DOI: 10.1148/rg.263055047
Delayed Enhancement MR Imaging: Utility in Myocardial Assessment1
Jens Vogel-Claussen, MD,
Carlos E. Rochitte, MD,
Katherine C. Wu, MD,
Ihab R. Kamel, MD, PhD,
Thomas K. Foo, PhD,
João A. C. Lima, MD, MBA and
David A. Bluemke, MD, PhD
1 From the Departments of Radiology (J.V.C., I.R.K., J.A.C.L., D.A.B.) and Cardiology (K.C.W., J.A.C.L., D.A.B.), Johns Hopkins Hospital, MRI, Room 143 (Nelson Basement), 600 N Wolfe St, Baltimore, MD 21287; the Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil (C.E.R.); and GE Health Systems, Baltimore, Md (T.K.F.). Recipient of a Certificate of Merit award for an education exhibit at the 2004 RSNA Annual Meeting. Received March 10, 2005; revision requested June 8 and received July 29; accepted August 9. The authors discuss an investigational or unlabeled use of a commercial product, device, or pharmaceutical that has not been approved for such purpose by the FDA. T.K.F. is an employee of GE Health Systems; J.A.C.L. is a member of the speakers bureau of GE Healthcare, Waukesha, Wis; all other authors have no financial relationships to disclose.
View larger version (31K):
[in a new window]
|
Figure 1a. (a) Relaxation of myocardium with delayed enhancement and normal myocardium. Optimal image contrast between myocardial areas of delayed enhancement (solid line) and normal myocardium (dashed line) is achieved by imaging at the null point of normal myocardium and adjusting the inversion time for each patient (3). In this example, the inversion time (dotted line) is 275 msec. MI = myocardial infarction. (b) Diagram of a delayed myocardial contrast-enhanced MR imaging sequence. The image acquisition starts after or around the center of the individually selected inversion time (TI), depending on the vendor. ECG = electrocardiogram.
|
|
View larger version (20K):
[in a new window]
|
Figure 1b. (a) Relaxation of myocardium with delayed enhancement and normal myocardium. Optimal image contrast between myocardial areas of delayed enhancement (solid line) and normal myocardium (dashed line) is achieved by imaging at the null point of normal myocardium and adjusting the inversion time for each patient (3). In this example, the inversion time (dotted line) is 275 msec. MI = myocardial infarction. (b) Diagram of a delayed myocardial contrast-enhanced MR imaging sequence. The image acquisition starts after or around the center of the individually selected inversion time (TI), depending on the vendor. ECG = electrocardiogram.
|
|
View larger version (128K):
[in a new window]
|
Figure 2. The inversion time (TI) is optimized for each patient by using low-resolution breath-hold images. The optimal inversion time (180 msec in this example) is visually selected to maximize both signal-to-noise ratio and contrast-to-noise ratio of the left ventricle.
|
|
View larger version (139K):
[in a new window]
|
Figure 3a. Acute myocardial infarction in a 53-year-old man with chest pain. (a) Short-axis first-pass perfusion MR image shows lack of subendocardial enhancement in the territory of the left anterior descending artery (arrows) due to microvascular obstruction. (b) Short-axis delayed MR image shows nearly transmural delayed myocardial enhancement in the territory of the left anterior descending artery (arrows). In addition, there is persistence of the region of microvascular obstruction.
|
|
View larger version (152K):
[in a new window]
|
Figure 3b. Acute myocardial infarction in a 53-year-old man with chest pain. (a) Short-axis first-pass perfusion MR image shows lack of subendocardial enhancement in the territory of the left anterior descending artery (arrows) due to microvascular obstruction. (b) Short-axis delayed MR image shows nearly transmural delayed myocardial enhancement in the territory of the left anterior descending artery (arrows). In addition, there is persistence of the region of microvascular obstruction.
