Dr. Rajiah is a Clinical Fellow, Cardiovascular Imaging Laboratory, Imaging Institute, and Dr. Flamm is Section Head, Cardiovascular ImagingLaboratory, Imaging Institute, and on the Cardiovascular Medicine staff, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH.
Cardiomyopathies are “a heterogeneous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction, which usually but not invariably exhibit inappropriate ventricular hypertrophy or dilatation, due to a variety of etiologies that frequently are genetic. Cardiomyopathies are either confined to the heart or are part of generalized systemic disorders and often lead to cardiovascular death or progressive heart-failure–related disability.”1 There are multiple classification systems for cardiomyopathies. The most commonly used are those by the World Health Organization (WHO) and American Heart Association (AHA).1,2 The WHO classified cardiomyopathies broadly into dilated, hypertrophic, restrictive subtypes, and arrhythmogenic right-ventricular cardiomyopathy (ARVD, Table 1).1 As a result of further insights into the morphological and functional expression of the heart-muscle diseases, based frequently on advances in molecular biology and genetics, the AHA proposed a comprehensive classification of primary cardiomyopathies, which is not restricted by strict morphological definitions (Table 2).
Cardiac MRI in the evaluation of cardiomyopathy
Cardiac magnetic resonance imaging (MRI) has become a “one-stop shop” imaging modality in the evaluation of various congenital and acquired cardiac disorders, including cardiomyopathies. Although MRI is helpful in evaluation of morphology and function, its most important role in cardiomyopathy is to determine the presence and extent of ischemic scar or interstitial fibrosis using viability imaging. Determination of the underlying cause of cardiomyopathy is essential in deciding further diagnostic and therapeutic options, and ultimately in determining prognosis. Echocardiography, cardiac catheterization and nuclear scintigraphy have limited roles in evaluation, as the appearances are nonspecific. Endomyocardial biopsy is not sensitive and is hindered by sampling error.3 Cardiac MRI employing viability imaging is an efficient, noninvasive method of characterization of the various cardiomyopathies based on the varied patterns of myocardial enhancement and distribution of scar. Identification of myocardial enhancement is useful in risk stratification, as it is a substrate for arrhythmias, indicates a higher incidence of cardiovascular events, and hence, is a negative prognostic factor.
Viability imaging and pathophysiology of delayed enhancement
Viability imaging depends on the ability of MRI, following contrast administration, to demonstrate scar or interstitial fibrosis as a bright area against the background of dark, normal myocardium. Viability is assessed in MRI by the delayed-enhancement sequence (DEMRI), which typically is acquired 10 to 20 minutes after administration of gadolinium-chelate (0.1 to 0.2 mmol/kg), most commonly using a segmented k-space inversion-recovery gradient-echo pulse sequence, where the inversion time is set to null signal from normal myocardium.
The gadolinium-chelate (Gad) is generally considered biologically inert and passively diffuses within the myocardium in the extracellular, interstitial space, with a half life in blood of approximately 20 minutes. Hyperenhancement in myocardial scar is secondary to the different wash-in and wash-out kinetics, and volume of distribution compared to normal myocardium. While normal myocardium has a rapid wash-in and wash-out rate, scar tissue has more delayed wash-in and wash-out of contrast. In addition, an increased volume of distribution is seen as a result of different pathophysiological states. In acute infarction, myocyte death and the resultant loss of sarcomere integrity converts the majority of intracellular space to interstitial space. In chronic infarction, interstitial space is increased due to fibrosis. In either scenario, the increased concentration of Gad per unit volume results in T1 shortening and increased signal intensity on T1-weighted images (T1W). Hyperenhanced areas demonstrate excellent contrast compared with normal myocardium (5 times the signal intensity relative to normal remote myocardium) and excellent spatial resolution (typically on the order of 1 to 2 mm). The location and size of myocardial infarction in DE-MRI correlates closely with irreversible damage seen in histopathology.4
The inversion time is selected to null the signal from normal myocardium, in order to maximize the contrast between the normal myocardium and scar. The optimal inversion time can be selected by:
- Obtaining a series of 2-dimensional DE-MRI images across a range of inversion times.
- Using a Look-Locker sequence (Figure 1).
