular Magnetic Resonance-Based Study

“…Acute myocardial injury and type 2 myocardial infarction are associated with an increased risk of MACE more than type 1 myocardial infarction [ 41 ], and the high prevalence of all forms of LGE observed in this study may contribute to the risks. Although generally considered a marker of myocardial fibrosis, LGE is not exclusively seen in fibrosis and can occur in acute myocardial necrosis [ 42 ]. Similarly, the vascular changes associated with a hypertensive crisis may result in areas of acute myocardial necrosis, elevated cardiac troponin, and focal/patchy LGE.…”

Sudden cardiac death during scuba diving: a case report of a patient with unknown hypertrophic cardiomyopathy

“…The exam confirmed LV concentric hypertrophy ( Figures 1 and 2 ) and showed myocardial fibrosis in the most hypertrophied area as well as extensive oedema (as a sign of acute myocardial damage; Figure 2 ). 8–10 …”

A Novel Approach to Cardiac Magnetic Resonance Scar Characterization in Patients Affected by Cardiac Amyloidosis: A Pilot Study

“…The former is mainly located in basal and mid-ventricular regions; it is mostly prevalent in the AL variant of CA and can be enhanced by dark-blood acquisitions. On the other hand, the transmural pattern is a better predictor of adverse outcomes [8][9][10][11]. A less described feature is atrial LGE; this finding represents another important marker of CA that is frequently associated with atrial dysfunction and carries a high specificity for the disease [12].…”