assessment of pericardial diseases and cardiac masses with cardiovascular magnetic resonance

Progress in Cardiovascular Diseases 54 (2011) 305–319www.onlinepcd.com

Assessment of Pericardial Diseases and Cardiac Masses withCardiovascular Magnetic Resonance

Dana Dawson, Raad Mohiaddin⁎

Department of Cardiovascular Medicine, University of Aberdeen and the Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital andNational Heart and Lung Institute, Imperial College, London, United Kingdom

Abstract Imaging plays an important diagnostic and prognostic role in the assessment of pericardial

Statement of Con⁎ Address reprin

FRCP, FESC, ProfessLung Institute, Imperi6NP, United Kingdom

E-mail address:

0033-0620/$ – see frodoi:10.1016/j.pcad.20

diseases and cardiac tumors and in differentiating these conditions from other cardiac andnoncardiac diseases. A number of imaging modalities are available for this task; each hasadvantages and limitation. Cardiovascular magnetic resonance (CMR) is a highly versatileimaging modality that provides detailed anatomical information, tissue characterization, cardiacfunction assessment, and evaluation of the impact of these conditions on hemodynamics. In thisreview we focus on the current state-of-the-art application of cardiovascular magnetic resonancein assessing pericardial diseases and cardiac tumors. (Prog Cardiovasc Dis 2011;54:305-319)
© 2011 Elsevier Inc. All rights reserved.
Keywords: Pericardium; Tamponade; Constriction; Pericarditis; Cardiac magnetic resonance; Echocardiography

Advanced imaging modalities have greatly facilitated thediagnosis of pericardial diseases and the detection of cardiacmasses. An integrated, multimodality assessment is oftennecessary to provide all the clinicians with completeinformation. This review will highlight the role that cardiacmagnetic resonance (CMR) plays in such clinical scenarios.

Special considerations on pericardial imaging

CMR is a very well suited and highly versatile imagingmodality to visualize fine structures such as the peri-cardium1 or to provide accurate evaluation of a mass andtissue characterization. In addition, it provides excellentassessment of cardiac function and hemodynamics.

There are, however, some technical issues that cancompromise accurate image collection; these need to be

flict of Interest: See page 318.t requests to Raad Mohiaddin, MD, PhD, FRCR,or, Royal Brompton Hospital, National Heart andal College, London Sydney Street, London [email protected] (R. Mohiaddin).

nt matter © 2011 Elsevier Inc. All rights reserved.11.08.001

understood and considered when images are acquired. It isimportant that the imaging personnel know in advancethose details of pericardial disease that are being lookedfor. The presence of epicardial and pericardial fat in CMRimaging is advantageous, as fat gives bright signal intensityon T1-and T2-weighted images, in contrast to the lowsignal intensity arising from pericardium.2 Sometimes thepericardium can be obscured by the chemical shift orcancellation artifacts; these need to be recognized. Atechnicality applicable to CMR is that the slice thickness ofroutine imaging is 7 mm as it is usually optimized formyocardial and not pericardial imaging. The normalpericardial thickness reported on CMR is up to 4 mm.3

These factors can contribute to some partial volume effect.Several CMR sequences are used to image the pericardium.On turbo-spin echo (TSE) images the pericardium gives arelatively low intensity signal,4 in contrast with the highsignal intensity given by the surrounding fat, on both T1-and T2-weighted imaging. Pericardium is also seen as lowsignal intensity on the steady-state free precession (SSFP)sequences. In addition, it is more easily distinguished atend-systole during cine imaging. Cine imaging also allowsassessment of the pericardial mobility. In acute inflamma-tion, the pericardium will appear very bright, due to a high

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mailto:[email protected]


Table 1Etiology of pericardial disease

1. Congenital abnormalitiesa. Partial or complete absence of the pericardiumb. Pericardial cystsc. Pericardial diverticulum2. Infectionsa. Viral (Echo, Coxakie, adenovirus)b. Bacterial: Mycobacterium tuberculosis, gram-positive cocci3. Postcardiac surgery4. Post-radiotherapy5. Trauma6. Post-myocardial infarction7. Connective tissue diseases: SLE, rheumatoid arthritis8. Granulomatous disorders: sarcoidosis9. Malignant conditions

