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Magnetic Resonance Imaging of Non‑Ischemic Cardiomyopathies: a Pictorial Essay

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Magnetic Resonance Imaging of Non‑Ischemic Cardiomyopathies: a Pictorial Essay Editor-in-Chief: Vikram S. Dogra, MD OPEN ACCESS Department of Imaging Sciences, University of Rochester Medical Center, Rochester, USA HTML format Journal of Clinical Imaging Science For entire Editorial Board visit : www.clinicalimagingscience.org/editorialboard.asp www.clinicalimagingscience.org PICTORIAL ESSAY Magnetic Resonance Imaging of Non‑ischemic Cardiomyopathies: A Pictorial Essay Cristina I Olivas‑Chacon, Carola Mullins, Kevan Stewart, Nassim Akle, Jesus E Calleros, Luis R Ramos‑Duran Department of Radiology, Texas Tech University Health Science Center El Paso, El Paso, Texas, USA Address for correspondence: Dr. Cristina Ivette Olivas Chacon, ABSTRACT Department of Radiology, 4800 Alberta Avenue, El Paso, Non-ischemic cardiomyopathies are defined as either primary or secondary diseases of Texas ‑ 79905, USA. the myocardium resulting in cardiac dysfunction. While primary cardiomyopathies are E‑mail: [email protected] confined to the heart and can be genetic or acquired, secondary cardiomyopathies show involvement of the heart as a manifestation of an underlying systemic disease including metabolic, inflammatory, granulomatous, infectious, or autoimmune entities. Non-ischemic cardiomyopathies are currently classified as hypertrophic, dilated, restrictive, or unclassifiable, including left ventricular non-compaction. Cardiovascular Magnetic Resonance Imaging (CMRI) not only has the capability to assess cardiac morphology and function, but also the ability to detect edema, hemorrhage, fibrosis, and intramyocardial deposits, providing a valuable imaging tool in the characterization of non-ischemic cardiomyopathies. This pictorial essay shows some of the most important non-ischemic cardiomyopathies with an emphasis on magnetic resonance imaging features. Received : 26‑03‑2015 Key words: Cardiac, delayed gadolinium enhancement, non-ischemic Accepted : 24‑05‑2015 cardiomyopathies, steady-state free precession Published : 30‑06‑2015 INTRODUCTION failure and dysrhythmias.[2] Clinical management and prognosis depend on the etiology of the cardiomyopathy Non‑ischemic cardiomyopathies include chronic and involved. Transthoracic ultrasound remains the major progressive myocardial diseases, either primarily of the imaging tool in identifying anatomic and functional cardiac muscle or secondary to generalized systemic characteristics of the heart, allowing the classification of disorders leading to progressive adverse effects on the size, hypertrophic, dilated, or restrictive cardiomyopathy. shape, and function of the cardiac muscle.[1] Occasionally, patients are asymptomatic or have only minimal symptoms, Cardiovascular Magnetic Resonance Imaging (CMRI) but commonly present with signs of advanced stage heart complements transthoracic ultrasound by allowing characterization of pathologic tissue and reliably assessing Video avaiable on www.clinicalimagingscience.org edema and fat infiltration using non‑contrast T1‑ and This is an open access article distributed under the terms of the Creative Access this article online Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows Quick Response Code: others to remix, tweak, and build upon the work non-commercially, as long as the Website: author is credited and the new creations are licensed under the identical terms. www.clinicalimagingscience.org For reprints contact: [email protected] How to cite this article: Olivas‑Chacon CI, Mullins C, Stewart K, Akle N, Calleros JE, DOI: Ramos‑Duran LR. Magnetic Resonance Imaging of Non‑ischemic Cardiomyopathies: A Pictorial Essay. J Clin Imaging Sci 2015;5:37. 10.4103/2156-7514.159564 Available FREE in open access from: http://www.clinicalimagingscience.org/text. asp?2015/5/1/37/159564 1 © 2015 Journal of Clinical Imaging Science | Published by Wolters Kluwer - Medknow Olivas‑Chacon, et al.: MRI of non‑ischemic cardiomyopathies: A pictorial essay T2‑weighted sequences. Phase‑contrast techniques throughout the body. Cardiac involvement manifests measure blood flow in concomitant valvular heart disease, as restrictive cardiomyopathy and is the cause of death and ischemia assessment can be performed with first‑pass in approximately half of the patients. On cine imaging, perfusion imaging during hyperemia.[2] glycoprotein deposition results in biventricular myocardial thickening and restrictive cardiomyopathy resulting in Late gadolinium enhancement (LGE) techniques accurately as global hypokinesis [Video 1, Figure 2a and b]. Late image areas of myocardial fibrosis or infiltration.