• Users Online: 415
  • Print this page
  • Email this page


 
 Table of Contents  
REVIEW ARTICLE
Year : 2019  |  Volume : 3  |  Issue : 2  |  Page : 78-84

Cardiac magnetic resonance imaging in infiltrative cardiomyopathy


Department of Imaging, Narayana Institute of Cardiac Sciences, Bengaluru, Karnataka, India

Date of Web Publication29-Aug-2019

Correspondence Address:
Vimal Raj
Department of Imaging, Narayana Institute of Cardiac Sciences, NH Health City, 258/A Bommasandra Industrial Area, Hosur Road, Bengaluru - 560 099, Karnataka
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jiae.jiae_2_19

Rights and Permissions
  Abstract 

Infiltrative cardiomyopathies are a wide spectrum of disorders characterized by deposition of abnormal substances in the myocardium. These have a varied etiology and can be idiopathic, familial, or secondary to systemic disorders. The infiltrative process primarily causes a diastolic dysfunction resulting in heart failure with preserved ejection fraction. Common infiltrative cardiomyopathies encountered are cardiac amyloidosis, sarcoidosis, Fabry disease, iron overload cardiomyopathy, endomyocardial fibrosis, and idiopathic restrictive cardiomyopathy. Early and accurate detection of cause of infiltration is very important to improve outcomes through disease-specific therapies. Cardiac magnetic resonance (CMR) plays an important role in the diagnosis, avoiding the need of invasive endomyocardial biopsy in many cases. The use of postcontrast late gadolinium enhancement and T1 and T2 mapping sequences in CMR is improving diagnosis of infiltrative cardiomyopathy. In this review, we highlight the role of CMR in detection of different types of infiltrative cardiomyopathy.

Keywords: Amyloidosis, cardiac magnetic resonance, hemochromatosis, infiltrative cardiomyopathy, restrictive cardiomyopathy, sarcoidosis


How to cite this article:
Pudhiavan A, Kothari R, Raj V. Cardiac magnetic resonance imaging in infiltrative cardiomyopathy. J Indian Acad Echocardiogr Cardiovasc Imaging 2019;3:78-84

How to cite this URL:
Pudhiavan A, Kothari R, Raj V. Cardiac magnetic resonance imaging in infiltrative cardiomyopathy. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2019 [cited 2019 Sep 15];3:78-84. Available from: http://www.jiaecho.org/text.asp?2019/3/2/78/265748


  Introduction Top


Cardiomyopathies are defined as “myocardial disorder in which there is an abnormality in the structure and function of the myocytes, in the absence of coronary artery disease, hypertension, valvular disease, and congenital heart disease that could justify this abnormality.”[1] In infiltrative cardiomyopathy, there is deposition of abnormal substances in the myocardium with or without an increase in wall thickness. This leads to restricted/impaired diastolic relaxation of the ventricles with reduced diastolic volume and subsequent dilatation of the atria. The systolic function of the ventricles is preserved until later in the disease process.[2]

Infiltrative/restrictive cardiomyopathy (RCM) is a challenging spectrum of diseases both in diagnosis and treatment. In primary RCM, the pathogenesis is predominantly confined to the heart, while in secondary RCM, the heart is involved as part of a systemic multi-organ disorder. Idiopathic RCM and endomyocardial fibrosis primarily involve the heart. The secondary RCM can be due to amyloidosis, sarcoidosis, glycogen/other storage disorders, iron overload, drug, or radiation induced.[3] In younger patients, RCM is usually due to genetic disorder causing fibrosis or deposition of various substances such as proteins, iron, or glycogen. In older adults, disease processes such as amyloidosis, sarcoidosis, iron overload cardiomyopathy, and radiation-induced RCM are more common. Idiopathic RCM are rare in this age group.[3]

Early and accurate detection of cause of infiltration is important to improve outcomes through disease-specific therapies. Echocardiography (echo) is good at picking up diastolic dysfunction of the left ventricle but often cannot differentiate between one cause of RCM and the other. Cardiac magnetic resonance (CMR) imaging has now become an important noninvasive imaging tool in diagnosis of RCM with its high spatial resolution and ability to assess myocardial morphology. Positron emission tomography (PET) imaging is also being increasingly used in assessment of patients with RCM, to assess for myocardial infiltration and also distant disease which could be easily sampled for histopathological assessment. With significant advancements in noninvasive testing, endomyocardial biopsy is now reserved as a problem-solving tool.