Abbreviations and Acronyms

CMR = cardiac magneticresonance

CT = computed tomography

IVRT = isovolumic relaxationtime

MSCT = multislice computedtomography

SSFP = steady-state freeprecession

TSE = turbo spin echo

Fig 1. Serial short axis view of SSFP, T1demonstrating thickening of both pericar

306 D. Dawson, R. Mohiaddin / Progress in Cardiovascular Diseases 54 (2011) 305–319

amount of water, there-fore giving a persistenthigh signal on T2-weighted imaging. Ifdoubt persists, the peri-cardium can be “separated”by the surrounding fat byapplying a fat saturationpre-pulse in addition toinf lammation/edemaT2-weighted imaging(short tau inversion re-covery). An inflamedpericardium will also en-

a. Primaryb. Secondary10. Metabolic: uremia11. Idiopathic

hance with administration of gadolinium contrast, appear-ing very bright on early and late gadolinium-enhancedimages.5,6 Real-time free breathing cine loops willdemonstrate abnormal motion of the right ventricle freewall or the interventricular septum, which enhances withbreathing.7 Finally, tagging can be applied to thepericardium to assess its mobility.8

Assessment of the pericardium

Brief review of anatomy and physiology

As a thin, elastic structure surrounding the heart, thepericardium has an important contribution to cardiacphysiology, governing the diastolic interaction betweenthe 2 ventricles.When diseased, the restraining effect of thepericardial apparatus can lead to significant morbidity andculminate into life-threatening situations. The 2 serosal

W-TSE, T2W-TSE with fat suppressidial layers with a small pericardial eff

layers (with a virtual space in between, accommodating10-50 mL of fluid) and the fibrous pericardium takentogether have a thickness between 0.5 and 1 mm.9 Thepericardium extends up 3 to 4 cm onto the great vessels andat this level it reflects as the transverse sinus. Behind theatria, at the level of the great veins it reflects as the obliquesinus.9,10 The pericardium anchors the heart in the thoraxonto the diaphragm inferiorly, the spine posterior, and thesternum anterior. Apart from the anchoring function, it alsoprovides an important mechanical function, facilitating theheart motion within the pericardial sac in the presence ofthe normal pericardial fluid.11 This range of motion isrelatively limited, a fact that contributes to the phenomenonof ventricular interdependence.

on, early and late after gadolinium administration (A to E, respectively),usion. Note that pericardium enhances with contrast.

Fig 2. Large pericardial effusion (asterix) seen on SSFP images of 4-chamber view, 3-chamber view and short axis (A-C) and late after gadoliniumadministration (D).

307D. Dawson, R. Mohiaddin / Progress in Cardiovascular Diseases 54 (2011) 305–319

The etiology of pericardial disorders is presentedin Table 1:

Acquired pericardial diseases

Acute pericardial inflammation. CMR plays an impor-tant role in delineating the pericardium in acute pericarditisand can demonstrate acute thickening of both pericardiallayers on T1-weighted TSE images and SSFP cines. T2-weighted short tau inversion recovery and contrastenhancement of the inflamed pericardium on late gado-linium enhancement can identify edema, inflammation,and pericardial effusion, if present. Fig 1 demonstrates

Table 2Imaging characteristics of cardiac tamponade

1. Pericardial fluid (usually a large amount)2. Right ventricular free wall early diastolic collapse3. Late diastolic right atrial inversion4. Swinging heart5. Abnormal ventricular septal motion6. Respiratory variation in chamber size7. Respiratory variation of trans-mitral Doppler inflow with N25%decrease during inspiration

such an example of a patient presenting with acutepericarditis in the context of generalized sepsis.

