cardiovasculcmriar mr fm basics to clinical applications

www.appliedradiology.com APPLIED RADIOLOGY©� 43November 2010

Cardiac magnetic resonanceimaging (CMR) is the soleimaging modality with the abil-

ity, in 3 dimensions, to assess cardiacmorphology, ventricular function, per-fusion, viability and imaging charac-teristics of the surrounding vasculaturewithout ionizing radiation.1 CMR usesthe same principles as other MR tech-niques with the addition of ECG gatingin order to suspend cardiac motion.The increasingly sophisticated treat-

ment of patients with cardiac disordershas created the need for accurate andreproducible measurements of cardiacchamber volumes and function.2 CMRhas the ability to provide this informa-tion as well as assess edema, perfusion,viability and vascular anatomy.

Techniques of CMRVentricular morphologyBlack blood imaging can be used to

create still-frame images with high spa-tial resolution for morphologic analysis(Figure 1). Bright-blood steady statefree precession (SSFP) sequences pro-vide moving cine images with a highsignal-to-noise ratio (SNR) and excel-lent endocardial definition. Standardviews are derived from their echocar-diography counterparts; 4-chamber, 2-chamber (vertical long axis), leftventricular outflow tract (3-chamber),and short axis stacks (Figure 2). Mor-phologic variants of atrial, ventricular,valvular, arterial and venous structurescan be imaged with unsurpassed defini-tion.3 The ability to image in any planewithin the thorax is a unique strength ofCMR, of particular advantage in con-genital disorders.

Left ventricular functionCardiovascular MRmeasurements of

left ventricular (LV) function (Figure 2),are usually obtained from a series ofECG-gated SSFP images obtained in theshort axis view.4 Using either the 2- or 4-chamber view as a reference, a short-axis stack is prescribed from the plane ofthe mitral valve orthogonal to the longaxis of the ventricle in end-diastole.A stack of images extending to the car-diac apex is then acquired during sus-pended respiration, at a slice thickness

of approximately 6 to 8 mm, with 2 mminterslice gap. Using either automated ormanual techniques, the endocardial andepicardial borders are traced for eachslice and the ventricular volumes are cal-culated. Reproducibility is best obtainedby including the papillary muscles andtrabeculae in the LV volume (Figure 2).5CMR remains the gold standard formeasurements of LVmass, volume andejection fraction (LVEF), as well asfor regional wall-motion abnormali-ties,6,7 and is more reproducible thanechocardiography.8The major source of error occurs at

the basal slice during ventricular sys-tole, because of• the fixed imaging plane, and• the descent of the mitral valvetowards the LV apex, movingthrough the imaging plane.Allow for LV shortening by careful

cross-referencing of planes to delineatethe position of the mitral annulus atend-systole and end-diastole.

Right ventricular functionAccurate right ventricular (RV)

assessment demands 3-dimensionaltechniques because of the non-geomet-ric shape of the ventricle. The RV posi-tion has also traditionally made reliableechocardiographic measurements diffi-cult. RV dysfunction, as assessed byCMR, predicts a poor prognosis lateafter myocardial infarction (MI),9 and

Cardiovascular magneticresonance from basicsto clinical applicationsChristian R. Hamilton-Craig, MD, FRACP, Richard E. Slaughter, MD, FRANZCR,and Jeffrey H. Maki, MD, PhD

Dr. Hamilton-Craig is a Staff Cardiol-ogist, Center of Excellence forCardiovascular MRI, University ofQueensland, Brisbane, Australia, andDepartment of Radiology, University ofWashington, Seattle, WA; Dr. Slaugh-ter is Director of Medical Imaging,Centre of Excellence in CardiovascularMRI, The Prince Charles Hospital,Brisbane, Australia; and Dr. Maki isDirector of Body MRI, University ofWashington Medical Centre, Seattle,WA. Dr Hamilton-Craig is supportedby the National Heart Foundation ofAustralia and the University of Wash-ington Trans-Pacific Fellowship.