In this review, we look at common infiltrative cardiomyopathies with emphasis on the role of CMR in their diagnosis.


  Clinical Characteristics Top


Patients with RCM often present with dyspnea on exertion, exercise intolerance, fatigue, and lower extremity edema. These are predominantly secondary to decreased compliance of the ventricles which inhibits rapid venous return and leads to fluid retention in the periphery. Increase in systemic filling pressures and reduced stroke volume can lead to renal dysfunction. Progressive atrial dilatation in the disease leads to atrial arrhythmias with increased risk of thromboembolic events. Mitral and tricuspid regurgitations are frequently present. Ventricular hypertrophy may or may not be present with a low-voltage QRS on electrocardiogram (ECG). The presence of tall p-waves may be seen due to atrial dilatation, and bundle branch/atrioventricular (AV) block is seen in sarcoidosis.


  Echocardiography Top


The most common echo findings are normal ventricular chamber volumes with preserved ejection fraction and biatrial dilatation. Decreased diastolic ventricular compliance is characterized by an increased early diastolic filling velocity (E-wave), decreased late filling velocity (A wave), an E/A ratio of >1.5, and a decreased mitral deceleration time (<120 ms).[4] Tissue Doppler and strain imaging can also help in assessing the regional myocardial function and contractility.[5] Echo lacks in tissue characterization of the myocardium in case of infiltrative cardiomyopathies. Echo is also helpful in differentiating between RCM and constrictive pericarditis (CP) by identifying respiratory ventricular septal shift which occurs due to exaggerated interventricular dependence and dissociation between intracardiac and intrathoracic pressures during respiration.[6]


  Cardiac Magnetic Resonance Imaging Top


CMR is a powerful tool in assessing and characterizing various infiltrative cardiomyopathies and can differentiate between RCM and CP. CMR accurately quantifies ventricular/atrial volumes and can quantify the severity of mitral and tricuspid regurgitation. Ventricular filling and E/A ratio can also be assessed with CMR helping in assessing diastolic dysfunction. CMR has the ability to assess myocardial morphology noninvasively using late gadolinium enhancement (LGE) and myocardial mapping. For LGE, imaging is performed 7–10 min after giving gadolinium contrast. In this time, the contrast accumulates in areas of myocardial fibrosis/extracellular interstitial space. Based on the pattern of LGE of the myocardium, it is possible to differentiate various forms of infiltration and also differentiate RCM from ischemic cardiomyopathy. LGE has become a gold standard in demonstration of myocardial fibrosis and provides incremental prognostic information.[7] Patients with ischemic cardiomyopathy have subendocardial enhancement which can extend to have transmural involvement. Patients with RCM can have patchy mid-myocardial to epicardial LGE. Some of these patients with early or diffuse myocardial fibrosis may not have positive LGE. In these patients, newer T1 mapping sequences are performed before and after administration of contrast agent.[8] T1 mapping looks at the magnetic property of the myocardial tissue and can assess for areas of fibrosis down to the level of a pixel of the myocardial tissue. Another form of myocardial mapping is using T2* (T2 star) which accurately quantifies iron overload in the myocardium.[9]


