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Year : 2007  |  Volume : 17  |  Issue : 2  |  Page : 109-119
Cardiac magnetic resonance in the assessment of cardiomyopathies

Department of Cardiac Radiology, Cardiothoracic Center, All India Institute of Medical Sciences, Ansari Nagar, New Delhi-110 029, India

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Cardiomyopathies (CMPs) are diseases of the myocardium, characterized by distinct morphological, electrophysiological and functional alterations of the heart. Cardiac magnetic resonance (CMR) offers distinct advantages over other imaging tests in the diagnosis and management of CMPs. This is primarily due to its ability to characterize the tissue abnormalities and demonstrate the functional alterations, all as part of a single examination. This review discusses the role of CMR, including the protocol, techniques and imaging features in the various CMPs. It also highlights the important role that CMR plays in the clinical decision making and follow-up of these patients.

Keywords: CMR, cardiomyopathy, MRI

How to cite this article:
Jagia P, Gulati GS, Sharma S. Cardiac magnetic resonance in the assessment of cardiomyopathies. Indian J Radiol Imaging 2007;17:109-19

How to cite this URL:
Jagia P, Gulati GS, Sharma S. Cardiac magnetic resonance in the assessment of cardiomyopathies. Indian J Radiol Imaging [serial online] 2007 [cited 2021 Mar 1];17:109-19. Available from:

   Introduction Top

Definition :

Cardiomyopathies (CMPs) are a spectrum of chronic progressive myocardial disorders with a distinct pattern of morphological, functional and electrophysiological changes. The expert consensus panel (2006) of the American Heart Association proposes the following definition: "Cardiomyopathies are a heterogeneous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction that usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilatation and are due to a variety of causes that frequently are genetic. Cardiomyopathies are either confined to the heart or are part of generalized systemic disorders, often leading to cardiovascular death or progressive heart failure-related disability". [1]

Classification :

CMPs are broadly classified into two major groups based on the predominant organ of involvement. Primary CMPs (genetic, nongenetic and acquired) comprise those conditions that are either solely or predominantly confined to heart muscle. These are relatively few in number. Secondary CMPs are those groups of conditions where the myocardial involvement occurs as part of a large number and heterogeneous variety of systemic disorders, usually affecting multiple organ systems.

For the purpose of the present review, however, we would be restricting the discussion to those CMPs that can be diagnosed based upon the currently available imaging modalities. These include dilated, hypertrophic, restrictive, arrhythmogenic right ventricular and certain miscellaneous group of CMPs.

Diagnostic techniques :

Determining the exact etiology of a Cardiomyopathy (CMP) is important since this determines the treatment and the patient survival time. [2] Currently available imaging modalities like echocardiography ( echo0 ) and radionuclide imaging cannot determine the exact etiology due to inadequate myocardial assessment (inferior spatial and contrast resolution and limited tissue characterization). Catheter angiography is limited to assessment of chamber lumen, with indirect demonstration of myocardial changes. Moreover, significant overlap of features between CMPs frequently exists. Endomyocardial biopsy (EMB), considered to be the gold standard technique, has limitations in the form of sampling errors and poor sensitivity. [3]

Cardiac MR (CMR) is now considered the ' in vivo ' gold standard imaging modality for the diagnosis and monitoring of treatment in patients with CMPs. It is capable of providing high-resolution images of the heart in any desired plane without any radiation. Spin-echo (SE) T1W and T2W imaging allows for tissue characterization. Cine-CMR can assess cardiac morphology and function. Gadolinium (Gd) can be administered and its passage through the LV myocardium can be imaged during its first pass at rest and this provides important information about contrast kinetics of the myocardium. Delayed-enhanced CMR (DE-CMR) is useful to differentiate ischemic from nonischemic CMP. Late enhancement occurs in any condition where the extracellular volume is enlarged due to myocardial fibrosis, inflammation or edema. [4],[5],[6] However, unlike ischemic heart disease, delayed enhancement in non-ischemic myocardial disease does not correspond to any coronary artery territory and is often midwall rather than subendocardial or transmural in location.