44 � APPLIED RADIOLOGY© www.appliedradiology.com November 2010

is of particular importance in pul-monary hypertension and adult con-genital heart disease.3In many centers, it is customary to

use the LV short axis view to assess RVvolume. However, the basal dimensionof the RV is considerably larger thanthe base of the LV, and when errors

occur in the base of the RV they maysignificantly affect accuracy, usuallyby underestimating RV volumes.8,10The tricuspid valve annular plane liesapical of the mitral valve plane. Whenthe same series of LV short axis viewsis used for RVmeasurements as for LVmeasurements, the basal end-diastolic

and end-systolic slice positions may bedifficult to determine. This is com-pounded because, in most cases, bothRV and atrial walls are thin, renderingit difficult to identify the exact plane ofthe tricuspid valve. RV quantificationcan be improved by using axial viewsor, preferably, dedicated RV sequenceswhere the tricuspid valve is imaged inthe margin of the slice.10,11 Axial imag-ing has disadvantages in congenitalheart diseases where the cardiac axisand the skeletal axis may not align,leading to inaccuracies in delineatingthe atrio-ventricular plane.

Late gadolinium enhancementTissue characterization with late

gadolinium enhancement (LGE) is oneof the unique properties of CMR. Thisphenomenon results from inherent rel-ative differences in the volume of dis-tribution of gadolinium (Gd) betweennormal and abnormal myocardium.12,13Gadolinium is normally confined tothe extracellular and interstitial space(e.g., it does not penetrate intactmyocardial cell membranes). Changesto the interstitium, such as infiltrationor fibrosis, increase the volume of dis-tribution, allowing a larger amount ofGd to penetrate into the tissue. T1-weighted (T1W) CMR imaging per-formed early after Gd administration isused for assessment of myocardial per-fusion during “first pass” entry into themyocardial microcirculation, analo-gous to single-photon emission com-puted tomography (SPECT) perfusionimaging of the myocardium. Imagingperformed late (10 to 20 min) after Gdadministration allows washout from themyocardial circulation. Myocardialsignal is nulled by the use of an inver-sion pulse, leaving normal myocardiumappearing black and areas of abnormalmyocardium appearing relativelybright due to residual Gd in the tissue(hence the term “late gadoliniumenhancement”).14-16 Myocyte necrosisresults in loss of cell membraneintegrity, allowing intracellular accu-mulation of Gd as occurs in LGE imag-ing of patients withMI.14,16-18

CARDIOVASCULAR MAGNETICRESONANCE

FIGURE 2. Standard CMR views. Vertical long axis (2-chamber, A), LVOT (3-chamber, B), 4-chamber (C), short axis (D).

A B

C D

FIGURE 1. Black blood images of the great vessels. Axial image (A) shows the relation-ship of the ascending and descending aorta to the right pulmonary artery (RPA). Obliquecoronal image (B) shows a patient with Marfanʼs syndrome and severe dilatation of theascending aorta.

A B



FIGURE 3. T2W CMR after acute myocardial infarction, shows a large area of myocardialedema as increased signal in the antero-septal wall (gray line, A). Late gadolinium enhance-ment image in the same patient (B) shows a large area of irreversible infarction (between thewhite arrows) with islands of low-signal within the infarct zone (*), signifying microvascularobstruction.

A B

FIGURE 4. Late gadolinium enhancement in ischemic cardiomopathy. Subendodardial infarc-tion in the basal inferior wall (lower arrows, A) with a small separate infarct in the anterior wall(upper arrow). Transmural infarction in the anterior wall (arrows, B).

A B

FIGURE 5. Extensive partial thickness LGE in the left ventricle is demonstrated (arrow, A) andin the right ventricle (arrow, B) in 2 patients with ischemic cardiomyopathy, severely dilatedventricles and poor systolic function.

Now an 80% dose reduction can mean...


T2-weighted ‘edema’ imagingT2-weighted (T2W) short-tau inver-

sion recovery (STIR) imaging is aCMR sequence sensitive to increasedmyocardial water content, allowing thedelineation of high-signal areas of

myocardial edema. Increased mobilewater content associated with edemaappears hyperintense on T2W-STIRimages (Figure 3).19 Quantification ofmyocardial edema, using tissue signalthresholds, has been shown to strongly

correlate with ischemic time.20-22Myocardial edema may be presentafter any form of myocardial injurysuch as myocardial ischemia, acuteinfarction, myocarditis, sarcoidosis ortrauma.19 CMR is able to assist in the


Table 1. Common Indications and Contraindications for CMR in Patients with Heart Failure