  Technique Top


For a CMR study, the patient has to lie supine in the scanner and ECG leads are attached to track patients' cardiac cycle. Scout images are taken to confirm the orientation of the heart and ensure that the heart is positioned in the middle of the magnet. The scout images are followed by images of the thorax in an axial plane to assess for extracardiac pathologies. Cine images are then performed in different imaging planes, including two-chamber, four-chamber, three-chamber, and LVOT views. A complete volumetric cine datum is acquired in short-axis plane covering the entire ventricular cavity for measuring volumes directly, which is less prone to error and is reproducible as it does not require geometric assumptions. T1 mapping with a modified look-locker inversion recovery sequence is done before and after administration of gadolinium contrast, which can be used to quantitate the tissue T1 values and the extracellular volume fraction (ECV).[8] A triple inversion short-tau inversion recovery sequence and T2 mapping is done to identify myocardial edema. T2* imaging can be done for quantification of iron in iron overload cardiomyopathies. LGE imaging is then performed in different planes including two and four chambers and short axis to assess for areas of fibrosis/scarring and their distribution.[7] Dynamic cine imaging can also be performed to look for septal bounce due to interventricular dependence in CP. Phase-contrast flow studies (similar to Doppler) are acquired across the mitral and tricuspid valves to demonstrate the restrictive ventricular filling due to diastolic dysfunction.


  Cardiac Amyloidosis Top


Cardiac amyloidosis is an infiltrative disorder, in which misfolded insoluble proteins are deposited in various tissues in the body including myocardium. There are two main types of amyloid deposition that occurs in the heart, namely immunoglobulin light chain-associated amyloid (AL type) and the transthyretin amyloid (ATTR type).[10] The typical CMR features are myocardial hypertrophy, valvular thickening, pericardial effusion, and diastolic dysfunction with biatrial dilatation. Associated AV valve regurgitation is also seen. The characteristic CMR features in cardiac amyloidosis include a diffuse LGE involving the subendocardium and the atrial walls, along with rapid washout of contrast from the myocardium [Figure 1]. The latter leads to difficulty in nulling normal myocardium in T1 scout look-locker images.[11] CMR is also helpful in differentiating the type of amyloid using the T1 mapping sequence where the AL type has the highest T1 values, followed by the ATTR type.[12] Left ventricular (LV) hypertrophy is more common in ATTR type with a more extensive LGE.
Figure 1: Amyloidosis: (a and b) Four-chamber and short-axis views showing concentric left ventricular hypertrophy. (c) Diffuse subendocardial enhancement in short-axis late gadolinium enhancement image. (d) Extracellular volume fraction map (derived from T1 maps) in the short axis with diffusely raised T1 and extracellular volume fraction values

Click here to view



  Cardiac Sarcoidosis Top


Sarcoidosis is a multisystem disorder of unknown etiology. It is characterized by deposition of granulomatous tissue in different organs including heart. Familial clustering of cases indicates a strong genetic predisposition.[13] Arrhythmias are often the most frequent feature of cardiac sarcoidosis, which include supraventricular tachycardia, ventricular tachycardia, bundle branch, and AV blocks. CMR is extremely useful in initial diagnosis and subsequent follow-up of treatment response in cardiac sarcoidosis. Noncontrast CMR findings are nonspecific with ventricular diastolic or systolic dysfunction, focal wall thinning, and regional wall motion abnormalities not corresponding to a vascular territory. Focal areas of myocardial edema indicate active inflammation. The presence and pattern of LGE are very important in differentiating cardiac sarcoidosis from other causes of myocardial infiltration. Sarcoidosis typically has a patchy and multifocal LGE with sparing of the endocardium.[14] LGE has a crucial role in prognostication with an increased amount of LGE associated with increased risk of ventricular arrhythmias and sudden cardiac death, irrespective of ejection fraction.[15] Atrial LGE on CMR is also associated with a three times greater likelihood of developing symptomatic atrial arrhythmias.[16] PET is another important tool in the identification of active inflammation and differentiating it from scarred myocardium, both of which will show LGE.[17] T1 and T2 mappings are increasingly used to identify subtle areas of inflammation and scarring which may not have positive LGE [Figure 2] and [Figure 3].[8]
Figure 2: Sarcoidosis: (a) Four-chamber balanced turbo field echo sequence showing septal thinning. (b) Short-axis short-tau inversion recovery image revealing patchy myocardial edema. (c and d) Four-chamber and short-axis phase-sensitive inversion recovery sequence showing patchy areas of transmural myocardial late gadolinium enhancement