According to the recently published appropriateness criteria for CMR/cardiac CT, the various CMPs, as described in this article, are all appropriate indications for performing a CMR examination. [7]

   CMR Protocol Top

  1. Following scout images in axial, sagittal and coronal planes, obtain axial set of steady state free precession (SSFP) or half-Fourier single shot turbo SE images through the chest.
  2. Single shot or cine, scout images to line up short axis (SA) images

    a. 2-chamber long axis (or vertical long axis) prescribed off an axial view showing the apex and mitral valve, bisecting the mitral valve (MV) and apex.

    b. Horizontal long axis (or 4-chamber long axis) prescribed off this view, again bisecting the apex and center of the MV.
  3. SSFP SA cine images, from the MV plane through the apex, prescribed from the previously acquired horizontal long axis image.

    a. Slice thickness 6-8 mm, inter-slice gap 2 mm

    b. Temporal resolution <45 msec between phases

    c. Use parallel imaging (factor 2) to reduce acquisition time
  4. SSFP long axis cine images

    a. 4-chamber long axis, prescribed off a basal SA image, bisecting the interventricular septum.

    b. 2-chamber long axis, prescribed off a basal SA image, bisecting the anterior and inferior walls.

    c. 3-chamber long axis, prescribed off the most basal SA including the plane of the left ventricular outflow tract (LVOT), bisecting the LVOT and the posterolateral wall. This is particularly important for cases of asymmetric septal hypertrophy in patients with hypertrophic CMP.
  5. SE T1W (or double inversion recovery) black blood imaging (slice thickness 5-6 mm; inter-slice gap 1-2 mm)

    a. 4-chamber long axis

    b. SA

    Perform SE T1W images with fat suppression and slice thickness ~ 4 mm in the axial and SA planes, if arrhythmogenic right ventricular dysplasia (ARVD) is suspected. Consider use of anterior surface coil only to improve resolution without "wrap around" artifacts.
  6. Consider SE T2W imaging (4-chamber long axis and SA) in the acute setting when necrosis/edema may be present (e.g. myocarditis). May add fat suppression to improve visualization of bright signal.
  7. First pass perfusion (at rest) - Saturation-recovery (SR) imaging with GRE-EPI hybrid, GRE or SSFP readout

    a. SA imaging (at least 3 slices per heart beat) - slice thickness 8 mm, parallel imaging, in-plane resolution ~ 2-3 mm, readout temporal resolution ~ 100 - 125 ms or shorter as available.

    b. Contrast is given (0.05 - 0.1 mmol/kg, i.v bolus @ 3-5 ml/sec) followed by at least 30 ml saline flush (@ 3-7 ml/sec).

    c. Breath-hold starts during early phases of contrast infusion, before contrast reaches the LV myocardium.

    d. Image for 40-50 heartbeats by which time contrast has passed through the LV myocardium.
  8. DE-CMR

    a. Wait at least 10 min after IV contrast administration (0.15-0.2 mmol/kg).

    b. Inversion time set to null normal LV myocardium (or use fixed TI with a phase-sensitive sequence). For ARVD, set the TI to null the RV myocardium. Typical inversion times lie between 200-275 msec.

    c. 2D segmented inversion recovery GRE imaging during diastole - same views as for cine imaging (SA and long axis views) with in-plane resolution ~1.4-1.8 mm.

    d. Estimate area (transmural extent) and location of enhancement within each segment (based on the American Heart Association 17-segment model).

   Dilated cardiomyopathy (DCM) Top

The anatomical abnormalities of DCM are clearly shown on echo0 or CMR; biatrial enlargement and increased size of the left (LV) and right (RV) ventricles [Figure - 1]. There may be pleural or pericardial effusion, SVC/IVC dilatation or ventricular thrombus. The functional abnormalities are in the form of segmental wall motion abnormalities or global dysfunction. Mitral or tricuspid regurgitation, if present, can be well demonstrated on cine-CMR.