|
|
View larger version (130K):
[in a new window]
|
Figure 4a. True aneurysm and thrombus in a 67-year-old man after a myocardial infarction. Two-chamber (a) and four-chamber (b) MR images show moderate thinning and delayed myocardial enhancement of the anterior left ventricular wall (arrows) with an aneurysm; these findings were due to a chronic full-thickness myocardial infarction. The aneurysm is complicated by a mural thrombus. True aneurysms, which are composed of pericardium adherent to underlying epicardium and scar tissue from infarcted myocardium, can be distinguished from false aneurysms, which consist of pericardium that contains a ruptured left ventricle. False aneurysms are not expected to demonstrate high signal intensity in the wall on delayed enhancement MR images due to lack of scar tissue. Because false aneurysms represent contained myocardial ruptures, they require urgent surgical repair.
|
|
View larger version (146K):
[in a new window]
|
Figure 4b. True aneurysm and thrombus in a 67-year-old man after a myocardial infarction. Two-chamber (a) and four-chamber (b) MR images show moderate thinning and delayed myocardial enhancement of the anterior left ventricular wall (arrows) with an aneurysm; these findings were due to a chronic full-thickness myocardial infarction. The aneurysm is complicated by a mural thrombus. True aneurysms, which are composed of pericardium adherent to underlying epicardium and scar tissue from infarcted myocardium, can be distinguished from false aneurysms, which consist of pericardium that contains a ruptured left ventricle. False aneurysms are not expected to demonstrate high signal intensity in the wall on delayed enhancement MR images due to lack of scar tissue. Because false aneurysms represent contained myocardial ruptures, they require urgent surgical repair.
|
|
View larger version (149K):
[in a new window]
|
Figure 5a. Acute and chronic transmural myocardial infarction in a 68-year-old man with chest pain. (a) Short-axis delayed enhancement MR image shows a transmural (100%) acute myocardial infarction in the lateral and inferior left ventricular wall (arrows), a site compatible with a dominant right coronary artery territory. No left ventricular atrophy in the infarcted territory has occurred. (b) Corresponding image obtained 5 months later shows persistent delayed enhancement in the infarcted area (arrows), which demonstrates thinning relative to its appearance on the acute-phase image.
|
|
View larger version (161K):
[in a new window]
|
Figure 5b. Acute and chronic transmural myocardial infarction in a 68-year-old man with chest pain. (a) Short-axis delayed enhancement MR image shows a transmural (100%) acute myocardial infarction in the lateral and inferior left ventricular wall (arrows), a site compatible with a dominant right coronary artery territory. No left ventricular atrophy in the infarcted territory has occurred. (b) Corresponding image obtained 5 months later shows persistent delayed enhancement in the infarcted area (arrows), which demonstrates thinning relative to its appearance on the acute-phase image.
|
|
View larger version (139K):
[in a new window]
|
Figure 6a. Idiopathic myocarditis in a 22-year-old woman. The patient presented 3 months earlier to an outside hospital with chest pain and fever. Follow-up MR imaging was performed to assess left ventricular function and evaluate scar extent. Four-chamber (a) and short-axis (b) delayed enhancement MR images show characteristic enhancement of the myocardial midwall at the septum and apex (arrow), an appearance typical of prior myocarditis.
|
|
View larger version (128K):
[in a new window]
|
Figure 6b. Idiopathic myocarditis in a 22-year-old woman. The patient presented 3 months earlier to an outside hospital with chest pain and fever. Follow-up MR imaging was performed to assess left ventricular function and evaluate scar extent. Four-chamber (a) and short-axis (b) delayed enhancement MR images show characteristic enhancement of the myocardial midwall at the septum and apex (arrow), an appearance typical of prior myocarditis.
|
|
View larger version (133K):
[in a new window]
|
Figure 7a. Acute idiopathic myocarditis in a 30-year-old man with frequent premature ventricular contractions and normal results at coronary angiography. Two-chamber long-axis MR image of the left ventricle (a) and short-axis MR image (b) show extensive scattered delayed enhancement in the anterior, lateral, and inferior wall and apex of the left ventricle and the right ventricular wall (arrows). The endocardium is relatively spared by the inflammation, which occurs predominantly in the epicardium and mid myocardial wall. This distribution is typical of myocarditis. (Case courtesy of Dr John Freeby.)
