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DOI:10.2214/AJR.07.2287
AJR 2007; 189:1344-1352
© American Roentgen Ray Society

Review

MRI of Hypertrophic Cardiomyopathy: Part 2, Differential Diagnosis, Risk Stratification, and Posttreatment MRI Appearances

Mark W. Hansen1,2 and Naeem Merchant2

1 Department of Medical Imaging, The Prince Charles Hospital, Rode Rd., Chermside, Brisbane, Queensland 4032, Australia.
2 Department of Medical Imaging, Toronto General Hospital, University Health Network and Mt. Sinai Hospital, Toronto, ON, Canada.

Received March 20, 2007; revised June 29, 2007;

 
Address correspondence to M. W. Hansen (mark.hansen{at}qscan.com.au).


Abstract
Top
 Abstract
Introduction
 Differential Diagnosis
 Sudden Cardiac Death and...
 Treatment of HCM
 Screening for HCM
 Summary
 References
 
OBJECTIVE. We present a two-part review about the use of MRI in patients with hypertrophic cardiomyopathy (HCM). This article, Part 2, covers the differential diagnosis, risk stratification, and posttreatment MRI follow-up appearances in these patients.

CONCLUSION. Cardiovascular MRI is a useful imaging tool for the diagnosis of HCM and follow-up of patients after either surgical myomectomy or septal ablation therapy. In addition, MRI can help to discriminate HCM from the differential diagnoses of other cardiomyopathies and cardiac disorders, and it can potentially identify the subset of patients at risk of sudden cardiac death.

Keywords: cardiac imaging • cardiomyopathy • cardiovascular imaging • Fabry's disease • hypertrophic cardiomyopathy • MRI • sarcoidosis • sports medicine


Introduction
Top
 Abstract
 Introduction
Differential Diagnosis
 Sudden Cardiac Death and...
 Treatment of HCM
 Screening for HCM
 Summary
 References
 
Cardiovascular MRI is now accepted as a valuable tool in the initial assessment and follow-up of many acquired and congenital disorders. In particular, assessment of cardiomyopathies with MRI has been successful owing to its unique ability to characterize different enhancement patterns in diseased myocardium with inversion recovery gadolinium-enhanced imaging. We present a two-part review about the use of MRI in hypertrophic cardiomyopathy (HCM). Part 1 of the review focuses on the MRI appearances of HCM [1]. This article, Part 2, covers the differential diagnosis, risk stratification, and posttreatment MRI follow-up appearances in these patients.


Differential Diagnosis
Top
 Abstract
 Introduction
 Differential Diagnosis
Sudden Cardiac Death and...
 Treatment of HCM
 Screening for HCM
 Summary
 References
 
In this section, we discuss the major differential diagnoses for HCM.

Amyloid
The presence of a thickened left ventricle with marked global systolic dysfunction should raise suspicion of HCM and of other diseases such as amyloidosis [2]. Researchers have suggested that all myocardial biopsies for thickened ventricular myocardium in patients older than 65 years should be assessed for cardiac amyloid given the prevalence of the disease in that age group [3]. Some imaging features, however, may help to distinguish this infiltrative cardiomyopathy from other causes of thickened left ventricles before biopsy.

Cardiac amyloidosis most commonly presents with symmetric left ventricular thickening, and although HCM more typically shows asymmetric left ventricular hypertrophy (LVH), symmetric disease is known to occur in up to 42% of HCM cases [3] (Figs. 1A, 1B, 1C, 1D, 2, 3A, 3B). Poorer ventricular wall contractility and lower ECG voltages should alert the physician to the diagnosis of amyloidosis [4, 5]. Both diseases may exhibit restrictive physiology and poor compliance. Morphologic changes of a thickened nodular right atrial free wall and interatrial septum are helpful in distinguishing cardiac amyloid from HCM (Fig. 2). In particular, thickening of the right atrial free wall of more than 6 mm has been shown to be a specific marker in diagnosing cardiac amyloid in suspected cases [4].