- Employing a lower resolution steady-state free-precession (SSFP) cine technique, incorporating an iteratively adjusted inversion time. Optimization of the inversion time is critical for DE-MRI imaging as an inappropriately short inversion time results in nulling of abnormal tissue and a long inversion time results in loss of contrast between normal and abnormal myocardium.
DE-MRI acquisition methods
There are multiple approaches for DE-MRI acquisition. In the 2-dimensional technique (usually a 2-dimensional segmented k-space gradient-echo inversion-recovery pulse sequence), each slice is acquired during a single breathhold with data acquired either every heartbeat or every other heartbeat. In the 3-dimensional volumetric technique (usually a 3-dimensional segmented k-space gradient-echo inversion recovery pulse sequence employing parallel acquisition acceleration), the entire left ventricle can be covered in a single breath. Although the overall acquisition time is shorter than the 2-dimensional acquisition, assuming equivalent coverage, and no slice misregistration (which is typically associated with 2-dimensional acquisition using multiple breathholds), the spatial resolution of 3-dimensional imaging is somewhat less than 2-dimensional imaging. The 3-dimensional volumetric techniques also can be acquired while free breathing, using navigator gating, which tracks the motion of the diaphragm as well as the electrocardiogram and synchronizes image acquisition, typically during expiration and end-diastole. Navigator-guided 3-dimensional sequences take more time to acquire, but have the advantage of potentially higher spatial resolution. Single-shot sequences acquire each image slice within a single heartbeat, which is particularly valuable in patients with arrhythmias or who have difficulty in breath holding.
All of the above sequences rely on the selection of an optimal inversion time. In contrast, the phase sensitive inversion recovery (PSIR) sequence eliminates the need for selecting the optimal inversion time. Magnitude, reference, and phase-sensitive images, with high spatial and contrast resolution, are acquired at a nominal value of T1, thus eliminating the need to acquire multiple images to find the precise nulling time.
Ischemic heart disease
Left ventricular (LV) dysfunction due to coronary artery disease (CAD) frequently is considered either irreversible with transmural myocardial damage, or consists of potentially reversible states of myocardial ischemia, such as stunning or hibernation. Irreversible damage may occur after coronary occlusion, as a wavefront of necrosis is initiated from the subendocardial region. If the damage is partial, only subendocardial enhancement occurs (Figure 2). If ischemia continues, the resultant necrosis gradually progresses outward to involve the epicardium with ensuing transmural enhancement (Figure 3) along the distribution of the involved epicardial coronary artery. Myocardial stunning, on the other hand, occurs when an acute, transient ischemic insult results in contractile dysfunction that persists despite restoration of coronary blood flow. Myocardial hibernation is sometimes considered a prolonged period of stunning, or secondary to repetitive stunning, as a result of chronic ischemia secondary to reduced coronary blood flow and oxygen supply. Viable myocardial cells may adapt to reduced oxygen supply by decreasing their function (contractility), but they retain the potential for recovery following restoration of coronary blood flow.
The aim of DE-MRI imaging is to detect segments of dysfunctional, but still viable myocardium that have the potential to recover or improve function following revascularization. Categorizing myocardium is based on the combination of wall motion and degree of segmental hyperenhancement. A pattern of normal wall motion and lack of hyperenhancement implies normal tissue. At the other extreme, the combination of wall-motion abnormality with >75% segmental hyperenhancement suggests nonviable infarcted tissue with little to no potential for function improvement. In between, are segments with wall-motion abnormality, but no degree or a mild degree (<25%) of hyperenhancement implying dysfunctional, but viable myocardial tissue with a high likelihood for functional improvement or recovery following revascularization. Other segments that are dysfunctional and have intermediate degrees of hyperenhancement (25% to 75%) have corresponding, intermediate potential for functional recovery.
While most ischemic patterns of enhancement are secondary to CAD, similar patterns also may be seen with transient events not associated with CAD, such as in embolism with spontaneous lysis of thrombosis (Figure 4), or vasospasm. In severe acute myocardial infarction, regions of myocardium may suffer severe microcirculatory damage, resulting in myocyte death, spilling of intracellulate contents, and severe sludging and occlusion of end-arteries and capillaries known as microvascular obstruction. As a result of lack of blood flow to the necrotic core, no Gad reaches the center of the infarcted zone and therefore no T1-shortening occurs. These areas are seen as a black core within an infarcted area (Figure 5), and portend poor prognosis with adverse remodeling.