Click here to view
Figure 3: Granulomatous cardiomyopathy: (a) Short-axis short-tau inversion recovery image revealing patchy myocardial edema. (b and c) Patchy areas of mid-myocardial and epicardial late gadolinium enhancement. (d) Raised native T1 values in the short-axis T1 map

Click here to view



  Iron Overload Cardiomyopathy Top


Liver and myocardium are two of the tissues where excess iron deposition happens. Common causes for iron deposition are due to increased iron absorption from the gastrointestinal tract, parenteral iron administration, and frequent blood transfusions in hereditary anemias. Due to iron deposition in myocardium, there is restricted LV relaxation with prominent early diastolic dysfunction that inevitably progresses to a dilated cardiomyopathy.[18],[19] On CMR, we see impaired diastolic LV function with restrictive filling patterns and atrial dilatation without LV hypertrophy. Noninvasive assessment of myocardial iron overload traditionally is performed by serial monitoring of serum ferritin. This is not reliable as ferritin is an acute phase reactant and can increase in various nonrelated causes. CMR is a reliable noninvasive diagnostic tool to accurately quantify the iron deposition in the myocardium.[19] Paramagnetic property of iron causes a reduction in T2 relaxation times resulting in a rapid signal loss [Figure 4]. This can help in determining the concentration of iron in different tissues. The T2* values of the myocardium with iron deposition are typically <20 ms, with a value of <10 ms denoting severe myocardial iron deposition at 1.5 T.[19] The T2* values are also shown to be independent of serum ferritin values.
Figure 4: Iron deposition cardiomyopathy: (a) Short-axis T2* images showing progressive signal drop with increasing echo time. (b) Axial T2* of the liver showing marked signal loss

Click here to view



  Lysosomal Storage Disorders Top


These are infiltrative cardiomyopathies secondary to a defect in lysosomal enzyme activity resulting in abnormal deposition of glycogen in various body tissues. The most common of these are Anderson–Fabry disease, Danon disease, and PRKAG2-deficient cardiomyopathy.[20] CMR features of these disorders are overlapping with most having LVH and showing restrictive ventricular diastolic filling [Figure 5]. Fabry disease has a typical pattern of mid-myocardial LGE along the basal inferolateral wall sparing the endocardium.[21] Danon disease also presents with concentric LVH with diffuse LGE in late stages. In early stages of disease, T1 mapping shows reduced native T1 values due to glycogen storage with an increase in T1 values with worsening fibrosis.[22]
Figure 5: Danon disease: (a and b) Four-chamber and three-chamber views showing concentric LV hypertrophy with LV dilatation and no LVOT narrowing. (c) No significant late gadolinium enhancement. (d) Diffuse reduction in native T1 values in the short-axis T1 map

Click here to view



  Idiopathic Restrictive Cardiomyopathy Top


Primary or idiopathic RCM is a rare disease with familial as well as sporadic incidence. The familial cases are believed to have an autosomal dominant inheritance with variable penetrance.[23],[24] On CMR, restrictive physiology is seen with biatrial dilatation and a restrictive ventricular filling pattern. The pericardium is normal with no evidence of respiratory exaggeration of ventricular dependence. T1 mapping can reveal a diffuse myocardial fibrosis which can be confirmed with endomyocardial biopsy. The pattern of LGE is very nonspecific with some patients having patchy mid-myocardial enhancement at right ventricular (RV) insertion sites [Figure 6].
Figure 6: Idiopathic restrictive cardiomyopathy: (a and b) Four- and two-chamber views showing reduced biventricular volumes with biatrial dilatation and atrioventricular valve regurgitation. (c) Four-chamber phase-sensitive inversion recovery sequence showing no late gadolinium enhancement. (d) Raised native T1 values in the short-axis T1 map