Figure 1
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  		Fig. 1A —64-year-old woman with cardiac amyloid. Inversion recovery delayed gadolinium-enhanced images (A and B) and steady-state free precession images (C and D) in the axial and short-axis oblique projections show extensive mid wall enhancement and symmetric thickening of the left ventricle that are typical of amyloid. Mild right ventricular wall thickening is also present. Although subendocardial extension of delayed enhancement is common in cardiac amyloid, large areas of mid wall enhancement, such as in this patient, are also commonly found.

 

Figure 2
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  		Fig. 1B —64-year-old woman with cardiac amyloid. Inversion recovery delayed gadolinium-enhanced images (A and B) and steady-state free precession images (C and D) in the axial and short-axis oblique projections show extensive mid wall enhancement and symmetric thickening of the left ventricle that are typical of amyloid. Mild right ventricular wall thickening is also present. Although subendocardial extension of delayed enhancement is common in cardiac amyloid, large areas of mid wall enhancement, such as in this patient, are also commonly found.

 

Figure 3
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  		Fig. 1C —64-year-old woman with cardiac amyloid. Inversion recovery delayed gadolinium-enhanced images (A and B) and steady-state free precession images (C and D) in the axial and short-axis oblique projections show extensive mid wall enhancement and symmetric thickening of the left ventricle that are typical of amyloid. Mild right ventricular wall thickening is also present. Although subendocardial extension of delayed enhancement is common in cardiac amyloid, large areas of mid wall enhancement, such as in this patient, are also commonly found.

 

Figure 4
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  		Fig. 1D —64-year-old woman with cardiac amyloid. Inversion recovery delayed gadolinium-enhanced images (A and B) and steady-state free precession images (C and D) in the axial and short-axis oblique projections show extensive mid wall enhancement and symmetric thickening of the left ventricle that are typical of amyloid. Mild right ventricular wall thickening is also present. Although subendocardial extension of delayed enhancement is common in cardiac amyloid, large areas of mid wall enhancement, such as in this patient, are also commonly found.

 

Figure 5
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  		Fig. 2 —Four-chamber view shows a small pericardial effusion and right pleural effusion in a 57-year-old woman with cardiac amyloid. Note thickening of the right atrial free wall.

 

Figure 6
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  		Fig. 3A —61-year-old man with biopsy-proven amyloid infiltration of the liver and spleen. Steady-state free precession image shows symmetric thickening of the left ventricular myocardium.

 

Figure 7
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  		Fig. 3B —61-year-old man with biopsy-proven amyloid infiltration of the liver and spleen. Delayed inversion recovery gadolinium-enhanced image shows there is no evidence of convincing delayed enhancement after administration of gadolinium within the heart; however, there is hepatomegaly with diffuse homogeneous enhancement of both the liver and spleen. This finding shows the ability of gadolinium to accumulate within expanded extracellular space not only in the heart but also in the remainder of the body.

 
Right ventricular wall thickening is less helpful in distinguishing between the two entities. One feature that may be helpful in assessing right ventricular free wall involvement is the distribution of hypertrophy. As with HCM involvement within the left ventricle, right ventricular involvement with HCM is typically asymmetric with thickening more commonly identified apically. In cases of amyloid, the right ventricular involvement is more commonly symmetric.

Patients with cardiac amyloid have been shown to have pericardial and pleural effusions in up to 50% of the cases [4] (Fig. 2).

A study of 29 patients with known cardiac amyloidosis by Maceira et al. [6] looked at both delayed enhancement and T1 mapping of the left ventricular myocardium. Those investigators found delayed enhancement in 69% of patients, with the dominant distribution of enhancement being predominantly subendocardial, diffuse, and not confined to one clear vascular territory (Fig. 1A, 1B, 1C, 1D). At autopsy, the distribution of delayed enhancement within the left ventricular myocardium of one patient premortem was found to coincide with the distribution of amyloid protein histologically. The authors concluded that it was the amyloid protein itself that was responsible for the delayed enhancement and not the minor accompanying diffuse interstitial fibrosis. The presence of delayed enhancement was also shown in that study to be associated with a higher left ventricular mass index and the presence of left ventricular systolic dysfunction [6].