Pericardial effusion. Clinical presentation of pericardialeffusion depends on the amount of fluid present in thepericardial sac and the rapidity with which this accumu-lates. Although a relatively large amount of fluid can buildup over a long time and result in relatively little or noclinical symptoms, the converse is also true: a relativelysmall amount of fluid that accumulates rapidly may resultin pericardial tamponade.12 Cardiac imaging is almostalways necessary to confirm the presence of fluid, assessthe size of the effusion and its distribution (global vsloculated) as well as to guide pericardiocentesis. Becauseof its urgent nature, this assessment is usually performedwith echocardiography, although CMR is gaining anincreasing role in recent years.

Cardiac tamponade is present when normal leftventricular filling is jeopardized. This represents amismatch between the ability of the pericardial layers tostretch relative to the amount and rate of fluid accumula-tion. To understand the pathophysiology of cardiactamponade, it is important to remember that under normalcircumstances, the intrathoracic pressure is transmitted to

image of Fig 2

Fig 3. (A) Global thickening of the pericardium (arrows) seen in transverse (A) and short-axis (B) T1-W Turbo spin-echo images and also on thecorresponding SSFP images (c-d). Note the bilateral pleural effusions. (B) Functional assessment of ventricular inter-dependence: a shows a normal septalposition during expiration and b demonstrates a marked leftward septal shift seen immediately after deep inspiratory effort. White arrows demonstrate therelative change in cavity size due to the septal shift.


image of Fig 3

Table 3Differentiation between pericardial constriction and restrictive cardiomyopathy

Pericardial Constriction Restrictive Cardiomyopathy Imaging Modality

➢ Pericardial thickness May be increased Normal CMR and CT➢ Pericardial calcification May be present Absent CT➢ LV systolic function Normal Normal until late stages CMR and echocardiography➢ LV diastolic function: echocardiography• Transmitral filling Respiratory variation No respiratory variation• E/A ratio Normal N2• Mitral septal annular E′ Normal b7 cm/s• Deceleration time Normal Short• IVRT Normal Short➢ Interventricular septal motion Abnormal (septal bounce

and shudder)Normal

➢ LV wall thickness Normal May be increased CMR, CT, and echocardiography➢ Invasive pressure monitoring “square root” sign Present May also be present Cardiac catheterization➢ Atrial size Increased but to a lesser degree Marked biatrial enlargement CMR, CT and Echocardiography➢ Color flow propagation N45 cm/sec b45 cm/sec Echocardiography➢ Hepatic vein flow Increased expiratory

flow reversalIncreased inspiratoryflow reversal

Echocardiography

Abbreviation: CT indicates computed tomography.


and equals the intrapericardial pressure. Physiologically,during inspiration, the return to the right ventricle ismomentarily increased. Because of the phenomenon of

Fig 4. A-B, SSFP images of a large pericardial cyst located in the right costophredemonstrating the cystic mass.

ventricular interdependence, there is a slight decrease inleft ventricular filling during inspiration. The oppositehappens during expiration. This little variation in the mitral

nic angle (arrows); (C) T1W-TSE and (D) T2W-TSE with fat suppression

image of Fig 4

Fig 5. A-B Turbo spin-echo image and C-D: SSFP image of total pericardial absence, which shows as a shift of the entire heart to the left and enlargement ofthe right heart.

Table 4Classification of cardiac masses

Benigna. Myxomab. Lipomac. Papillary fibroelastomad. Rhabdomyomae. Fibromaf. Hemangiomag. TeratomaMalignant1. Primarya. Angiosarcomab. Rhabdomyosarcomac. Fibrosarcomad. Lymphomae. Pericardial mesothelioma2. SecondaryNontumoral masses1. Thrombus2. Lipomatous hypertrophy of the interatrial septum3. Hydatid cyst4. Pericardial cyst