Click here to view



  Endomyocardial Fibrosis Top


Endomyocardial fibrosis is a tropical disease and prevalent in equatorial countries. In India, it is more common in the southern coastal state of Kerala. There is diffuse subendocardial fibrosis with apical thrombus formation and diastolic dysfunction. The right ventricle is preferentially involved compared to left ventricle.[25] CMR demonstrates restrictive diastolic dysfunction in the ventricles with biatrial dilatation and AV valve regurgitation [Figure 7]. CMR is superior to echocardiography in demonstrating the presence of thrombus, especially in RV, and reveals a diffuse endocardial and subendocardial LGE.[26]
Figure 7: Endomyocardial fibrosis: (a and b) Four- and two-chamber views showing reduced biventricular volumes with biatrial dilatation. (c and d) Late gadolinium enhancement images showing diffuse endocardial enhancement with a thin linear LV thrombus in the apical cavity

Click here to view



  Hypereosinophilic Syndromes Top


Hypereosinophilia is defined as an absolute peripheral blood eosinophil count of >1500 cells/l. Eosinophilic heart disease has three stages: an acute necrotic phase, an intermediate phase with thrombus formation, and a late fibrotic phase.[27] Echocardiography is typically normal during the acute stage which presents with elevated cardiac enzymes. CMR detects the acute stage in which there is subendocardial infiltration of eosinophils and demonstrates diffuse subendocardial edema and LGE.[28] Cavity thrombus can be well depicted by CMR. The late fibrotic stage demonstrates cavity distortion, fibrotic deformation of chordal structures, and AV valve regurgitation.


  Radiation/drug-Induced Cardiomyopathy Top


Radiation- and drug-induced cardiomyopathy is becoming an increasing concern with more use of radiation for diagnostic and therapeutic purpose and improved long-term survival of cancer patients. The common drugs associated with RCM are anthracyclines, chloroquine, and ergotamine.[3],[29] The pathogenesis of radiation-induced RCM is inflammation leading to microvascular injury, reduced capillary density causing ischemia, and replacement fibrosis.[29] CMR features are of diffuse LGE with associated pericardial thickening and enhancement in late stages. Early identification is possible with T1 mapping, which reveals elevated native T1 values and ECV with a restrictive pattern.[30]


  Constrictive Pericarditis Top


Considerable overlap exists between the CMR features of idiopathic RCM and CP, with both showing diastolic dysfunction with restrictive early diastolic ventricular filling. Tuberculosis is by far the most common cause in India and often involves myocardium. CMR has a very high accuracy of 93% in detecting a thickened pericardium of >4 mm.[30] Cine CMR sequences with myocardial tagging are also useful in detecting tissue tethering.[31] Dynamic cine images demonstrate septal bounce and early diastolic septal flattening due to exaggerated ventricular dependence during respiration. CMR also helps in identifying extracardiac abnormalities such as presence of mediastinal adenopathy, pulmonary lesions, and pleural and pericardial effusions [Figure 8].
Figure 8: Constrictive pericarditis: (a) Four-chamber view showing reduced biventricular volumes with biatrial dilatation. (b and c) Postcontrast black blood T1 showing pericardial and pleural thickening and bilateral pleural effusions. (d) Noncontrast computed tomography showing diffuse pericardial calcification

Click here to view



  Conclusion Top


Comprehensive evaluation of infiltrative cardiomyopathies remains a challenge. Early identification of restrictive physiology and type of infiltration is important to prevent irreversible injury. Echo is the first-line imaging and is able to detect gross morphological and functional abnormalities, though it lacks specificity and sufficient sensitivity. CMR has shown immense promise in the evaluation of all types of infiltrative cardiomyopathies. Apart from identifying typical morphological and functional changes, it is also useful in assessing disease activity, prognostication, and serial assessment of treatment response. The newer CMR techniques will have increasing role to play in infiltrative cardiomyopathies as these do not require any contrast.