Another feature noted in cardiac amyloid by Maceira et al. [6] was the rapid washout of gadolinium from blood and myocardium, probably as a result of distribution into the total body amyloid load (Fig. 3A, 3B). This washout was noted to occur in patients with reduced creatinine clearance; however, comparison of gadolinium clearance with estimates of total body amyloid load showed no direct correlation. The poor correlation was considered to be secondary to inaccuracies with serum amyloid P component scintigraphy as a technique for making this estimate [6].

The alteration in distribution kinetics of gadolinium chelates within both the blood and myocardium and the diffuse myocardial delayed enhancement in patients with amyloidosis may result in perceived difficulties in selecting an appropriate inversion time for the delayed enhancement imaging pulse sequence, a point to keep in mind when imaging patients with LVH [7].

Athlete's Heart
Although sudden cardiac death is rare among the athletic population (estimated to be less than 1:200,000), it is nonetheless a devastating occurrence [8, 9]. Up to 90% of deaths occur during training or competition, which suggests that vigorous physical activity in the setting of certain cardiovascular diseases is a trigger for sudden cardiac death [9]. HCM is known to be the most common cause of sudden death in young athletes, usually male [2, 8, 10]. In the United States, HCM is the most common culprit accounting for one third of deaths, whereas arrhythmogenic right ventricular dysplasia (ARVD) has been found to be more common in Italian athletes [8, 9].

Morphologic adaptations of an athlete's heart may mimic cardiovascular diseases such as HCM, dilated cardiomyopathy, and ARVD. Approximately 2% of highly trained male athletes will have mild symmetric increase in wall thickness (usually < 16 mm), increased left ventricular volumes, and increased left ventricular mass, but no evidence of diastolic dysfunction [2, 5, 9, 11]. Similar changes may be seen within the right ventricle.

The diastolic wall thickness (DWT) divided by the left ventricular end-diastolic volume (LVEDV) ratio (DWT/LVEDV) was identified by Petersen et al. [12] as the best parameter to differentiate an athlete's heart from all other pathologic causes of hypertrophy. Those investigators found that by using the various geometric indexes of LVEDV, left ventricular end-systolic volume (LVESV), left ventricular ejection fraction (LVEF), wall thickness, and the DWT/LVEDV ratio, they were able to correctly identify an athlete's heart in 100% of the cases. Most important, no athlete was misdiagnosed with a pathologic form of LVH, despite wall thicknesses of up to 16 mm in some athletes [12]. A cutoff for the DWT/LVEDV ratio of less than 0.15 mm/m2/mL gave a sensitivity of 80% and a specificity of 99% [12] (Fig. 4A, 4B, 4C, 4D, 4E, 4F).


Figure 8
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  		Fig. 4A —28-year-old male athlete with athlete's heart. Steady-state free precession images show maximal left ventricular wall thickness was measured as 16 mm. Note biventricular dilatation (E). This male athlete's end-diastolic volume (EDV) was calculated as 325 mL (120 mL/m2). Diastolic wall thickness (DWT) and left ventricular end-diastolic volume (LVEDV) ratio (DWT/LVEDV) of 0.13 falls below the cutoff of 0.15 suggested by Petersen et al. [12]. This quantitative evaluation makes diagnosis of athlete's heart more likely than other pathologic causes of thickened left ventricles.

 

Figure 9
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  		Fig. 4B —28-year-old male athlete with athlete's heart. Steady-state free precession images show maximal left ventricular wall thickness was measured as 16 mm. Note biventricular dilatation (E). This male athlete's end-diastolic volume (EDV) was calculated as 325 mL (120 mL/m2). Diastolic wall thickness (DWT) and left ventricular end-diastolic volume (LVEDV) ratio (DWT/LVEDV) of 0.13 falls below the cutoff of 0.15 suggested by Petersen et al. [12]. This quantitative evaluation makes diagnosis of athlete's heart more likely than other pathologic causes of thickened left ventricles.