Nonischemic dilated cardiomyopathy
Nonischemic dilated cardiomyopathy (DCM) is characterized by dilation and impaired contraction of the LV or both ventricles, which is not explained by CAD. DCM may be idiopathic, familial, genetic, viral, autoimmune, alcoholic or toxic in etiology. Arrhythmias, thromboembolism and sudden death are common complications. Cardiac MRI plays an important role in characterization and risk stratification of these patients. 30% to 35% demonstrate mid myocardial linear enhancement on DE-MRI in a noncoronary distribution, predominantly in the basal and mid interventricular septum, due to fibrosis (Figure 6). Etiologic considerations for this fibrosis include inflammation as well as microvascular ischemia. Pathologic specimens have demonstrated both reactive (perivascular, interstitial) and reparative (replacement) fibrosis. The pattern of fibrosis, similar to that seen in myocarditis suggests that, at least in a subset, DCM may be a sequelae of chronic myocarditits. The presence of interstitial fibrosis in DCM is a predictor of all-cause mortality, cardiovascular hospitalization, ventricular tachycardia and sudden death.5
Hypertrophic cardiomyopathy (HCM) is a primary disorder of the cardiac sarcomere due to inherited mutations in contractile proteins, and characterized by left- and sometimes right-ventricular myocardial hypertrophy. Complications may be severe and include arrhythmia and sudden death. Pathologically, HCM is characterized by myocyte hypertrophy and myofibrillar disarray surrounding loose connective tissue. The most common pattern is asymmetrical, septal hypertrophy. Other phenotypical variants are symmetrical, apical, mid ventricular, mass-like and burnt-out subtypes. Typically, the LV volume is normal or reduced and systolic function is normal or increased. Systolic gradients may be seen in the LV outflow tract (LVOT) or mid ventricle due to dynamic outflow obstruction at the site(s) of maximal hypertrophy, and when involving the LVOT systolic anterior motion of the mitral valve precipitates mitral regurgitation. Diastolic dysfunction is seen due to altered ventricular compliance.
There is a direct correlation between histologic collagen in HCM and increased delayed enhancement.6 Delayed enhancement is seen in the hypertrophied areas frequently in a patchy, sand-like pattern. In asymmetric hypertrophy, it is seen in the mid and basal anteroseptum, commonly at the anterior and posterior RV insertion points to the interventricular septum (Figure 7). In other patterns of hypertrophy, it is seen at the sites of maximal hypertrophy (Figure 8). Transmural enhancement in a thinned wall may be seen in the burned-out phase. Scarring is believed to be secondary to replacement interstitial fibrosis or plexiform fibrosis in areas of myofibrillar disarray, expansion of interstitial space due to abundant connective tissue in hypertrophied areas, or ischemia-related necrosis.7 Ischemia may be seen due to reduced capillary density, hyperplasia of the media of the arterioles, increased perivascular fibrosis and myocardial bridging. Increasing volumes of delayed enhancement are associated with regional wall-motion abnormalities and global decrease in LV function.
The presence of scar is becoming an important factor in risk stratification as interstitial fibrosis is a substrate for arrhythmia, and is associated with sudden death and cardiac failure.
DE-MRI also is used to assess HCM patients following transcatheter septal ablation, where the presence of new septal hyperenhancement with decrease in size and mass of the hypertrophied segment corresponds to successful percutaneous therapy (Figure 9).
Restrictive cardiomyopathies and constrictive pericarditis
Restrictive cardiomyopathy is characterized by restrictive filling and reduced diastolic volume of either or both ventricles, atrial dilation, and normal or near-normal systolic function and wall thickness.8 Increased interstitial fibrosis may be present. The main differential diagnosis is constrictive pericarditis. MRI is helpful in differentiating these 2 conditions as management options differ. DE-MRI may demonstrate varying patterns of myocardial enhancement in restrictive cardiomyopathy depending on the underlying pathology.