inflow (not more than 10%) is called physiologicalparadox.13 Any disease that limits the normal complianceof the pericardium (inflammation, thickening, or effusion)prevents the transmission of the intrathoracic pressures tothe pericardium and intracardiac cavities.14 This creates alarge respiratory-dependent variation in the left-sidedfilling gradient (between pulmonary capillaries and leftatrium). With inspiration the intrathoracic pressure falls,but this is not transmitted to the intrapericardial space,therefore the driving gradient between pulmonary capil-laries and the left atrium decreases. On the other hand, thereturn to the right atrium is increased, as in the normalsituation. With expiration, the intrathoracic pressureincreases, encouraging more return to the left atrium. Asthe intrapericardial space is fixed, the phenomenon ofventricular interdependence dictates that less left ventric-ular filling occurs during early inspiration whereas the rightventricle fills more. As a result, the interventricular septummoves toward the left. In expiration, the left ventricle fillsbetter and the septum returns to a normal position.15,16

This characteristic septal motion is known as a “septalbounce” or “septal shift.” The respiratory variation of leftventricular filing can be assessed clinically by palpatingthe pulse or by recording the blood pressure, or with

Doppler echocardiography where it is seen as a N25%variation of the transmitral peak E wave of the diastolicinflow, which is recognized as a highly sensitive sign.16 In

image of Fig 5

Fig 6. A-B SSFP images of a left atrial myxoma attached to the inter-atrial septum; C-D late gadolinium enhancement images showing enhancement of thecore of the tumour with contrast.

Fig 7. A well-circumscribed mass (arrow) is seen in the right atrium with high signal intensity on T1W-TSE images (A) and suppressed signal on T2-WTSE with fat suppression (B).


image of Fig. 6

image of Fig 7

Fig 8. Small mass attached to the tricuspid valve seen in a SSFP image (A), with high signal intensity on a T2W-TSE (B) and markedly enhancing on thelate gadolinium enhanced images (C-D).


addition to the septal bounce, there is also a discrete septal“shudder” that is seen during any cardiac cycle indepen-dent of breathing. This is thought to occur because of thedifferential filling rates of the 2 ventricles during diastole:in early diastole the suction resulting from ventricularrelaxation is stronger on the left side; toward mid-diastolethe filing rate of the right ventricle is facilitated. Inaddition, the mitral valve opens before the tricuspid valve.These phenomena result in a septal movement first towardthe right, then toward the left. If the right ventricular freewall is not adherent, then an early diastolic rightventricular collapse is easily seen on cine imaging.17 Insome cases, the acute inflammatory process is character-ized by the formation of granulation and fibrinousdeposition, which is highly adherent onto the free rightventricular wall and the early diastolic right ventricularcollapse may be obscured. Fig 2 demonstrates a largeeffusion. The main imaging characteristics of cardiactamponade are summarized in Table 2.

The use of CMR in pericardial effusions has been alsoused in an attempt to characterize the type of effusiondepending on the signal intensity: on T1-weighted TSE

images, transudates most likely appear black, whereasexudates or fresh hemorrhagic content may appear to havehigher signal intensity. On T2-weighted TSE imaging,both have high signal intensity. An older hemorrhagicpericardial effusion should appear to have lower signal onT2-weighted due to the shortening of T2 relaxation time bymet-hemoglobin.

Chronic constrictive pericarditis. Chronic constrictivepericarditis refers to the fibrotic transformation of thepericardium that becomes thickened and noncompliant.18

The most common settings or causes of pericardialconstriction are postcardiac surgery, post-pericarditis/effusion, radiotherapy, bacterial infections (classicallytuberculosis), autoimmune disorders, longstanding uremia,posttraumatic, or methysergide therapy. Patients presentwith dyspnea, vague abdominal complaints, and signs ofright ventricular failure and hepatic congestion; a pericar-dial knock may occasionally be heard.19 The pathophys-iology is similar to that described for tamponade20: thenoncompliant pericardium prevents the transmission ofintrathoracic pressures to the cardiac chambers and the

image of Fig 8

Fig 9. Large intramyocardial mass located within the interventricular septum of similar signal intensity to the myocardium seen on SSFP images (A) andsignificant late gadolinium retention denoting an increased volume of distribution (B). C shows the specimen after surgical resection.