 

Figure 10
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  		Fig. 4C —28-year-old male athlete with athlete's heart. Steady-state free precession images show maximal left ventricular wall thickness was measured as 16 mm. Note biventricular dilatation (E). This male athlete's end-diastolic volume (EDV) was calculated as 325 mL (120 mL/m2). Diastolic wall thickness (DWT) and left ventricular end-diastolic volume (LVEDV) ratio (DWT/LVEDV) of 0.13 falls below the cutoff of 0.15 suggested by Petersen et al. [12]. This quantitative evaluation makes diagnosis of athlete's heart more likely than other pathologic causes of thickened left ventricles.

 

Figure 11
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  		Fig. 4D —28-year-old male athlete with athlete's heart. Steady-state free precession images show maximal left ventricular wall thickness was measured as 16 mm. Note biventricular dilatation (E). This male athlete's end-diastolic volume (EDV) was calculated as 325 mL (120 mL/m2). Diastolic wall thickness (DWT) and left ventricular end-diastolic volume (LVEDV) ratio (DWT/LVEDV) of 0.13 falls below the cutoff of 0.15 suggested by Petersen et al. [12]. This quantitative evaluation makes diagnosis of athlete's heart more likely than other pathologic causes of thickened left ventricles.

 

Figure 12
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  		Fig. 4E —28-year-old male athlete with athlete's heart. Steady-state free precession images show maximal left ventricular wall thickness was measured as 16 mm. Note biventricular dilatation (E). This male athlete's end-diastolic volume (EDV) was calculated as 325 mL (120 mL/m2). Diastolic wall thickness (DWT) and left ventricular end-diastolic volume (LVEDV) ratio (DWT/LVEDV) of 0.13 falls below the cutoff of 0.15 suggested by Petersen et al. [12]. This quantitative evaluation makes diagnosis of athlete's heart more likely than other pathologic causes of thickened left ventricles.

 

Figure 13
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  		Fig. 4F —28-year-old male athlete with athlete's heart. Steady-state free precession images show maximal left ventricular wall thickness was measured as 16 mm. Note biventricular dilatation (E). This male athlete's end-diastolic volume (EDV) was calculated as 325 mL (120 mL/m2). Diastolic wall thickness (DWT) and left ventricular end-diastolic volume (LVEDV) ratio (DWT/LVEDV) of 0.13 falls below the cutoff of 0.15 suggested by Petersen et al. [12]. This quantitative evaluation makes diagnosis of athlete's heart more likely than other pathologic causes of thickened left ventricles.

 
In cases that cannot be distinguished, a period of deconditioning to assess for a return to more normal cardiac dimensions may be necessary [2]. Most (90%) athletes with dilated left ventricles will show a reduction in LVEDV after a period of deconditioning [11]. Similarly, nearly all athletes with an increased left ventricular wall thickness will show a return to normal left ventricular wall thickness, some in as little as 13 weeks [9, 11]. This period of deconditioning is, however, unacceptable to many athletes.

Another feature of the cardiac remodeling identified in athletes is the lack of areas of delayed enhancement within the left ventricular myocardium. However, it should be noted that the absence of myocardial delayed enhancement does not exclude the diagnosis of HCM.

Fabry's Disease
Fabry's disease is a rare X-linked autosomal recessive metabolic storage disorder caused by a lack of lysosomal {alpha}-galactosidase A, leading to accumulation of glycosphingolipid in various tissues. Histologic ultrastructural findings include concentric lamellar bodies or myelin figures within the sarcoplasm of myocytes. The disease is more typically systemic in onset, but one variant may cause predominant heart involvement, typically later in life [3, 13]. Studies suggest a prevalence of 3% in all male patients who present with LVH. This prevalence increases to 6% in male patients and 12% in female patients referred to tertiary referral centers for late-onset HCM evaluation [3, 13, 14].

Fabry's disease leads to increased, usually concentric, left ventricular wall thickening [13, 15] (Fig. 5A, 5B, 5C, 5D). However, asymmetric septal thickening mimicking HCM can occur [13, 16].