[3] To perform fibrotic stages of restrictive cardiomyopathy secondary LGE, a segmented gradient‑recalled echo (GRE) sequence to amyloidosis can develop atrioventricular valvular with an inversion pulse preparation is generally used. To abnormalities such as mitral and tricuspid insufficiency, obtain imaging of the entire heart (stack of short‑axis which can be seen on cine imaging [Video 2]. slices), the acquisition is ECG gated, performed 10–15 min after bolus injection of 1 mmol/kg of gadolinium, and Amyloid deposition within the heart results in the expansion typically requires 10–12 breath‑holds and a stable sinus of the extracellular space, allowing gadolinium‑based rhythm. Gadolinium tends to accumulate in fibrotic regions contrast agents to be retained appearing as diffuse of the myocardium, creating a hyperintense signal, which enhancement in the subendocardial region on LGE can be differentiated from normal myocardium after imaging[5] [Figure 2c and d], which along with the abnormal choosing a correct time of inversion (TI) to null the signal gadolinium kinetics found in amyloidosis, makes choosing from normal viable myocardium. Since choosing the right the right TI difficult. PSIR sequence can be helpful in these TI can present a challenge, phase‑sensitive inversion cases as it is independent of the TI value. In amyloidosis, recovery (PSIR) can be used to alleviate the dependence on the TI value. Single‑shot steady‑state free precession (SSFP) Table 1: Common sequences used in the evaluation of sequences can be used to accelerate imaging for patients non‑ischemic cardiomyopathies with arrhythmia or those unable to breath‑hold with Sequence name Sequence usefulness conventional protocols, but come with the cost of lower Cine SSFP Myocardial structure and function Cine fast gradient echo Myocardial structure and function [4] signal‑to‑noise ratio and spatial resolution. Table 1 T1‑weighted black blood Myocardial fat imaging summarizes the common sequences used in the evaluation T2‑weighted black blood Tissue edema of non‑ischemic cardiomyopathies and their application. Inversion recovery late Late gadolinium enhancement enhancement T2* Myocardial iron content Various enhancement patterns can be recognized using SSFP: Single-shot steady-state free precession LGE. Subendocardial or transmural LGE located within the perfusion territory of an epicardial coronary artery can be classified as ischemic type, and abnormal enhancement not confined to a known vascular distribution is consistent with non‑ischemic causes[1] [Figure 1]. Subendocardial enhancement Amyloidosis a b Amyloidosis is a systemic glycoprotein deposition of misfolded proteins within the extracellular spaces c d Figure 2: 60-year-old female with shortness of breath, diagnosed with systemic amyloidosis secondary to end-stage renal disease. 3 T CMRI gradient-recalled echo (GRE) cine images were taken to minimize the flow artifacts related to mitral insufficiency systolic jet. Two‑chamber views (a and b) demonstrate myocardial wall thickening and global hypokinesis, along with a mitral insufficiency systolic jet (black arrows). Single‑shot, phase‑sensitive inversion recovery (PSIR) late gadolinium enhancement (LGE) with two-chamber (c) and short-axis (d) views show increased signal intensity diffusely distributed in the subendocarium, involving large areas of the left ventricle in a non-coronary artery distribution and also affecting the right ventricle (black arrowhead) and left atrium (white arrow). LGE is demonstrated transmurally involving the subepicardium at the apex and at the apical aspects of the anterior and inferior Figure 1: LGE patterns of ischemic and non-ischemic cardiomyopathies. walls (white arrowheads). ED = End diastole, ES = End systole. 2 Journal of Clinical Imaging Science | Vol. 5 | Issue 2 | Apr-Jun 2015 Olivas‑Chacon, et al.: MRI of non‑ischemic cardiomyopathies: A pictorial essay high myocardial uptake in addition to fast clearance and until the final fibrotic pathologic stage is reached due to blood washout of intravenous administered gadolinium scarring of the chordae tendinae and the endocardium is result in similar T1 values for blood and myocardium on cine reached. Disruption of the anticoagulant endothelial lining imaging. Therefore, image acquisition should be performed along with blood stasis in areas of hypokinesis leads to shortly after contrast injection.[5] thrombus formation within the endomyocardial surface [Figure 3a and b]. Thrombi found in Loeffler endocarditis Loeffler endocarditis (hypereosinophilic syndrome) differ from the thrombi found in apical myocardial infarction Hypereosinophilic syndrome is a rare disorder characterized as they lack transmural enhancement with LGE, myocardial by eosinophilia with organ‑system dysfunction caused by thinning, and perfusion defects in first‑pass perfusion eosinophil‑associated tissue damage. Cardiac involvement imaging in the subjacent myocardial wall [Video 3, Figure 3e]. has traditionally
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