ventricular diastolic filling is dominated by ventricularinterdependence occurring within a rigid pericardialspace.21 As a result, marked respiratory variations in leftand right ventricular filling rates will determine theabnormal septal motion seen shortly after inspiration.7,22,23

The diagnosis of pericardial constriction can often bechallenging and will require careful clinical assessment aswell as use of most available imaging techniques. There areseveral additional morphologic features to consider whendiagnosing pericardial constriction that pertain mostly toadvanced imaging. (1) The pericardium is usuallythickened, in some cases calcified, but normal pericardialthickness does not preclude the diagnosis of constriction.24

Pericardial thickening, if present, is a good diagnosticmarker.25 However, this can only be focal (characteristi-cally in the atrioventricular groove4). Both cardiac CT andCMR can provide accurate measurements of pericardialthickness. (2) Calcification of the pericardium is not wellseen on CMR and CT is the modality of choice to identifythis. (3) Chronically constrictive pericardium has a ragged,irregular appearance compared to an effusion where theedges are smooth. (4) Associated findings of the heart:

tubular-shaped ventricles, atrial and inferior vena cavaenlargement, although not specific for constriction mayadd to the diagnostic confidence. Fig 3 shows CMRexamples from a patient with pericardial constriction.

Constrictive-effusive pericarditis refers to tampo-nade/constrictive physiology that persists even after aneffusion is drained and the intrapericardial pressuredecreases. This can persist for a while or becomepermanent, resulting in constrictive pericarditis, and it isconceivable that this clinical entity represents an interme-diate or transitional status between an effusion andpericardial constriction.26

Differentiation of constrictive pericarditis fromrestrictive cardiomyopathy

Although the former represents decreased pericardialcompliance and the latter results as decreased myocardialcompliance, these 2 clinical entities are often confounded,mainly because their clinical signs of diastolic heart failureoverlap significantly. When a restrictive cardiomyopathyis the result if an infiltrative myocardial process (such asamyloidosis, glycogen storage diseases), cine-imaging

image of Fig 9


with CMR tissue characterization is very helpful inestablishing the diagnosis.27 Left ventricular systolicfunction is normal in both situations with the exceptionof late stages of restrictive cardiomyopathies, when itdeclines. Abnormal septal motion is only found inconstriction. A summary of the anatomical and hemody-namic indices derived from cardiac CT, CMR, orechocardiography are presented in Table 3.

Congenital anomalies: pericardial cysts and absenceof pericardium

Pericardial cysts. Pericardial cysts are usually incidentalfindings and typically occur in the cardiophrenic sulcusand most often right sided. Pericardial cysts are notconnected to the pericardial cavity and appear as mediumintensity on T1-weighetd TSE, and high signal on T2-weighted TSE or SSFP.28 They do not enhance withcontrast (Fig 4).

Absence of pericardium. Total absence shows as a shiftof the entire heart to the left and enlargement of the rightventricle, usually with significant tricuspid regurgitation.29

Fig 5 shows a SSFP frame of a total absence of peri-cardium. Partial absence may lead to myocardial hernia-tion, and patients present with chest pain.30

Cardiac tumors

Primary tumors of the heart, with the exception ofatrial myxomas, occur rarely; metastatic tumors to ordirectly invasive of the heart are far more common.About 75% of primary tumors are benign and 75% ofthese are atrial myxomas. The benign tumors includerhabdomyomas, fibromas, papillary fibroelastomas, hem-angiomas, pericardial cysts, lipomas, hamartomas, tera-tomas, and paragangliomas/pheochromocytomas. The last2 may also be malignant. The malignant tumors consist ofvarious sarcomas: myxosarcoma, liposarcoma, angiosar-coma, fibrosarcoma, leiomyosarcoma, osteosarcoma,synovial sarcoma, rhabdomyosarcoma, undifferentiatedsarcoma, lymphoma , neurofibrosarcoma, and malignantfibrous histiocytoma.31