Non-invasive tests have their limitations in distinguishing dysfunction related to DCM or coronary artery disease (CAD) because of the presence of segmental wall motion abnormalities in both. Catheter angiography is usually performed to distinguish ischemic from non-ischemic pathology, but this approach is deficient since significant CAD may exist without 'infarction', whereas 'normal' coronaries may exist with myocardial damage. McCrohon et al , [9] on the basis of their study involving DE-CMR, concluded that the pattern of enhancement in the myocardium can help distinguish LV dysfunction related to DCM or CAD on CMR. The majority of DCM patients did not show contrast uptake, while in some patients, the late enhancement was seen in the mid-myocardium in a non-coronary pattern, clearly distinguishable from CAD. CMR is also useful in quantifying the effects of drug therapy [10],[11] in these patients.

   Hypertrophic CMP Top

Hypertrophic CMP is a condition characterized by significant myocardial hypertrophy. It may be symmetric, when it involves all the walls of the LV [Figure - 2]a or asymmetric, when it is regional in distribution.

Though ECHO is the most commonly used modality, asymmetric hypertrophy at the LV apex may not be well assessed with this technique. CMR precisely defines the site and extent of hypertrophy, especially at the LV apex. [12],[13]

Cardiac function and flow dynamics of the outflow in cases of hypertrophic obstructive CMP (HOCM), including systolic anterior motion of the mitral valve, are well seen on cine-CMR [Figure - 2]b and c. [14] Precise planimetric measurements of the LVOT area during systole can also be determined. [15] Myocardial tagging on CMR identifies regional myocardial strain and shear abnormalities. [16] DE-CMR demonstrates a pattern of contrast uptake in areas of fibrosis that is distinct from ischemic CMP, in that it does not preferentially involve the subendocardium. It is usually seen in the areas of hypertrophy or at the RV insertion points on the septum [Figure - 2]d. Patients showing hyperenhancement are at increased risk of sudden cardiac death. Bello et al [17] showed that patients with late enhancement usually will not respond to heart failure drug therapy. They may benefit from an implantable defibrillator. [18] CMR has also been used to monitor the functional and anatomical outcome of surgical and pharmacological septal reduction. [14],[19]

CMR is useful to screen the relatives of probands. It is the technique of choice for the diagnosis and follow-up of all variants of HCM. Assessment of total LV mass and its progression over time can be evaluated better with CMR compared to echo. [20]

   Restrictive CMP (RCM) Top

The World Health Organization (WHO) defines RCM as a myocardial disease characterized by restrictive filling and reduced diastolic volume of either or both ventricles with normal or near-normal systolic function and wall thickness. It accounts for nearly 5% of all primary heart muscle disorders. [21]

RCM is identified on CMR by normal LV size and normal or mildly impaired systolic function, abnormal severe diastolic ventricular function and biatrial enlargement [Figure - 3]. Primary infiltrative disorders of the myocardium, characterized by replacement of muscle by fibrous and other types of tissue, can lead to RCM. CMR can characterize tissue, identify anatomic alterations and can quantify myocardial mass, ventricular volumes and ejection fraction, thus making it a useful modality for investigating the various infiltrative CMPs.

Common infiltrative disorders of the heart include amyloidosis, sarcoidosis, hemochromatosis (or siderotic CMP) and endomyocardial fibrosis. Rarer causes include storage disorders such as  Anderson-Fabry disease More Details and Gaucher's disease.