|
|
View larger version (137K):
[in a new window]
|
Figure 7b. Acute idiopathic myocarditis in a 30-year-old man with frequent premature ventricular contractions and normal results at coronary angiography. Two-chamber long-axis MR image of the left ventricle (a) and short-axis MR image (b) show extensive scattered delayed enhancement in the anterior, lateral, and inferior wall and apex of the left ventricle and the right ventricular wall (arrows). The endocardium is relatively spared by the inflammation, which occurs predominantly in the epicardium and mid myocardial wall. This distribution is typical of myocarditis. (Case courtesy of Dr John Freeby.)
|
|
View larger version (165K):
[in a new window]
|
Figure 8. Chagas myocarditis in a 34-year-old man from Brazil. Two-chamber MR image shows patchy delayed enhancement at the apex and mid anterior wall of the left ventricle (arrows). The patient was infected with Trypanosoma cruzi, and the myocardial areas of delayed enhancement represent inflammation due to Chagas disease (12). This parasite can spread via the bloodstream into many organ systems and often affects the heart.
|
|
View larger version (142K):
[in a new window]
|
Figure 9. Cardiac sarcoidosis in a 56-year-old woman with chronic coughing and occasional wheezing. Four-chamber delayed enhancement MR image shows foci of myocardial enhancement in the septum, lateral left ventricular wall, and right ventricular wall (arrows). Other foci of delayed enhancement were seen in the anterior-lateral segments and inferior wall.
|
|
View larger version (178K):
[in a new window]
|
Figure 10a. Kawasaki syndrome in an 18-year-old man. (a) Maximum intensity projection steady-state free precession image shows a 1.5-cm aneurysm (arrow) at the origin of the right coronary artery. There was also an aneurysm in the distribution of the left coronary artery with thrombosis; this aneurysm resulted in an extensive infarction of the left anterior descending artery. (b) Short-axis delayed enhancement MR image shows wall thinning and delayed enhancement (arrows) due to infarction.
|
|
View larger version (131K):
[in a new window]
|
Figure 10b. Kawasaki syndrome in an 18-year-old man. (a) Maximum intensity projection steady-state free precession image shows a 1.5-cm aneurysm (arrow) at the origin of the right coronary artery. There was also an aneurysm in the distribution of the left coronary artery with thrombosis; this aneurysm resulted in an extensive infarction of the left anterior descending artery. (b) Short-axis delayed enhancement MR image shows wall thinning and delayed enhancement (arrows) due to infarction.
|
|
View larger version (142K):
[in a new window]
|
Figure 11a. Hypertrophic obstructive cardiomyopathy in a 48-year-old patient with chest pain. (a) Four-chamber black blood MR image shows marked hypertrophy of the ventricular septum and left ventricular wall (arrows). (b) Short-axis delayed gadolinium-enhanced MR image shows subendocardial areas of delayed myocardial enhancement (arrows) in the left ventricular wall and septum. These areas of delayed enhancement are related to the myofibrillar disarray and scattered fibrosis present in hypertrophic obstructive cardiomyopathy.
|
|
View larger version (150K):
[in a new window]
|
Figure 11b. Hypertrophic obstructive cardiomyopathy in a 48-year-old patient with chest pain. (a) Four-chamber black blood MR image shows marked hypertrophy of the ventricular septum and left ventricular wall (arrows). (b) Short-axis delayed gadolinium-enhanced MR image shows subendocardial areas of delayed myocardial enhancement (arrows) in the left ventricular wall and septum. These areas of delayed enhancement are related to the myofibrillar disarray and scattered fibrosis present in hypertrophic obstructive cardiomyopathy.