In constrictive pericarditis, there is reduced ventricular filling and diastolic volumes, similar to restrictive cardiomyopathy. However, constrictive pericarditis classically demonstrates focal or diffuse pericardial thickening (>4 mm) or calcification (Figure 10a). In a subset of patients, the pericardium is of normal thickness. Specific physiological features of constrictive pericarditis seen in cine imaging are: Diastolic restraint and diastolic septal bounce due to ventricular interdependence, conical deformity of the RV, and tubular deformity of the LV. Real-time cine imaging reveals early inspiratory flattening and inversion of the interventricular septum.9 Secondary features include biatrial dilation, enlarged SVC/IVC/hepatic veins, bilateral pleural effusions, and ascites. There may be focal or diffuse enhancement of the pericardium in DE-MRI images (Figure 10b).
Sarcoidosis is a multisystem disorder characterized by noncaesating granulomas. Cardiac symptoms are seen in 5% of patients, although cardiac involvement may be as high as 50% in autopsy specimens. Cardiac sarcoidosis is a poor prognostic indicator and is associated with ventricular tachyarrhythmias, conduction abnormalities, and LV dysfunction. Pathologically, there are nonspecific inflammatory changes such as lymphocytic infiltration, interstitial edema, and damaged cardiac myocytes that result in interstitial fibrosis or scarring. DE-MRI demonstrates enhancement predominantly in the mid myocardial/subepicardial regions (Figure 11).10 Localization to the subepicardium might be due to the inflammatory myocardial lesion. Previous studies suggested a predilection for the septum, though a recent study11 revealed no specific regional predilection. Occasionally, subendocardial or transmural enhancement is seen, the latter more typically in older, burned-out phases of disease. Areas of enhancement are associated with wall-motion abnormalities, but with normal myocardial thickness (unlike myocardial infarction). Severe hyperenhancement is associated with poor LV function.
Amyloidosis is characterized by extracellular accumulation of a ß-pleated sheet fibrillary protein. The various types include:
- Primary, which is the most common and severe, with cardiac involvement common (50%);
- Familial, which is autosomal dominant, and has high penetrance with uncommon cardiac involvement;
- Senile-systemic amyloidosis, which is seen exclusively in the heart; and,
- Reactive-systemic amyloidosis, which rarely has cardiac involvement.
Cardiac amyloidosis typically has myocardial thickening, reduced systolic and diastolic function, and biatrial enlargement with diffuse wall thickening. Morphologic features that differentiate amyloidoses from HCM include nodular atrial thickening and interatrial septal thickening.
DE-MRI demonstrates a typical pattern of global, diffuse subendocardial enhancement that may be patchy, and extends to varying degrees into the myocardium, in a noncoronary distribution.12 Enhancement is caused by interstitial expansion from amyloid infiltration, though without fibrosis, and is associated with increased ventricular mass and impaired systolic function.13 Enhancement on DE-MRI also is seen in the thickened atrial walls, interatrial septum and valves (Figure 12).
Cardiac amyloidosis also is characterized by abnormal myocardial and blood pool Gad kinetics.13 As a result of diffuse amyloid infiltration, the myocardium has a shorter T1 value at 4 minutes than in normal individuals. In addition, Gad washes out faster than normal from blood and myocardium due to distribution into the total amyloid load in the body, which results in rapidly similar T1 values for blood and myocardium. In a normal person, the null point of blood typically occurs earlier than myocardium (Figure 1), but in amyloidosis, due to diffuse infiltration and Gad uptake, the myocardium appears the darkest at an inversion time earlier than that of the blood pool (Figure 13).
Technical challenges occur in detecting delayed enhancement in amyloidosis because of the altered kinetics. The inversion time is shorter than normal and lengthens in large incremental steps. Enhancement fades with equalization of inversion time between subendocardium and epicardium at approximately 8 minutes. Hence DE-MRI should be performed more quickly following Gad administration than in other cardiomyopathies.