Common Indications Contraindications• Accurate assessment of left ventricular ejection Absolutefraction for device implantation (ICD/CRT) • Non-MR compatible implantable devices• Myocardial viability (ischemic cardiomyopathies) • Severe claustrophobia• Detection of interventricular thrombus Relative• Interstitial fibrosis (dilated and infiltrative cardiomyopathies) • Dysrhythmia affecting ECG-gating• Congenital heart disease • Severe renal impairment (risk of nephrogenic• Right ventricular quantification systemic fibrosis)• Evaluation for ARVD/C• Post cardiac transplantation surveillance• Constrictive pericarditis• Quantification of valvular dysfunction• Aortic and vascular measurement• Iron overload quantification (T2*)

ICD = implantable cardiac defibrillator. CRT = cardiac resynchronization therapy, ARVD/C = arrythmogenic right ventricular dysplasia/cardiomyopathy.

Table 2. Delayed Enhancement Patterns in CMR

Ischemic cardiomyopathies • Subendocardial or full thickness enhancement in a typical coronary distribution(Figure 4)

Non-ischemic cardiomyopathies • Mid-wall, oftenmild enhancement

Hypertrophic cardiomyopathy • Patchymid-wall enhancement in the areas of myocardial thickening• Faint “plexiform fibrosis” enhancement• Auto-infarction due to burnt-out disease (Figure 7E)

Sarcoidosis • Patchy,often bright LGE in a non-coronary distribution

Myocarditis • Mid-wall LGE in the lateral LV (Figure 7A)

Amyloidosis • Thickenedmyocardiumwith diffuse LGE of relatively low signal, involving bothventricles and the atria.

Systemic auto-immune syndromes • Subendocardial and/or subepicardial enhancement• Areas of full thickness LGE (Figure 7B)

Endomyocardial fibrosis • Bright subendocardial enhancement in a shortened ventricle• Often with triangular-shaped LV apical thrombus (Figure 7F).

Iron overload • Low signal on SSFP imaging• Quantification with T2*

LGE = late gadolinium enhancement, SSFP = steady state free precession, LV = left ventricle


diagnosis and surveillance of a rangeof cardiac disorders (Table 1).

Clinical role and indications for CMRIschemic cardiomyopathyEarly studies show that increased

signal in the myocardium followingintravenous Gd accurately depictedirreversible ischemic myocardialinjury independent of age.23,24 Thiswas subsequently confirmed byothers.25 The presence and transmuralextent of LGE following myocardialischemia (Figures 3B and 4) givesimportant predictive information aboutthe likelihood of functional recoveryafter revascularization.26-29 CMR isnow considered the gold standardinvestigation for the assessment ofmyocardial viability.The extent of LGE is also predictive

of LV remodelling in patients with HFfrom both ischemic and non-ischemiccauses.30 Previous reports have shownthat the presence of LGE can distin-guish ischemic from non-ischemic

dilated cardiomyopathy with good sen-sitivity and specificity (Figure 5).31,32However, patients with either severeleft main or diffuse coronary diseasemay not have undergone infarction,and therefore may not exhibitischemic-type LGE, despite large areasof ventricular hibernation. CMR withLGE combined with CT coronaryangiography may improve the non-invasive detection of ischemia as acause for heart failure with high sensi-tivity and specificity.33 Stress CMRperfusion imaging may also have a rolein this scenario.34

Interstitial fibrosisThe presence of mid-wall fibrosis as

demonstrated by LGE (Figure 5) hasalso been shown to correlate with ahigher rate of all-cause mortality andhospitalization in patients with non-ischemic dilated cardiomyopathy(DCM).35,36 In a group of patients withDCM, the presence of mid-wall LGEoccurred with poorer ejection fractions


FIGURE 6. Early-enhancement image demonstrating 2 separate mural thrombi (arrows).

…a cleaner image with the patient in mind.


and larger volumes when compared witha group of patients with DCM andabsence of mid-wall enhancement (Fig-ure 6).37 The extent of this interstitialfibrosis has also been assessed by the useof T1 mapping following intravenousGd.38 Interstitial fibrosis is a final com-mon pathway formany patients suffering

myocardial damage from various etiolo-gies.39 Measurements of T2 signal inten-sity and relaxation times also correlatewith biopsy-proven heart transplantrejection.40 The degree of interstitialfibrosis on CMR also correlates withincreased arrhythmic events in patientswith hypertrophic cardiomyopathy.41,42