|
|
View larger version (186K):
[in a new window]
|
Figure 12. Hypertrophic obstructive cardiomyopathy in a 46-year-old man with dyspnea, chest discomfort, and exertional syncope. Transarterial alcohol ablation was performed via the first perforating branch off the left anterior descending artery for treatment of left ventricular out-flow tract obstruction. MR images show delayed myocardial enhancement in the proximal septum (arrow) beginning directly after the ablation procedure and persisting over time. Note the gradually decreasing septal wall thickness due to iatrogenically induced myocardial infarction and subsequent scar formation.
|
|
View larger version (163K):
[in a new window]
|
Figure 13. Ischemic dilated cardiomyopathy in a 60-year-old woman with three-vessel coronary artery disease. Short-axis delayed enhancement MR image shows marked dilatation of the left ventricle, which was 8 cm in diameter. There is mild subendocardial delayed enhancement and thinning of the inferior wall (arrows) due to an old infarction of the right coronary artery. Delayed enhancement is not usually seen in non-ischemic dilated cardiomyopathy.
|
|
View larger version (140K):
[in a new window]
|
Figure 14a. Cardiac amyloidosis in a 56-year-old man with chest pain, renal failure, and diabetes. Short-axis (a) and two-chamber (b) MR images show delayed, patchy, inhomogeneous gadolinium enhancement of the left ventricular wall in a nonvascular distribution (arrows). A low normal ejection fraction of 55% and a restrictive wall motion pattern were observed at cine MR imaging.
|
|
View larger version (147K):
[in a new window]
|
Figure 14b. Cardiac amyloidosis in a 56-year-old man with chest pain, renal failure, and diabetes. Short-axis (a) and two-chamber (b) MR images show delayed, patchy, inhomogeneous gadolinium enhancement of the left ventricular wall in a nonvascular distribution (arrows). A low normal ejection fraction of 55% and a restrictive wall motion pattern were observed at cine MR imaging.
|
|
View larger version (179K):
[in a new window]
|
Figure 15a. Metastatic breast cancer involving the heart and pericardium in a 55-year-old woman. (a) Axial T2-weighted MR image shows a large bulky mass at the left ventricular apex (arrow) and a moderate-sized pericardial effusion. (b) Axial delayed enhancement MR image shows diffuse delayed enhancement of the mass (arrows).
|
|
View larger version (182K):
[in a new window]
|
Figure 15b. Metastatic breast cancer involving the heart and pericardium in a 55-year-old woman. (a) Axial T2-weighted MR image shows a large bulky mass at the left ventricular apex (arrow) and a moderate-sized pericardial effusion. (b) Axial delayed enhancement MR image shows diffuse delayed enhancement of the mass (arrows).
|
|
View larger version (126K):
[in a new window]
|
Figure 16a. ARVD in a 43-year-old woman. Long-axis (a) and short-axis (b) delayed enhancement MR images show diffuse delayed enhancement (arrows). Delayed enhancement is present in about two-thirds of patients with ARVD. Delayed enhancement of the right ventricle in association with reduced function or an aneurysm is highly suggestive of ARVD in patients who have nonsustained ventricular tachycardia with left bundle-branch block.
|
|
View larger version (138K):
[in a new window]
|
Figure 16b. ARVD in a 43-year-old woman. Long-axis (a) and short-axis (b) delayed enhancement MR images show diffuse delayed enhancement (arrows). Delayed enhancement is present in about two-thirds of patients with ARVD. Delayed enhancement of the right ventricle in association with reduced function or an aneurysm is highly suggestive of ARVD in patients who have nonsustained ventricular tachycardia with left bundle-branch block.
|
|
View larger version (138K):
[in a new window]
|
Figure 17. Duchenne muscular dystrophy in an 18-year-old man with heart failure. Coronary angiography showed normal coronary arteries. Short-axis MR image shows extensive, nearly transmural delayed enhancement of the anterior and lateral left ventricular wall (arrows) and left ventricular dilatation (ejection fraction of 34%). The findings are compatible with fibrosis of the left ventricular wall due to muscular dystrophy.
|
|
Copyright © 2006 by the Radiological Society of North America.