Amyloidosis is characterized by expansion of the interstitium with amyloid protein. [22],[23] Cardiac involvement is seen with most forms of amyloidosis, although it is most common and most often clinically significant with type AL amyloidosis (primary amyloidosis), often associated with multiple myeloma or other monoclonal gammopathies. [24] It is the most common cause of RCM outside the tropics. Cardiac involvement leads to thickening of the left and right ventricular walls, sometimes associated with thickened atrial walls and the atrio-ventricular valves. On CMR, the presence of the latter two findings, in combination with pericardial and pleural effusions has been reported to be useful in differentiating amyloidosis from hypertrophied myocardium. An increase in the thickness of the interatrial septum or the posterior right atrial wall to greater than 6 mm is fairly specific for amyloid infiltration [Figure - 4]a. [25] There is also a diffuse decrease in the myocardial signal intensity on both T1W- and T2W-weighted images [Figure - 4]b. A ratio of myocardial to skeletal muscle signal intensity of < 1.0 at 20 ms TE has been reported to be an important feature of cardiac amyloidosis. [25]

On DE-CMR, contrast uptake is seen typically in the subendocardial location. In comparison with ischemic heart disease, however, this enhancement is usually global and does not match any specific coronary artery perfusion territory [Figure - 4]c. [26] Many a times, the entire LV myocardium may enhance. This may make it very difficult to determine the optimal inversion time, which will null the normal myocardium, as it becomes difficult to identify the normal myocardial areas clearly. Mahrholdt et al [27] found that if more than 50% of LV myocardium nulls earlier than LV cavity and if this region is not in a coronary artery distribution territory, then the diagnosis of cardiac amyloidosis is highly likely. While performing the DE-CMR examination, imaging must be performed earlier than usual and completed quickly since the inversion time is shorter than normal. [26] CMR can also be used to follow-up patients on drug therapy in amyloidosis. [28]


Cardiac involvement, though found in about 25% of patients with sarcoidosis, is symptomatic in only 5% of cases. [29] An early diagnosis is important since early corticosteroid therapy can help prevent malignant arrhythmias, which can result in sudden death. Biopsy may miss sarcoidosis because of patchy infiltration of the heart muscle.

CMR shows characteristic abnormalities in cardiac sarcoidosis. In the acute phase, T2W- and early Gd-enhanced images show focal areas of increased signal intensity [Figure - 5]a. [30],[31] This is because of edema associated with inflammation. Confluent sarcoid granulomas show increased peripheral signal and low signal in the center on T2W- images. Focal myocardial thickening because of edema may be seen. Cine-CMR may show segmental wall motion abnormalities.

On DE-CMR, patchy or focal enhancement is seen that is usually quite bright, discrete, does not correspond to any coronary artery distribution and is often mid-wall rather than subendocardial or transmural [Figure - 5]b. The enhancement may be seen in the interventricular septum in the basal region and sometimes in the LV wall. Rarely, papillary muscles and the RV wall may be involved. [32] In the late post-inflammatory phase, features of DCM may be seen.

In patients already on corticosteroids, follow-up CMR may show focal increased signal on T2W- images but without myocardial thickening and without Gd uptake. [32] CMR may also show associated features like pericardial effusion, mediastinal adenopathy [Figure - 5]c etc.

Siderotic (or iron overload) CMP

Iron overload CMP may be seen in patients with hemochromatosis or in those with inherited severe anemias like thalassemia, who require multiple and regular blood transfusions. Cardiac complications (heart failure and arrhythmias) lead to early death.

CMR offers a noninvasive and highly reproducible technique for quantifying heart iron deposition, before overt clinical and echocardiographic picture of heart failure takes place. CMR reveals extensive myocardial signal loss on T1W and T2W- images, a finding which is more prominent on T2* images. This pattern of focal signal loss in dysfunctional myocardium, associated with a dark liver, is enough to confirm the diagnosis of systemic hemochromatosis. [33]

Measurement of myocardial T2* [Figure - 6] on CMR has been found to correlate with LV dysfunction [33] and has been chemically validated through various studies. Calibration curves for MRI parameters R2 and R2* (or their reciprocals, T2 and T2*) have been developed for the liver and the heart. [34] In thalassemia patients with heart failure, myocardial T2* has been shown to increase as the LV function recovers. CMR has also been found useful for evaluation of different chelation regimes in these patients. [35]

Endomyocardial fibrosis (EMF)

EMF is a common cause of RCM in the tropics. This disease entity is characterized by extensive subendocardial fibrosis, apical thrombus formation and progressive diastolic dysfunction. [36] It involves the RV more commonly than the LV. The etiology is unknown, though eosinophilia and immuno-pathological processes are thought to play a role in its pathogenesis.