Infiltrative cardiomyopathiesInfiltrative cardiomyopathies, which

may present either with systolic or dias-tolic heart failure, arrhythmias or sud-den cardiac death, can be difficult todiagnose with traditional imaging tech-niques. CMR provides accurate assess-ment of ventricular morphology andLGE, allowing imaging of abnormalareas of myocardium, with particularpatterns of LGE correlating with theunderlying infiltrative diagnosis.43 Suchconditions include sarcoidosis, hyper-trophic cardiomyopathy, connective tis-sue diseases, endomyocardial fibrosisand amyloid infiltration (Figure 7).44-47These conditions have patterns of LGEthat may be characteristic, and assist indiagnosis, when combined with theclinical features and ventricular mor-phology (Table 2). Knowledge of suchetiologies in patients presenting withHF may influence treatment decisions,such as a need for implantable defibril-lator insertion, and provide an opportu-nity for disease-specific therapy. CMRcan readily determine the extent of ironinfiltration in thalassemia, hemochro-matosis, and other states of iron over-load, and quantify them with the use ofthe T2* sequence.48

Intraventricular thrombusCMRhas advantages over echocardio-

graphy in the detection of intraventricularthrombi.49 Following IV Gd, the bloodpool signal is enhanced on T1W imagesand the signal from thrombus remains low(black). T1W images acquired immedi-ately after administration of Gd can dis-tinguish thrombus from surroundingmyocardium or tumor. When imagingimmediately after Gd contrast administra-tion, myocardium or tumor demonstrateincreased signal due to vascularity andperfusion, whereas thrombus, being avas-cular, remains dark. Left atrial appendagethrombus can also be seen on CMR, butthe diagnostic accuracy of CMR in thisarea is yet to bedetermined.50

Valvular dysfunctionThe anatomic mechanisms and

quantification severity can be assessed


FIGURE 7. Infiltrative myopathies. Myocarditis (A): Mid-wall LGE in the lateral LV. Systemiclupus erythematosis/overlap syndrome (B): sub-endocardial, sub-epicardial and full thicknessareas of LGE. Sarcoidosis (C): Patchy, bright LGE in a non-coronary distribution. Amyloid (D):Thickened myocardium with diffuse LGE of relatively low signal involving both ventricles andthe atria, due to amyloid infiltration. Burnt-out hypertrophic cardiomyopathy (E): Patient withknown HCM presenting with HF, showing focal areas of LGE. Endomyocardial fibrosis (F):Thick, sub-endocardial LGE is seen in a shortened ventricle, with a large triangular-shapedLV apical thrombus.

A B

C D

E F



by CMR. Echocardiographic measure-ments of regurgitation may be inaccu-rate, particularly in dilated ventricles.51The 3-dimensional volumetric natureof CMR helps overcome the problemswith inhomogeneity and eccentricity ofregurgitant jets.52 Comparison of LVstroke volume from volumetric LVmeasurements can be compared withaortic forward flow measurementsusing phase contrast flow imaging inthe ascending aorta. The regurgitantvolume can readily be calculated.53-55Regurgitant orifice area, most oftencalculated by the proximal isovelocitysurface area (PISA) method in echocar-diography, can also be performed byCMR.56 The CMR measurement ofanatomic orifice area, however, has notbeen prospectively evaluated to pro-vide equivalent prognostic informationto echocardiography.Similar CMR techniques can be

used for quantification of tricuspid,aortic and pulmonary regurgitation. Inparticular, phase-contrast flow quan-tification across the semilunar valvesoffer an accurate measurement of for-ward and backward flow,57 and mayoffer superior reproducibility toechocardiography.

Diastolic functionEchocardiography is the best-estab-

lished non-invasive technique for theevaluation of diastolic dysfunction.58CardiovascularMR analysis of ventricu-lar filling velocity, 3-dimensionalmyocardial strain analysis and real-timeCMR tissue tagging are promisingmeth-ods to assess regional diastolic func-tion.59 Cardiovascular MR using phasecontrast flow imaging is capable of mea-suring flow across themitral valve and inpulmonary veins. Measurements ofmitral A-wave and E-wave velocity anddeceleration times, and systolic and dias-tolic wave velocities in the pulmonaryflow traces, have been shown to be reli-able and easy to obtain.60 CardiovascularMR measurements show good correla-tion with echocardiographic measure-ments in limited numbers of patientswith normal and abnormal ventricles.60,61

