Otwarty dostęp

The Current Role of Cardiovascular Magnetic Resonance Imaging According to European Society of Cardiology Guidelines and Statements (Second part)

Ramona Bica
Ramona Bica
, 
Virgil Ionescu
Virgil Ionescu
, 
Jan Bogaert
Jan Bogaert
 oraz 
Anca Florian
Anca Florian
   | 05 maj 2022
Romanian Journal of Cardiology's Cover Image
O artykule
Poprzedni artykuł
Następny artykuł
Zacytuj
Article Category: Review
Data publikacji: 05 maj 2022
Zakres stron: 807 - 818
DOI: https://doi.org/10.47803/rjc.2020.31.4.807
© 2021 Ramona Bica et al., published by Sciendo
This work is licensed under the Creative Commons Attribution 4.0 International License.

Figure 1

Schematic exemplification of a rest CMR protocol used in the work-up of patients with non-ischemic and inflammatory cardiomyopathies, including functional (cine), rest contrast myocardial perfusion and tissue characterization: T2-STIR, T2-mapping, pre- and post-contrast T1-mapping, and late gadolinium enhancement (LGE) sequences. * - 0.15 mmol/kg.
Schematic exemplification of a rest CMR protocol used in the work-up of patients with non-ischemic and inflammatory cardiomyopathies, including functional (cine), rest contrast myocardial perfusion and tissue characterization: T2-STIR, T2-mapping, pre- and post-contrast T1-mapping, and late gadolinium enhancement (LGE) sequences. * - 0.15 mmol/kg.

Figure 2

Exemplary LGE images in three patients with different forms of hypertrophic cardiomyopathy (HCM) (A, B, C) and in one patient with inherited primary mitochondrial disease (D). In the first case, with non-obstructive HCM (A), a typical, non-ischemic, patchy LGE in the hypertrophied septum (white arrow) together with focal LGE in the RV insertion points (red arrows) is present. In the second case, with mid-ventricular obstructive HCM (B), transmural LGE with apical aneurysm formation and small apical thrombus can be noticed (white arrow). In the third case, with apical HCM (C), diffuse, non-ischemic LGE in the hypertrophied apical segments can be depicted (white arrow). Lastly, in the mitochondriopathy patient (D), extensive, circular, subepicardial/intramural (non-ischemic) LGE (white arrows) and concentric LV hypertrophy are seen.
Exemplary LGE images in three patients with different forms of hypertrophic cardiomyopathy (HCM) (A, B, C) and in one patient with inherited primary mitochondrial disease (D). In the first case, with non-obstructive HCM (A), a typical, non-ischemic, patchy LGE in the hypertrophied septum (white arrow) together with focal LGE in the RV insertion points (red arrows) is present. In the second case, with mid-ventricular obstructive HCM (B), transmural LGE with apical aneurysm formation and small apical thrombus can be noticed (white arrow). In the third case, with apical HCM (C), diffuse, non-ischemic LGE in the hypertrophied apical segments can be depicted (white arrow). Lastly, in the mitochondriopathy patient (D), extensive, circular, subepicardial/intramural (non-ischemic) LGE (white arrows) and concentric LV hypertrophy are seen.

Figure 3

Exemplary LGE images in three patients with dilated cardiomyopathy (DCM). In the first case, with idiopathic DCM (A), a characteristic, mid-wall (non-ischemic) LGE is seen in the basal and mid-ventricular septum (red arrows). In the second case, with post-inflammatory (myocarditis) DCM, a typical, almost “ring-like” subepicardial/intramural (non-ischemic) LGE in the basal and mid-ventricular segments can be depicted (white arrows). In the third case, with Becker muscular dystrophy and cardiac involvement, extensive LGE with a myocarditis-like pattern is present (arrow heads).
Exemplary LGE images in three patients with dilated cardiomyopathy (DCM). In the first case, with idiopathic DCM (A), a characteristic, mid-wall (non-ischemic) LGE is seen in the basal and mid-ventricular septum (red arrows). In the second case, with post-inflammatory (myocarditis) DCM, a typical, almost “ring-like” subepicardial/intramural (non-ischemic) LGE in the basal and mid-ventricular segments can be depicted (white arrows). In the third case, with Becker muscular dystrophy and cardiac involvement, extensive LGE with a myocarditis-like pattern is present (arrow heads).

Figure 4

Exemplary LGE images and corresponding, color-coded native T1 maps (no contrast needed) in a normal control and in two patients with hypertrophic phenotypes. In the first case, with Anderson-Fabry cardiomyopathy, a reduced septal native T1 time (where fibrosis is absent) due to lipid accumulation together with characteristic intramural fibrosis (LGE) in the basal lateral wall (white arrow) can be seen. In the second case, with AL cardiac amyloidosis, an elevated native T1 myocardial time together with extensive, almost circular LGE, more pronounced in the subendocardium and involving also the RV (septum and inferior wall) can be depicted.
Exemplary LGE images and corresponding, color-coded native T1 maps (no contrast needed) in a normal control and in two patients with hypertrophic phenotypes. In the first case, with Anderson-Fabry cardiomyopathy, a reduced septal native T1 time (where fibrosis is absent) due to lipid accumulation together with characteristic intramural fibrosis (LGE) in the basal lateral wall (white arrow) can be seen. In the second case, with AL cardiac amyloidosis, an elevated native T1 myocardial time together with extensive, almost circular LGE, more pronounced in the subendocardium and involving also the RV (septum and inferior wall) can be depicted.

Figure 5

Edema sensitive T2-STIR (A, B, C) and LGE images (D, E, F) in a patient with acute viral myocarditis. Acute, non-ischemic, inflammatory changes with edema (T2-hyperintensity, red arrows) and LGE (white arrows) in the subepicardium of the inferior and lateral walls, extending towards the anterior wall, can be noticed.
Edema sensitive T2-STIR (A, B, C) and LGE images (D, E, F) in a patient with acute viral myocarditis. Acute, non-ischemic, inflammatory changes with edema (T2-hyperintensity, red arrows) and LGE (white arrows) in the subepicardium of the inferior and lateral walls, extending towards the anterior wall, can be noticed.

Figure 6

Cine images at end-diastole (A) and end-systole (B) as well as LGE images in basal short-axis (C) and four-chamber view (D) in a patient with arrhythmogenic RV cardiomyopathy. A dilated RV with dys-kinetic basal and apical lateral wall (B, red arrows) and corresponding fibrotic changes (LGE) in the basal inferior/lateral and apical lateral RV walls (C, D, white arrows) can be seen.
Cine images at end-diastole (A) and end-systole (B) as well as LGE images in basal short-axis (C) and four-chamber view (D) in a patient with arrhythmogenic RV cardiomyopathy. A dilated RV with dys-kinetic basal and apical lateral wall (B, red arrows) and corresponding fibrotic changes (LGE) in the basal inferior/lateral and apical lateral RV walls (C, D, white arrows) can be seen.
eISSN:
2734-6382
Język:
Angielski
Częstotliwość wydawania:
4 razy w roku
Dziedziny czasopisma:
Medicine, Clinical Medicine, Internal Medicine, Cardiology, Pediatrics and Juvenile Medicine, Paediatric Cardiology, Surgery, Cardiac Surgery
Kanał RSS czasopisma