Differentiation between benign and malignant cardiactumors by their MR signal characteristics is usuallydisappointing with few exceptions such as lipomas andfibromas, since most tumors show low to intermediatesignal intensity on T1-weighted images and high signalintensity on T2-weighted images. However, the combi-nation of MR signal characteristics, tissue characteriza-tion, location, and morphological appearances of thetumors are usually relied upon to give clues. Malignantprimary tumors can be differentiated from benignprimary tumors because of the former's large size withwide points of attachment, involvement of more than onecardiac chamber or great vessel, and pericardial orextracardiac extension. Angiosarcomas and haemangio-

mas show signal enhancement after administration of anMR contrast agent.

Special considerations on imaging of cardiac masses

The advantages that CMR offers are a superb spatialresolution without use of ionizing radiation, the inherentcontrast of flowing blood in cine imaging, the ability toprovide tissue characterization either by suppressingsignals from certain types of tissues (eg, fat suppression),or by assessing the vascular/fibrotic/necrotic compositionof a mass after administration of paramagnetic contrastagents. T1- and T2-weighted TSE offer excellent anatom-ical visualization of the heart and mediastinum. Fluid(such as in cystic lesions or tissue edema) appears as highsignal intensity on T2-weighted images. Fat containingstructures (lipomas, lipomatous hypertrophy of theinteratrial septum, or fat transformation within an infarct)appear as very bright signal on T1-weighed images andcan be suppressed with fat specific inversion recoverysequence. Hemorrhage can have a mixed signal intensitydepending on how much elemental vs particulate iron iscontained within a specific tissue. Paramagnetic contrastagents will accumulate quickly in high concentrations instructures that are abundantly vascular but will not entercystic or nonvascular areas (such as a thrombus).Gadolinium will be retained on late images in structureswith necrotic cores or fibrosis. SSFP sequences will allowassessment of a mass mobility and suggest or visualize itsinsertion points.

Cardiac masses

It is important to recognize the difference betweenstructures normally present in the heart, which may bemistaken by the inexperienced observer as a cardiac mass,and true cardiac masses. Structures that are normallypresent in the heart but are sometimes misinterpreted aspathology are:

1. Crista terminalis, seen as a muscular ridge at theentry site of the superior vena cava into the rightatrium, demarcating the part of the right atrium thatis embryologically derived from the sinus venosus;

2. Eustachian valve, variably present in the right atriumas a remnant structure, which conveys the bloodtoward the foramen ovale during fetal life;

3. Chiari network in the right atrium;4. The moderator band of the right ventricle that

uniquely identifies the anatomical right ventricle;5. False tendons of the left ventricle.

A classification of all cardiac masses is presented inTable 4.

Table 5Main CMR imaging characteristics of cardiac masses

T1-weighted TSE T2-weighted TSEGradient EchoImages

Enhancement AfterAdministration ofGd-DTPA

Myxoma Intermediate varying SI,calcified areas: hypointenseand hemorrhage: increased SI

Low SI, especially in ironcontaining myxomas

Very low SI comparedto the surroundingblood pool

Hyperintense

Lipoma/Lipomatoushypertrophy

Brightest SI similar tosubcutaneous fat, usingfat presaturation technique:reduced SI

Intermediate SI paralleling tosubcutaneous fat

Nonspecific Nonspecific

Fibroma Intermediate to slightlyhyperintense SI comparedto myocardium, whencalcification (hypointense)and hemorrhage (hyperintense)are present: heterogeneous.

Decrease in SI compared to TI Nonspecific Slight and heterogeneous

Rhabdomyoma Homogeneous, slightlylower SI than myocardium

Strong increased SI Very low comparedto myocardium

Nonspecific

Hemangioma Intermediate SI Increased SI (Due to slowflowing blood in the tumor vessels),higher than myocardium

Nonspecific Significant increasingSI, heterogeneous.