Figure 14
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  		Fig. 5A —60-year-old man with Fabry's disease and cardiac involvement. Steady-state free precession and delayed inversion recovery gadolinium-enhanced images show symmetric left and right ventricular hypertrophy with mid wall delayed enhancement of the basal posterolateral wall (C and D). Further enhancement of the basal left ventricular septum (C) is noted.

 

Figure 15
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  		Fig. 5B —60-year-old man with Fabry's disease and cardiac involvement. Steady-state free precession and delayed inversion recovery gadolinium-enhanced images show symmetric left and right ventricular hypertrophy with mid wall delayed enhancement of the basal posterolateral wall (C and D). Further enhancement of the basal left ventricular septum (C) is noted.

 

Figure 16
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  		Fig. 5C —60-year-old man with Fabry's disease and cardiac involvement. Steady-state free precession and delayed inversion recovery gadolinium-enhanced images show symmetric left and right ventricular hypertrophy with mid wall delayed enhancement of the basal posterolateral wall (C and D). Further enhancement of the basal left ventricular septum (C) is noted.

 

Figure 17
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  		Fig. 5D —60-year-old man with Fabry's disease and cardiac involvement. Steady-state free precession and delayed inversion recovery gadolinium-enhanced images show symmetric left and right ventricular hypertrophy with mid wall delayed enhancement of the basal posterolateral wall (C and D). Further enhancement of the basal left ventricular septum (C) is noted.

 
Delayed gadolinium-enhanced imaging has been shown to be useful in diagnosing Fabry's disease. Moon et al. [17] found that delayed contrast enhancement occurred in up to 50% of patients with Fabry's disease. Enhancement was typically mid wall and occurred in the basal inferolateral segment in 92% of patients [17] (Fig. 5A, 5B, 5C, 5D). Distinction between Fabry's disease and HCM is important because enzyme replacement or enhancement therapy for patients with Fabry's disease is now available [3].

Other inherited metabolic disorders, such as mitochondrial myopathy and glycogen storage disease, are considered in the differential diagnosis of HCM but are not discussed here.

Thickened Left Ventricular Apex
The differential diagnosis of a thickened left ventricular apex on echocardiography includes apical HCM, mural thrombus, hypertrabeculation or noncompaction, and hypereosinophilic cardiomyopathy. These entities may be evaluated more clearly on MRI using steady-state free precession (SSFP) imaging techniques and delayed gadolinium-enhanced imaging [18]. Contrast-enhanced echocardiography is superior to standard transthoracic echocardiography but is no substitute for MRI [19].

Mural thrombus can be easily detected on delayed gadolinium-enhanced imaging when it is associated with an underlying myocardial infarct. The low signal of the mural thrombus in these instances stands out against a background of intermediate blood pool signal and the underlying hyperintense area of infarcted subendocardium.

Patients with left ventricular apical hypertrabeculation or noncompaction are well suited to imaging with cardiovascular MR. The high signal intensity of the blood pool achieved by SSFP imaging techniques allows reliable differentiation of compacted and noncompacted layers of the left ventricular myocardium (Fig. 6A, 6B). The presence of echogenicity within the blood pool trapped between the interstices of the trabeculae on echocardiography can sometimes lead to the incorrect diagnosis of apical HCM.


Figure 18
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  		Fig. 6A —36-year-old man with biventricular dilatation and reduced function. Steady-state free precession four-chamber (A) and short-axis oblique (B) projection images show left ventricular noncompaction. Note presence of prominent trabeculae within the right ventricle as well. Echocardiography (not shown) suggested possible left ventricular apical thickening; however, the diagnosis of left ventricular noncompaction was considered, and MRI was requested to investigate further.

 

Figure 19
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  		Fig. 6B —36-year-old man with biventricular dilatation and reduced function. Steady-state free precession four-chamber (A) and short-axis oblique (B) projection images show left ventricular noncompaction. Note presence of prominent trabeculae within the right ventricle as well. Echocardiography (not shown) suggested possible left ventricular apical thickening; however, the diagnosis of left ventricular noncompaction was considered, and MRI was requested to investigate further.