Cardiac involvement in amyloidosis indicates a poorer prognosis. As treatment options are limited with onset of heart failure; cardiac MRI with DE-MRI plays an important role in early diagnosis and the initiation of aggressive treatment. Presence of delayed enhancement is not a significant predictor of mortality, but a 2 minute postGad T1 difference between subepicardium and subendocardium of <23 ms indicates diffuse infiltration and is associated with decreased survival.14
Anderson-Fabry disease is an X-linked glycogen storage disorder caused by deficiency of alpha-galactosidase A. It results in accumulation of sphingolipids in multiple organs. Cardiac involvement is one of the biggest contributors of mortality. The disease is more common in heterozygote females, and there is an isolated cardiac variant that occurs in men (6%). Cardiac involvement is characterized morphologically by symmetrical, concentric myocardial hypertrophy (occasionally asymmetrical septal hypertrophy like HCM), and functionally by reduced LV volume and increased EF, which can be confused with HCM. Arrhythmias, valvulopathy, and restrictive cardiomyopathy are common complications. Delayed enhancement is due to intramyocyte-sphingolipid deposition or expansion of interstitial space due to fibrosis and collagen deposition. Delayed enhancement is seen in 50% of patients15 and tends to be subepicardial and midmyocardial, predominantly in the basal inferolateral wall (Figure 14); this pattern of enhancement helps to differentiate the entity from HCM. Differentiating these two is important in that the treatment options are disparate, and for Fabry’s disease the presence of delayed enhancement predicts lack of response to enzyme replacement therapy. Of further importance is that 6% to 12% of patients initially diagnosed as HCM, were ultimately found to have Fabry’s disease.
Acute myocarditis is a cause of acute, fulminant cardiac failure and is usually secondary to viral infections, such as enteroviruses, adenoviruses, parvovirus B19 (PVB19) and human herpesvirus 6 (HHV6). Delayed enhancement is seen in the vast majority of patients with acute myocarditis. The enhancement pattern is often characteristic, beginning in the epicardial zone and extending to varying degrees into the midmyocardium, with usual sparing of the endocardium, and frequently localized to the inferolateral and lateral walls, and less frequently to the anteroseptal walls (Figure 15). The combination of focal-myocardial enhancement on DE-MRI and associated wall-motion abnormality has a strong correlation with active myocarditis. As the disease progresses, enhancement can become diffuse. With time, enhancement may decrease in size or disappear.
Recent work has suggested different patterns of enhancement and progression of disease based on the etiologic agent. For example, in a recent study, patients with PVB19 presented with typical subepicardial Gad enhancement in the lateral wall, and they recovered within months. However, patients who presented with HHV6 and new onset of heart failure had septal enhancement; they frequently progressed toward chronic heart failure.16
Delayed midwall enhancement has been seen in ≤84% of patients with chronic active myocarditis, and ≤44% of those with borderline myocarditis.17 The pattern of enhancement in these patients is similar to patients with dilated cardiomyopathy, lending potential credence to the hypothesis that episodes of myocarditis are a component of their pathophysiology.17
Endomyocardial fibrosis is an idiopathic disorder characterized by patchy fibrosis of the endocardial surface of the heart, resulting in restrictive cardiomyopathy. It is considered part of a spectrum of single-disease processes that includes Loeffler endocarditits (nontropical eosinophilic endomyocardial fibrosis or fibroplastic parietal endocarditis with eosinophilia). In the initial phase, there is eosinophilic infiltration of the myocardium with subendocardial necrosis, similar to myocarditis. The second stage (after 10 months), is characterized by thrombi formation with decreased inflammatory activity. Finally, in the chronic-fibrotic stage, the endocardium is replaced with collagenous fibrosis and calcification. DE-MRI reveals a diffuse, intense, linear enhancement of thickened endocardium involving either or both the LV and RV. The enhancement can be a result of either an inflammatory exudate or fibrosis, with higher signal intensity in the former.18 Thrombi, when present, are seen as areas of low signal intensity on DE-MRI (Figure 16).
Arrhythmogenic right ventricular dysplasia/cardiomyopathy
Arrhythmogenic right-ventricular dysplasia or cardiomyopathy (ARVC/D) is an RV-myocardial disorder characterized by progressive fibrofatty replacement of the myocardium. The etiology is uncertain and could be secondary to apoptosis, abnormal development, degeneration or inflammation. It is a familial condition in 30% to 50% of individuals with autosomal-dominant inheritance, and it has variable penetrance and phenotypic expression. Ventricular arrhythmia with a left-bundle branch pattern is the usual clinical presentation. It may account for ≤20% of sudden deaths in adults <35 years of age.
