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Myocardial Late Enhancement in Contrast-Enhanced Cardiac MRI: Distinction Between Infarction Scar and Non–Infarction-Related Disease

Peter Hunold1, Thomas Schlosser1, Florian M. Vogt1, Holger Eggebrecht2, Axel Schmermund2, Oliver Bruder3, Walter O. Schüler3 and Jörg Barkhausen1

1 Department of Diagnostic and Interventional Radiology and Neuroradiology, University Hospital Essen, Hufelandstrasse 55, 45122 Essen, Germany.
2 Department of Cardiology, West German Heart Center, University Hospital, 45122 Essen, Germany.
3 Department of Cardiology, Elisabeth Hospital, 45138 Essen, Germany.



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Fig. 1. Schematic of midventricular short-axis image of left ventricle after contrast material administration. Black area is normal myocardium; late enhancement (LE) within myocardium is indicated in gray. Different patterns of LE are shown.

A, Transmural LE in anterior wall.

B, Subendocardial LE in lateral and inferior walls.

C, Midmyocardial LE in interventricular septum.

D, Subepicardial LE in inferior wall.

 


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Fig. 2. 78-year-old man with known history of chronic myocardial infarction. Horizontal and vertical long-axis views and two short-axis slices of left ventricle show extensive subendocardial late enhancement, confirming nontransmural infarction of segments 7, 10, 13, 14, and 16. Typical pattern of ischemic lesion with only subendocardial involvement of large area is shown.

 


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Fig. 3. 23-year-old man (patient 1) with chest pain and shortness of breath during exercise. Systemic signs of inflammation, reduced left ventricle function (ejection fraction, 42%), and MRI led to diagnosis of acute myocarditis. Contrast-enhanced turbo FLASH images in horizontal long-axis (A) and short-axis (B) orientations show clearly demarcated intramural late enhancement in parts of septum and anterior, anteroseptal, and lateral walls (segments 1, 6–8, 11–14). Small subepicardial rim is seen in inferior wall (segment 10) (C). T2-weighted turbo spin-echo image in horizontal long-axis orientation shows hyperintense signal in corresponding areas, indicating edema.

 


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Fig. 4. 60-year-old man (patient 3) with suspected perimyocarditis in adolescence. Shown are turbo FLASH images in long-axis (A) and short-axis (B and C) orientations. Small area of central late enhancement (LE) can be seen in midseptum (A and C; segment 9). Another area of subepicardial LE is shown in inferolateral, inferior, and inferoseptal walls in midventricle, which cannot clearly be separated from pericardium (A, B, and C; segments 9, 10, and 11) and basal lateral wall (A; segment 5).

 


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Fig. 5. 48-year-old man (patient 5) with myocardial involvement of acute sarcoidosis. Contrast-enhanced turbo FLASH images in horizontal (A), vertical (B), and short-axis (C) orientation show clearly defined late enhancement (LE) in large parts of left ventricle myocardium. Mainly, LE presents transmural extent. Basal parts of septum, however, show subendocardial LE. Note subepicardial LE with unenhanced subendocardial layer in anterior and anteroseptal regions in panel C.

 


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Fig. 6. 48-year-old woman (patient 10) with history of sustained ventricular tachycardia and echocardiographic diagnosis of hypertrophic cardiomyopathy. Manual planimetry of left ventricle (LV) short axes revealed LV myocardial mass index of 178 g/m2. Turbo FLASH images after administration of gadopentetate dimeglumine in vertical long-axis (A) and short-axis (B) show diffuse, poorly demarcated late enhancement of midmyocardial layer of LV mid portion and apical portion (A; segments 7, 10, 13, and 15) and lateral and anterior walls (B; segments 7, 11, and 12).

 


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Fig. 7. 59-year-old woman (patient 15) with multiple strokes due to embolism from histologically proven endomyocardial fibrosis in right and left ventricles. Contrast-enhanced turbo FLASH images in horizontal long-axis orientation immediately after injection of gadopentetate dimeglumine (A), 4 min after injection (B), and 11 min after injection (C) are shown. Thrombotic and fibrotic material in both ventricles reveals no early perfusion, whereas it enhances centripetally during course of several minutes, indicating partly fibrotic organization of thrombi.

 


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Fig. 8. 62-year-old man (patient 15) with hypertrophic obstructive cardiomyopathy (HOCM), with left ventricle myocardial mass index of 119 g/m2. Invasively measured intraventricular pressure gradient approximated 100 mm Hg. Patient underwent transcoronary ablation of septal hypertrophy (TASH) 14 months before MRI study. There is "subepicardial" nontransmural scar from TASH in middle portion of intraventricular septum, which failed to improve gradient because of wrong localization of scar. Another scar is shown in basal and midventricular portions of the lateral wall caused by subendocardial myocardial infarction that occurred 4 years previously.

 

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