The structural and functional alterations of EMF can be well seen on CMR. Reported CMR findings in EMF include high signal intensity along the endocardium of the apex on T2W sequences, an overlying non-enhancing thrombus and a distinct high signal intensity plane separating the thrombus from the underlying myocardium on gradient- echo cine sequences. [37] Cine-CMR may demonstrate mitral and tricuspid regurgitation besides obliterated apices of the ventricles [Figure - 7]a.

DE-CMR has been shown to reveal subendocardial hyperenhancement of the apex, related to endocardial fibrosis [Figure - 7]b. [37],[38]

Anderson-Fabry disease (AFD)

AFD is an X-linked disorder of lysosomal metabolism, which is characterized by accumulation of glycosphingolipid in various tissues. In patients with the cardiac variant of AFD, myocardial hypertrophy is the main feature. This hypertrophy appears to be similar to that seen in HCM, but on DE-CMR the pattern of enhancement is different, with the basal inferolateral wall being the commonest segment showing enhancement. Unlike myocardial infarction, the subendocardium is commonly spared. [39] The mechanism of enhancement in AFD is thought to be interstitial expansion due to myocardial fibrosis associated with the accumulation of intracellular glycolipids. Presence of myocardial scarring may imply that treatment with enzyme replacement therapy may be less effective at this stage, making a case for early initiation of this treatment before fibrosis has developed.


Tuberculosis of the heart generally involves the pericardium and may result in constrictive pericarditis. Myocardial tuberculosis is very rare, the reported autopsy incidence being 0.14 - 0.3%. [40] Myocardial tuberculosis presenting as RCM is extremely unusual, with only one report till date. [41] We came across one case (not biopsy proven) of treated pulmonary tuberculosis presenting as RCM on echo0 . CMR shows diffuse myocardial thickening contiguous with the pericardial involvement, alongwith dilated atria [Figure - 8]a. DE-CMR showed dense myocardial and pericardial enhancement [Figure - 8]b.

   Arrhythmogenic Right Ventricular Dysplasia (ARVD) Top

ARVD is a myocardial disorder of uncertain etiology, marked by progressive fibrosis and fatty replacement of the myocardium. It most commonly involves the anterior wall of the RV, in the so-called "triangle of dysplasia" (the sub-tricuspid area, the apex and the infundibulum). It is more common in young males and has a familial occurrence. The condition usually leads to progressive RV failure and dilatation and is an important cause of sudden cardiac death due to ventricular arrhythmias. In one series, it accounted for 20% of sudden deaths in all individuals younger than 35 years and 22% of sudden deaths in young athletes. [42]

According to the task force criteria of 1994 laid down by McKenna et al , [43] the diagnosis of ARVD is based on the presence of major and minor criteria encompassing genetic, electrocardiographic, pathophysiologic and histopathologic factors. To fulfill the appropriate criteria for ARVD, patients must have two major criteria, one major and two minor criteria or four minor criteria.

The traditional imaging modalities used to evaluate right ventricular abnormalities include conventional angiography, echo0 and radionuclide angiography. However, all of them have low sensitivity and specificity for diagnosing ARVD, primarily because of their inability to accurately characterize structural and functional abnormalities of the RV. Besides, all these imaging modalities are limited by a lack of spatial resolution in diagnosing the typical fatty and fibro-fatty changes of the RV myocardium. EMB suffers from sampling errors, since the disease generally occurs in a segmental fashion. Also, ARVD commonly involves the anterior RV wall, while the biopsy specimen is usually obtained from the interventricular septum.

Due to its high resolution, large field of view and ability to quantify RV abnormalities, CMR has emerged as the imaging modality of choice for investigating ARVD. T1W SE images show fatty infiltration as bright signal with thinning of the RV wall and dysplastic trabecular structures [Figure - 9]a. [44] Cine-CMR shows decreased global function, regional wall motion abnormalities or aneurysms [Figure - 9]b. [44],[45] DE-CMR may show hyperenhancement in regions of fibro-fatty replacement [46] and thus may be useful to guide EMB [Figure - 9]c.