Acknowledgment

The authors would like to thank the technicians and our colleagues who have contributed immensely in this work.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Elliott P, Andersson B, Arbustini E, Bilinska Z, Cecchi F, Charron P, et al. Classification of the cardiomyopathies: A position statement from the European Society of Cardiology working group on myocardial and pericardial diseases. Eur Heart J 2008;29:270-6.  Back to cited text no. 1
    
2.
Ammash NM, Seward JB, Bailey KR, Edwards WD, Tajik AJ. Clinical profile and outcome of idiopathic restrictive cardiomyopathy. Circulation 2000;101:2490-6.  Back to cited text no. 2
    
3.
Pereira NL, Grogan M, Dec GW. Spectrum of restrictive and infiltrative cardiomyopathies: Part 1 of a 2-part series. J Am Coll Cardiol 2018;71:1130-48.  Back to cited text no. 3
    
4.
Vaitkus PT, Kussmaul WG. Constrictive pericarditis versus restrictive cardiomyopathy: A reappraisal and update of diagnostic criteria. Am Heart J 1991;122:1431-41.  Back to cited text no. 4
    
5.
Pieroni M, Chimenti C, Ricci R, Sale P, Russo MA, Frustaci A, et al. Early detection of Fabry cardiomyopathy by tissue Doppler imaging. Circulation 2003;107:1978-84.  Back to cited text no. 5
    
6.
Garcia MJ. Constrictive pericarditis versus restrictive cardiomyopathy? J Am Coll Cardiol 2016;67:2061-76.  Back to cited text no. 6
    
7.
Rapezzi C, Arbustini E, Caforio AL, Charron P, Gimeno-Blanes J, Heliö T, et al. Diagnostic work-up in cardiomyopathies: Bridging the gap between clinical phenotypes and final diagnosis. A position statement from the ESC working group on myocardial and pericardial diseases. Eur Heart J 2013;34:1448-58.  Back to cited text no. 7
    
8.
Iles L, Pfluger H, Phrommintikul A, Cherayath J, Aksit P, Gupta SN, et al. Evaluation of diffuse myocardial fibrosis in heart failure with cardiac magnetic resonance contrast-enhanced T1 mapping. J Am Coll Cardiol 2008;52:1574-80.  Back to cited text no. 8
    
9.
Anderson LJ, Holden S, Davis B, Prescott E, Charrier CC, Bunce NH, et al. Cardiovascular T2-star (T2*) magnetic resonance for the early diagnosis of myocardial iron overload. Eur Heart J 2001;22:2171-9.  Back to cited text no. 9
    
10.
Fontana M, Banypersad SM, Treibel TA, Maestrini V, Sado DM, White SK, et al. Native T1 mapping in transthyretin amyloidosis. JACC Cardiovasc Imaging 2014;7:157-65.  Back to cited text no. 10
    
11.
Maceira AM, Joshi J, Prasad SK, Moon JC, Perugini E, Harding I, et al. Cardiovascular magnetic resonance in cardiac amyloidosis. Circulation 2005;111:186-93.  Back to cited text no. 11
    
12.
Dungu JN, Valencia O, Pinney JH, Gibbs SD, Rowczenio D, Gilbertson JA, et al. CMR-based differentiation of AL and ATTR cardiac amyloidosis. JACC Cardiovasc Imaging 2014;7:133-42.  Back to cited text no. 12
    
13.
Birnie DH, Nery PB, Ha AC, Beanlands RS. Cardiac sarcoidosis. J Am Coll Cardiol 2016;68:411-21.  Back to cited text no. 13
    
14.
Greulich S, Deluigi CC, Gloekler S, Wahl A, Zürn C, Kramer U, et al. CMR imaging predicts death and other adverse events in suspected cardiac sarcoidosis. JACC Cardiovasc Imaging 2013;6:501-11.  Back to cited text no. 14
    
15.
Cain MA, Metzl MD, Patel AR, Addetia K, Spencer KT, Sweiss NJ, et al. Cardiac sarcoidosis detected by late gadolinium enhancement and prevalence of atrial arrhythmias. Am J Cardiol 2014;113:1556-60.  Back to cited text no. 15
    
16.
Pellegrino D, Bonab AA, Dragotakes SC, Pitman JT, Mariani G, Carter EA. Inflammation and infection: Imaging properties of 18F-FDG-labeled white blood cells versus 18F-FDG. J Nucl Med 2005;46:1522-30.  Back to cited text no. 16
    