Arrhythmogenic RV dysplasiaCMR provides the best imaging tech-

nique available for assessment of RVfree wall contraction abnormalities andis particularly valuable in assessingpatients with suspected arrhythmogenicRV dysplasia (ARVD).62,63 Regionalwall motion abnormalities are more dif-ficult to interpret in the RV than in theLV because of the structure of the RVfree wall. Exaggerated diastolic distor-tion of the RV free wall, or the “accor-dion sign,” is also associated withgenotype-positive ARVD.64 However,some systolic distortion of the RV, due tocontraction of the moderator band andinsertion of the trabeculae into the thinRV free wall, may be present in normalpatients. There is also growing recogni-tion of LV involvement in ARVD,whichcan be imaged by CMR.62 Identificationof fatty infiltration of the RV wall byCMR can be supportive of a diagnosis ofARVD, but is not a reliable sign due tothe thinness of the RVwall. It should benoted that fatty infiltration, as defined inthe current diagnostic criteria, is a histo-logical diagnosis not an imaging diagno-sis, and the prevalence of RV fat byCMR in the normal population has notbeen fully elucidated.

DyssynchronyImproved temporal resolution ECG-

gated SSFP images allow approxi-mately 40 frames per heart beat to beobtained. In the 4-chamber view, theLV lateral wall and septal contractilitycan be carefully evaluated frame-by-frame in relation to tricuspid andmitral valve opening as well as atrialcontraction. Cardiac MR techniquesusing SSFP imaging show promise inthe evaluation of mechanical dyssyn-chrony.65 The improved spatial resolu-tion of CMR, combined with hightemporal resolution or real-time imag-ing, may offer improved reproducibil-ity for the assessment of dyssychrony,which has proven difficult in random-ized echocardiographic trials of dys-synchrony quantification.66-68 Theability for CMR to predict respondersto cardiac resynchronization therapy isan area of ongoing research. It hasbeen well demonstrated, however,that patients with a large volumeof myocardial scar, as determinedby CMR, respond poorly to biventricu-lar pacing.6

Constriction and constrictivepericarditisContstrictive pericarditis is notori-

ously difficult to diagnose, often withsubtle echocardiographic and invasivehemodynamic findings. CMR pro-vides an accurate assessment of peri-cardial thickness, using double andtriple inversion recovery sequences, aswell as being able to non-invasivelydemonstrate ventricular interdepen-dence. Real-time imaging allowsassessment of the ventricular interde-pendence and abnormal septal motionseen in constrictive physiology. This isdone in the LV short axis view withimages, including the domes of thediaphragm, in order to observe respi-ratory motion.

Magnetic resonance angiographyThe anatomy of the great vessels and

branches are exquisitely shown onCMR,particularly with contrast-enhanced3-dimensional magnetic resonance

FIGURE 8. MR pulmonary angiography inchronic thromboembolic pulmonary hyper-tension. Image demonstrates severelyabnormal vasculature with stenosis, vesselcut-off, webs and poor perfusion.



angiography (3D-MRA). Lack of ioniz-ing radiation and high reproducibilitymake 3D-MRA useful for longitudinalfollow-up of patients with vascularabnormalities, particularly surgicalshunts or dissection. MR pulmonaryangiography is also useful in evaluationand surgical planning for chronic throm-boembolic disease (Figure 8).70In spite of its advantages, CMR does

have some limitations in patients withdysrythmias that affect ECG-gating,claustrophobia, implantable devices,and severe renal impairment. Parallelimaging has improved acquisition time,and automated software has reducedanalysis time, however CMR remains aspecialized technique requiring consid-erable expertise for both acquisition andinterpretation.

ConclusionCMR uniquely provides accurate and

reproducible measures of volumes andfunction of all 4 cardiac chambers andsurrounding vasculature. It providesexcellent morphological informationwith unparalleled definition betweenblood pool and myocardium. Combinedwith the known patterns of LGE, CMRprovides a powerful tool for the diagno-sis and quantification of myocardialinfarction. It provides prognostic infor-mation prior to either revascularizationor ventriculoplasty. Non-ischemic pat-terns of LGE may reveal infiltrativeconditions that are often difficult todiagnose with other techniques, andwhich may significantly alter clinicalmanagement. CMR is an ideal tech-nique to evaluate complications such asintracardiac thrombus or valve dysfunc-tion. It has significant advantages inevaluation of the RV, which is increas-ingly recognized as an important andprognostic factor in HF and congenitalheart disease.

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