 

Hypereosinophilic syndrome with cardiac involvement and endomyocardial fibrosis (with or without peripheral hypereosinophilia) are a complex group of disorders that may lead to both endomyocardial fibrosis and obliteration of the left ventricular apical cavity. Imaging appearances may mimic apical HCM; therefore, these disorders should be considered in the differential diagnosis [20–24].

Hypereosinophilic syndrome typically induces cardiac damage through three distinct phases: an acute necrotic stage, a thrombotic stage, and a fibrotic stage. The disorder may result in endomyocardial fibrosis, valvular lesions, mural thrombus formation, infiltration of the myocardium with eosinophils, and pericardial effusions [24–27] (Fig. 7A, 7B).


Figure 20
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  		Fig. 7A —49-year-old man with hypereosinophilic syndrome cardiomyopathy. Steady-state free precession four-chamber view shows apparent apical left ventricular thickening, small pericardial effusion, and bilateral pleural effusions.

 

Figure 21
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  		Fig. 7B —49-year-old man with hypereosinophilic syndrome cardiomyopathy. Delayed enhancement four-chamber view clearly shows diffuse subendocardial enhancement and triangular-shaped apical thrombus. These findings are typical of hypereosinophilic syndrome cardiomyopathy.

 
The imaging appearances of hypereosinophilic syndrome on cardiovascular MR are therefore characterized by subendocardial enhancement; distortion of the mitral valve apparatus, with resultant regurgitation; and mural thrombus formation [24, 27, 28]. Fibrosis at the cardiac apex frequently results in obliteration of the apical cavity. These changes, when combined with apical mural thrombus, commonly lead to a misdiagnosis of apical HCM (Fig. 7A, 7B).

Cardiac Sarcoidosis
Sarcoidosis is a multisystem disorder that shows cardiac involvement in up to 27% of patients with the disorder at autopsy [29]. Clinical evidence of myocardial involvement is apparent during life in only 5% of affected patients. Sarcoidosis is characterized by the presence of noncaseating granulomatous infiltration. Sudden death is the most common cardiac manifestation of patients with severe cardiac sarcoid involvement, with ECG changes being the most predictive of cardiac sarcoid in general [29]. The incidence of sudden cardiac death in these patients highlights the importance of identifying cardiac sarcoid early because prompt initiation of corticosteroid therapy has been shown to improve left ventricular function and prevent malignant arrhythmia [30, 31].

Common MRI findings in patients with cardiac sarcoid include delayed enhancement, which may be either mid wall or transmural; nodular mid wall hyperintense foci on black blood T2-weighted imaging; and areas of focal myocardial thickening (Fig. 8A, 8B). Disease may involve either the left or the right ventricle but more commonly involves the left ventricle, where the basal septum is often involved, giving an appearance that can mimic asymmetric HCM [30, 32–36].


Figure 22
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  		Fig. 8A —54-year-old man with heart block and confirmed cardiac sarcoid. Steady-state free precession four-chamber view shows three separate areas of nodular left ventricular thickening. Two nodules are noted within the left ventricular septum and a third at the lateral apical left ventricular free wall.

 

Figure 23
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  		Fig. 8B —54-year-old man with heart block and confirmed cardiac sarcoid. After gadolinium administration, the three areas seen in A show nodular delayed enhancement. Note also delayed enhancement and inflammatory thickening of the right ventricular trabeculae.

 

In a study by Tadamura et al. [36], 10 patients with cardiac sarcoidosis were imaged with MRI, 201Tl scintigraphy, and 67Ga scintigraphy. They found delayed gadolinium enhancement in all patients. Assessment for wall motion abnormalities, 201Tl perfusion defects, and abnormal 67Ga uptake was shown to be less sensitive in detecting disease [35, 36]. Patients in whom transmural delayed gadolinium enhancement was identified were more likely to show abnormalities on both 201Tl and 67Ga scintigraphy and to show region wall motion abnormalities [36].