Intravenousleiomyomatosis

Similar to myocardium Similar to myocardium Nonspecific Nonspecific

Pericardial cysts(simple fluid)(proteinaceous fluid)

Lowest SI, flow void Highest SI Nonspecific Signal enhancement,visualization ofintracystic septae

Low SI, but higher than innormal fluid, no flow void

High SI

Angiosarcoma Central hyperintense spot(blood vessels, hemorrhageor necrosis), surrounded byintermediate SI regions.

No change Nonspecific Strong

Lymphoma Isointense to hypointense tocardiac muscle

Isointense to myocardium Nonspecific Heterogeneous withless enhancing centralregions

Liposarcoma Bright SI equal to subcutaneousfat, but heterogeneous: decreasein SI, when fat presaturationis used

Not published Not published Not published

Leimyosarcoma High SI, slightly higherthan liver parenchyma, but notas high as subcutaneous fathomogeneous, commonlyconnected with proteinaceouspericardial effusion

Not published Not published Not published

Thrombus Intermediate, often slightlyhigher SI than myocardium,slightly higher than blood

Surrounding slowly flowingblood becomes higher SI thanthrombus, contrast betweenthrombus and myocardium isfurther accentuated

Thrombus has thelowest SI

No signal enhancement,unless the thrombusis organized.

Fresh High SI (oxyhemoglobin) Decreased SIChronic (Olderthan 2weeks)

Higher SI (deoxyhemoglobin)

Abbreviation: SI = signal intensity. Adapted from Hoffmann et al. Eur Heart J. 1998;19:553–563.


Benign tumors

1. Myxoma is the most common benign cardiac tumor.The commonest occurrence is in the left atrium, buttumors located in all cardiac chambers have beenreported.32 Myxomas are pedunculated and the usualinsertion site is the interatrial septum (Fig 6). The tumoris mobile, often protruding through the mitral valve

orifice, well circumscribed, and has a heterogeneousappearance.33 Depending on whether there are areas ofnecrosis (described as “gelatinous” in pathologyspecimens), intratumoral hemorrhage, or calcification,there will be variable signal intensity on MR images.Myxomas usually have vascular center,34 and this partenhances during the early and late phase aftergadolinium administration. Because of their tendency

Fig 10. Large mass with irregular edges (arrows), occupying the back of the right atrium, extending beyond the borders of the heart with destruction ofthe myocardial walls (white arrows) seen on HASTE images (A), enhancing with contrast after gadolinium administration (B), showing aninhomogenous signal intensity on T1W-TSE (C) and also seen on SSFP images. A large, hemorrhagic pericardial effusion is also seen. Histologydemonstrated an angiosarcoma.


to embolize, detection of a cardiac myxoma shouldprompt immediate surgical removal.35 Rarely, myxo-mas can be multiple. Carney complex is an autosomaldominant syndrome characterized by cutaneous disease(lentigines, ephelides, and blue nevi) associated withintracardiac myxomas.2. Lipomas are also well circumscribed and can befound within the heart chambers (right atrium) but moreoften they are contained within the myocardial walls.36

They are incidental findings and do not commonlycause symptoms. CMR offers in vivo tissue character-ization, as on T1W TSE lipomas have high signalintensity but on T2W TSE they have intermediatesignal intensity (in contrast, acute intramyocardialhemorrhage has high signal intensity on both T1- andT2-weighted images). In addition, fat suppressionsequences will clearly demarcate a lipoma (Fig 7).3. Papillary fibroelastomas are small tumors (maxi-mum ~1 cm), pedunculated, less mobile, and exhibitfinger-like projections emerging from the maintumor.37 Most often they insert onto the cardiac valves(either valvular side). They are composed of avascular

connective tissue and if they are of enough size to beseen on CMR they would not enhance on the first passperfusion and early after gadolinium administration,but they enhance significantly on the late phase aftergadolinium (Fig 8). They do not cause valvulardysfunction but have a propensity to embolize;therefore, the embolic risk commands surgical exci-sion. They need to be differentiated from valvularvegetations and Lambl's excrescences, and this is bestdone by transesophageal echocardiography.4. Rhabdomyomas are usually intramural and multi-ple. They are mostly found in children and areassociated with tuberous sclerosis.38