CMR can accurately quantify intramyocardial fat, which can help monitor evolution of the disease. [47] However, it is important to note that significant fatty infiltration occurs in more than 50% of normal hearts in elderly people. Also, in 15% of control subjects, some degree of intramyocardial fat is seen in the anterior apex of RV. Hence, focal wall motion abnormalities are considered to be a more reliable indicator of ARVD than the presence of isolated intramyocardial fat.

Since first-degree relatives of individuals with ARVD have an increased chance of having the disease, with an increased risk of sudden death, CMR serves as an important tool for screening them for the presence of pre-clinical disease.

   Miscellaneous Myocardial Diseases Top

Left Ventricular Noncompaction

Noncompaction of the ventricular myocardium is a CMP thought to be caused by arrest of normal embryogenesis of the endocardium and myocardium. This results in persistence of deep inter-trabecular recesses in communication with both the ventricular cavity and the coronary circulation. [48] On imaging, the inner myocardial layer is less compacted compared to the outer compacted myocardium. CMR images this differential myocardial compactness with high spatial resolution, particularly in the ventricular apex where echo0 has inherent diagnostic limitations. The other common site of involvement is the lateral wall of the LV. Lesser degrees of myocardial layering may however, be seen in other CMPs. Peterson et al [49] reported that a noncompacted/compacted myocardium ratio of >2.3 in diastole distinguished pathological noncompaction from other CMPs, with a specificity and negative predictive value of 99% each.

Takotsubo Cardiomyopathy

Also known as "transient apical ballooning syndrome", this condition is characterized by basal hypercontractile myocardium and a dyskinetic apex. Affected patients usually present with all clinical manifestations of an ST elevation myocardial infarction including chest pain, ECG changes and enzyme elevation. However, coronary angiography is normal. The condition is likely thought to be due to stress related catecholamine upsurge causing cardiac dysfunction. CMR is useful to show the functional abnormalities. Various studies on CMR report complete reversal of wall motion changes on repeat imaging performed a few weeks later. [50],[51] Generally, no enhancement on DE-CMR is seen. [51]


This is characterized by inflammation of the myocardium and is usually viral in origin. Although spontaneous recovery is common, active myocarditis may occasionally lead to sudden death and 5-10% of cases may progress to chronic dilated CMP. [52]

The clinical diagnosis may be difficult because of variable and often non-specific symptoms. Patchy involvement limits the use of EMB for diagnostic purposes.

CMR may show focal areas of increased signal on T2W images, representing active inflammation/edema. Both early and late Gd enhancement has been shown to correlate well with foci of myocardial necrosis on histology. [52] Cine-CMR may show wall motion abnormalities. The late hyperenhancement is typically subepicardial and has a nonischemic pattern of distribution. It is known to occur predominantly in the lateral free wall. [53] This hyperenhancement has been shown to decrease during healing and can be almost invisible after recovery. [52] Persistent hyperenhancement is a sign of fibrosis and may be clinically relevant as it may be a substrate for lethal arrhythmias. [54]

   Conclusion Top

CMPs are a heterogeneous group of myocardial disorders associated with distinct anatomical, functional and electrophysiological alterations of the heart. They arise either primarily in the heart muscle or are a result of secondary cardiac involvement in a variety of systemic multi-organ diseases. Traditional imaging techniques are limited in their assessment of the myocardium in CMPs. CMR has emerged as a virtual "one-stop shop" for imaging in CMPs. Its utility in imaging patients proven or suspected to have CMP is likely to evolve further in the coming years as more research into the development of improved techniques for myocardial characterization and assessment of contrast kinetics takes place.

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Correspondence Address:
Gurpreet S Gulati
Department of Cardiac Radiology, All India Institute of Medical Sciences, Ansari Nagar, New Delhi-110 029
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-3026.33620

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