The fatty type is characterized by fat infiltration, without wall thinning, while the fibrofatty type has fibrofatty infiltration and significant RV-wall thinning. Less commonly, either type may involve the LV. Diagnosis is made based on the presence of major and minor criteria according to published Task Force criteria.19
Fatty replacement is seen in spin-echo black-blood images as high signal intensity within the RV-free wall. Functional images may show RV dilation, wall-motion abnormalities, global systolic or diastolic dysfunction, or aneurysms. Fibrofatty replacement presents with diffuse or segmental replacement of RV myocardium with scar in the DE-MRI images (Figure 17). It is more common in the RV outflow tract and anterobasal wall (67%), and has associated wall thinning. Delayed enhancement predicts induction of ventricular tachycardia and correlates with decreased RV EF and increasing RV EDV, and may be important for risk stratification.20
LV noncompaction is characterized by exaggerated hypertrabeculated, noncompacted myocardium typically in mid and distal LV segments. Complications include systolic dysfunction, thromboemboli, arrhythmias and sudden death. Cardiac MRI may demonstrate delayed enhancement in the deep trabecular recesses of the noncompacted segments (Figure 18). The amount and degree of trabecular delayed enhancement correlates inversely with the global LV function.21
Muscular dystrophies are X-linked recessive disorders that involve skeletal and cardiac muscles. Duchenne and Becker dystrophy are the 2 most common subtypes, characterized by absent and abnormal or reduced dystrophin, respectively, which results in myocardial necrosis and replacement with fat or fibrous tissue. Death is due to cardiac or respiratory failure. Early diagnosis of cardiac involvement helps in early initiation of heart-failure treatment, before manifestation of symptoms, and to monitor treatment response. Delayed enhancement on DE-MRI has been seen in 70% of patients in one study22 with a typical subepicardial distribution predominantly in the lateral wall (Figure 19). Patients with fibrosis have lower EF than those without. In a recent study of Becker dystrophy patients 80% had reduced LVEF and 73% had delayed enhancement, which was most commonly present in the subepicardial portion of the inferolateral wall.23
Chagas disease is caused by Trypanosoma cruziand can result in cardiomyopathy in 20% of patients. Delayed enhancement is seen in the epicardial or mid myocardial portions of the LV, more commonly in the mid inferolateral wall and apex. Enhancement is diffuse in instances of more severe involvement. Delayed enhancement can be seen during the prolonged asymptomatic phase, and when identified, treatment can be initiated prior to the onset of heart-failure symptoms. Delayed enhancement is seen in 100% of patients with established heart failure.3
A global subendocardial pattern of enhancement is also seen in uremic cardiomyopathy, post cardiac transplant,3 systemic sclerosis, and Churg-Strauss syndrome.24 Mid myocardial scarring can be seen in glycogen storage disease.24
DE-MRI is an excellent technique for accurate, reproducible detection and quantification of myocardial scar, due to its high spatial and contrast resolution and absence of radiation. Cardiac MRI with delayed enhancement is also useful in the differentiation of ischemic from nonischemic cardiomyopathies and in the characterization of various non-ischemic cardiomyopathies, based on the distribution and enhancement patterns of scar tissue and interstitial fibrosis (Table 3). The presence of scar/interstitial fibrosis is a substrate for arrhythmia and increases the risk of ad-verse cardiovascular events, making DE- MRI an important tool for prognosis.
- Maron BJ, Towbin JA, Thiene G, et al. American Heart Association; Contemporary definitions and classification of the cardiomyopathies. Circulation. 2006;113:1807-1816.
- Richardson PJ, McKenna W, Bristow M, et al. Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the definitionand classification of cardiomyopathies. Circulation. 1996; 93:841-842.
- White JA, Patel MR. The role of cardiovascular MRI in heart failure and cardiomyopathies. Cardiol Clin. 2007;25:71-95.
- Shan K, Constantine G, Sivanathan M, Flamm SD. Role of Cardiac Magnetic Resonance Imaging in the assessment of myocardial viability.Circulation. 2004;109:1328-1334.
- Assomull RG, Prasad SK, Lyne J, et al. Cardiovascular magnetic resonance, fibrosis, and prognosis in dilated cardiomyopathy.J Am Coll Cardiol. 2006;48:1977-1985.