5. Fibromas are also intramural and located within theventricular myocardium (Fig 9). They have a tendencyto calcify.39 They have a similar signal intensity as thesurrounding myocardium on the T1W TSE and SSFPbut early after gadolinium administration a poorlyvascular fibrous core may become apparent withintense enhancement on the late gadolinium images.40

6. Intrapericardial pheochromocytomas are a veryrare variety of extraadrenal pheochromocytomas, are

image of Fig 10

Fig 11. Multiple masses present in the myocardium, with irregular borders and local invasion extramyocardially (arrows), seen on T1W-TSE (A), T2W-TSE, enhancing variably with contrast after gadolinium administration (C). The histology later demonstrated an aggressive T-cell lymphoma (D).

Fig 12. Metastatic right renal cell carcinoma. Coronal (A) and transverse (B) spin-echo image showing large right sided mass invading the inferior venacava and extending into the right atrium (arrows). ra indicates right atrium; la, left atrium; rv, right ventricle; lv, left ventricle.


image of Fig. 11

image of Fig 12


usually located cranial to the left atrium or along theatrioventricular groove.41 They show high signalintensity on T2W images and have marked enhance-ment after gadolinium administration.7. Hemangiomas are rare. They occur intramurally andare highly vascular, hence they enhance markedly withcontrast. Hemangiomas typically show peripheralenhancement with poorly vascular core.8. Teratomas occur in infants, are located intraper-icardially and accompanied by a epicardial effusion.CMR helps locate the mass and surgical removal iscurative (Table 5).

Primary malignant tumors of the heart are rare.Generally, primary cardiac tumors within the ventricletend to be intramural, whereas those located in the atriatend to be intracavitary. Their prognosis in general isextremely unfavorable.

1. Sarcomas are the most common of these (angio-sarcoma, rhabdomyosarcoma, fibrosarcoma, liposar-coma, leiomyosarcoma, and undifferentiatedsarcomas). Metastases are common at the time ofdiagnosis. The right ventricle is most commonlyinvolved. Quite often there is architectural distortionof the myocardial walls involved and extension into thepericardium, with an associated pericardial effusion.Tissue characterization of tumors may be difficult withthe exception of lipomas and liposarcomas.42 They arehighly vascular, enhancing with contrast administra-tion. Extraskeletal cardiac osteosarcomas characteristi-cally develop near the junction of the pulmonary veinsand the left atrium. Figs 10 and 11 demonstrateexamples of malignant tumors of the heart.2. Pericardial mesothelioma usually involves bothpericardial layers, encasing the heart but not invadingit.43 Occasionally they can be surgically resected.

Cardiac metastases are much more common and aremost often secondary to lung or breast carcinoma orlymphoma; they are usually pericardial and are associatedwith hemorrhagic pericardial effusions.44 Not uncom-monly, extension through the inferior vena cava fromabdominal malignant tumors can be seen to invade theheart; such an example is illustrated in Fig 12.

In conclusion, CMR offers an extremely versatilemode of examination for the pericardium and cardiacmasses that can be used as a stand-alone technique or asan add-on to other imaging modalities. Its uniquecontribution comes from its ability to use a variety ofhighly specialized sequences which enables in vivotissue characterization.

Statement of Conflict of Interest

All authors declare that there are no conflicts of interest.

Acknowledgments

Dr. Dawson is supported by the Scottish AcademicHealth Sciences Collaboration. This work was supportedby the NIHR Cardiovascular Biomedical Research Unit ofRoyal Brompton and Harefield NHS Foundation Trust andImperial College London.

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assessment of pericardial diseases and cardiac masses with cardiovascular magnetic resonance

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