17.
Murphy CJ, Oudit GY. Iron-overload cardiomyopathy: Pathophysiology, diagnosis, and treatment. J Card Fail 2010;16:888-900.  Back to cited text no. 17
    
18.
Gujja P, Rosing DR, Tripodi DJ, Shizukuda Y. Iron overload cardiomyopathy: Better understanding of an increasing disorder. J Am Coll Cardiol 2010;56:1001-12.  Back to cited text no. 18
    
19.
Wood JC. History and current impact of cardiac magnetic resonance imaging on the management of iron overload. Circulation 2009;120:1937-9.  Back to cited text no. 19
    
20.
Nagueh SF. Anderson-Fabry disease and other lysosomal storage disorders. Circulation 2014;130:1081-90.  Back to cited text no. 20
    
21.
De Cobelli F, Esposito A, Belloni E, Pieroni M, Perseghin G, Chimenti C, et al. Delayed-enhanced cardiac MRI for differentiation of Fabry's disease from symmetric hypertrophic cardiomyopathy. AJR Am J Roentgenol 2009;192:W97-102.  Back to cited text no. 21
    
22.
Angelini A, Calzolari V, Thiene G, Boffa GM, Valente M, Daliento L, et al. Morphologic spectrum of primary restrictive cardiomyopathy. Am J Cardiol 1997;80:1046-50.  Back to cited text no. 22
    
23.
Hayashi T, Shimomura H, Terasaki F, Toko H, Okabe M, Deguchi H, et al. Collagen subtypes and matrix metalloproteinase in idiopathic restrictive cardiomyopathy. Int J Cardiol 1998;64:109-16.  Back to cited text no. 23
    
24.
León D, Martín M, Corros C, Santamarta E, Costilla S, Lambert JL. Usefulness of cardiac MRI in the early diagnosis of endomyocardial fibrosis. Rev Port Cardiol 2012;31:401-2.  Back to cited text no. 24
    
25.
Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood 1994;83:2759-79.  Back to cited text no. 25
    
26.
Syed IS, Martinez MW, Feng DL, Glockner JF. Cardiac magnetic resonance imaging of eosinophilic endomyocardial disease. Int J Cardiol 2008;126:e50-2.  Back to cited text no. 26
    
27.
Pereira NL, Grogan M, Dec GW. Spectrum of restrictive and infiltrative Cardiomyopathies: Part 2 of a 2-part series. J Am Coll Cardiol 2018;71:1149-66.  Back to cited text no. 27
    
28.
Darby SC, Cutter DJ, Boerma M, Constine LS, Fajardo LF, Kodama K, et al. Radiation-related heart disease: Current knowledge and future prospects. Int J Radiat Oncol Biol Phys 2010;76:656-65.  Back to cited text no. 28
    
29.
Mukai-Yatagai N, Haruki N, Kinugasa Y, Ohta Y, Ishibashi-Ueda H, Akasaka T, et al. Assessment of myocardial fibrosis using T1-mapping and extracellular volume measurement on cardiac magnetic resonance imaging for the diagnosis of radiation-induced cardiomyopathy. J Cardiol Cases 2018;18:132-5.  Back to cited text no. 29
    
30.
Masui T, Finck S, Higgins CB. Constrictive pericarditis and restrictive cardiomyopathy: Evaluation with MR imaging. Radiology 1992;182:369-73.  Back to cited text no. 30
    
31.
Bogabathina H, Biederman RW. Lack of slippage by cardiovascular magnetic resonance imaging is sine qua non for constrictive pericarditis. Circulation 2011;123:e418-9.  Back to cited text no. 31
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Clinical Charact...
Echocardiography
Cardiac Magnetic...
Technique
Cardiac Amyloidosis
Cardiac Sarcoidosis
Iron Overload Ca...
Lysosomal Storag...
Idiopathic Restr...
Endomyocardial F...
Hypereosinophili...
Radiation/drug-I...
Constrictive Per...
Conclusion
References
Article Figures

 Article Access Statistics
    Viewed42    
    Printed0    
    Emailed0    
    PDF Downloaded12    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]