- Moon JC, Reed E, Sheppard MN, et al. The histologic basis of late gadolinium enhancement cardiovascular magnetic resonance in hypertrophic cardiomyopathy. J Am Coll Cardiol. 2004; 43:2260-2264.
- Moon JCC, McKenna WJ, McCrohon JA, et al. Toward clinical risk assessment in hypertrophic cardiomyopathy with gadolinium cardiovascular magnetic resonance. J Am Coll Cardiol. 2003; 41:1561 -1567.
- Kushwaha SS, Fallon JT, Fuster V. Restrictive cardiomyopathy. N Engl J Med. 1997;336:267-276.
- Francone M, Dymarkowski S, Kalantzi M, et al. Real-time cine MRI of ventricular septal motion: A novel approach to assess ventricular coupling. J Magn Reson Imaging. 2005;21:305-309.
- Vignaux O. Cardiac sarcoidosis: spectrum of MRI features. AJR. 2005;184:249-254.
- Ichinose A, Otani H, Oikawa M, et al. MRI of cardiac sarcoidosis: Basal and subepicardial localization of myocardial lesions and their effect on left ventricular function. AJR. 2008;191:862-869.
- Vogelsberg H, Mahroldtr H, Deluigi C, et al. Cardiovascular magnetic resonance in clinically suspected cardiac amyloidosis: Nonivasive imaging compared to endomyocardial biopsy.J Am Coll Cardiol. 2008;51:1022-1030.
- Maceira AM, Joshi J, Prasad SK, et al. Cardiovascular magnetic resonance in cardiac amyloidosis. Circulation. 2005;111;186-193.
- Maceira AM, Prasad SK, Hawkins PN, et al. Cardiovascular magnetic resonance and prognosis in cardiac amyloidosis. J Cardiovas Magn Reson. 2008;10:54-65
- Moon JC, Sheppard M, Reed E, et al. The histological basis of late gadolinium enhancement cardiovascular magnetic resonance in a patient with Anderson-Fabry disease.J Cardiovasc Magn Reson. 2006;8:479-482.
- Mahrholdt H, Wagner A, Deluigi CC, et al. Presentation, patterns of myocardial damage, and clinical course of viral myocarditis. Circulation. 2006;114:1581-90.
- De Cobelli F, Pieroni M, Esposito A, et al. Delayed gadolinium-enhanced cardiac magnetic resonance in patients with chronic myocarditis presenting with heart failure orrecurrent arrhythmias. J Am Coll Cardiol. 2006;47:1649-1654.
- Syed IS, Martinez MW, Feng DL, Glockner JF. Cardiac magnetic resonance imaging of eosinophilic endomyocardial disease. Int J Cardiol. 2008;126:50-52.
- Kayser HWM, van der Wall EE, Sivananthan MU, et al. Diagnosis of arrhythmogenic right ventricular dysplasia: A review.RadioGraphics. 2002; 22:639-650.
- Tandri H, Saranathan M, Rodriguez ER, et al. Noninvasive detection of myocardial fibrosis in arrhythmogenic right ventricular cardiomyopathy using delayed enhancementmagnetic resonance imaging. J Am Coll Cardiol. 2005;45: 98-103.
- Petersen SE, Selvanayagam JB, Wiesmann F, et al. Left ventricular non-compaction: Insights from cardiovascular magnetic resonance imaging. J Am Coll Cardiol. 2005;46:101-105.
- Silva MC, Meira ZM, Gianneti FJ, et al. Myocardial delayed enhancement by magnetic resonance imaging in patients with muscular dystrophy. J Am Coll Cardiol. 2007;49:1874-1879.
- Yilmaz A, Gdynia HJ, Baccouche H, et al. Cardiac involvement in patients with Becker muscular dystrophy: New diagnostic and pathophysiological insights by a CMRapproach. J Cardiovasc Mag Reson. 2008;10:50-55.
- Silva C, Moon JC, Elkington AG, et al. Myocardial late gadolinium enhancement in specific cardiomyopathies by cardiovascular magnetic resonance: A preliminary experience. J Cardiovasc Med. 2007;8:1076-1079.