Imaging features that should alert the radiologist to a diagnosis of cardiac sarcoid over HCM include clinical, hematologic, pulmonary, and mediastinal manifestations of sarcoidosis; nodular myocardial thickening confined to areas of myocardial delayed enhancement (Fig. 8A, 8B) or T2 hyperintensity; associated 67Ga scintigraphy changes; and pericardial granulomatous disease characterized by effusions, thickening, and delayed enhancement.

Aortic Stenosis and Hypertensive Heart Disease
These diseases tend to cause symmetric left ventricular wall thickening and are a diagnosis of exclusion. Aortic stenosis is readily evaluated on cardiovascular MR, and evidence of this finding should be sought when imaging patients for suspected HCM.


Sudden Cardiac Death and Risk Stratification in Patients with HCM
Top
 Abstract
 Introduction
 Differential Diagnosis
 Sudden Cardiac Death and...
Treatment of HCM
 Screening for HCM
 Summary
 References
 
Sudden cardiac death occurs in 1% or less per year of adult patients, rising to 2–4% per year in children and adolescents [2]. Disorganized cellular architecture, myocardial replacement scarring, and an expanded interstitial collagen compartment are thought to be the primary arrhythmogenic substrate in some susceptible patients [37]. The best clinical correlate of sudden cardiac death is ventricular tachyarrhythmias [2, 3]. Appendix 1 includes a list of classic predictors of sudden cardiac death in HCM patients [37].

The ability to detect areas of myocardial enhancement in hearts with HCM has generated interest in trying to identify patients who harbor an "arrhythmogenic substrate." Teraoka et al. [38] found that the presence of delayed enhancement and the number of involved segments correlated with the presence of ventricular tachycardia. Furthermore, delayed enhancement has been shown to be increased in patients with more clinical risk factors for sudden cardiac death [39–41].


Figure 24
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  		Fig. 9A —Diagrams looking at the left ventricular interventricular septum and outflow tract. Diagram depicts subaortic surgical myomectomy.

 


Figure 25
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  		Fig. 9B —Diagrams looking at the left ventricular interventricular septum and outflow tract. Diagram depicts area of iatrogenic infarction resulting from injection of ethanol into an appropriate septal perforator as shown.

 

Treatment of HCM
Top
 Abstract
 Introduction
 Differential Diagnosis
 Sudden Cardiac Death and...
 Treatment of HCM
Screening for HCM
 Summary
 References
 
Although most patients with HCM are treated medically, septal reduction techniques involving either surgical septal myomectomy or catheter-based septal alcohol ablation are generally indicated in patients who do not respond to medical therapy and have either resting or inducible left ventricular outflow tract (LVOT) gradients. Other techniques involving atrioventricular sequential pacing and insertion of an implantable cardioverter-defibrillator are used in certain circumstances; however, because these patients do not undergo follow-up cardiovascular MR, they are not discussed here.


Figure 26
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  		Fig. 10A —52-year-old man with hypertrophic cardiomyopathy and left ventricular outflow tract (LVOT) obstruction treated with alcohol septal ablation. Steady-state free precession (A and B) and delayed enhancement (C and D) images of the basal left ventricular septum show full-thickness infarction. The area of delayed enhancement (C and D) is well remodeled with marked thinning of the involved septum. This remodeling creates a greater cross-sectional dimension of the LVOT and reduces gradients in this region.

 


Figure 27
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  		Fig. 10B —52-year-old man with hypertrophic cardiomyopathy and left ventricular outflow tract (LVOT) obstruction treated with alcohol septal ablation. Steady-state free precession (A and B) and delayed enhancement (C and D) images of the basal left ventricular septum show full-thickness infarction. The area of delayed enhancement (C and D) is well remodeled with marked thinning of the involved septum. This remodeling creates a greater cross-sectional dimension of the LVOT and reduces gradients in this region.

 


Figure 28
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  		Fig. 10C —52-year-old man with hypertrophic cardiomyopathy and left ventricular outflow tract (LVOT) obstruction treated with alcohol septal ablation. Steady-state free precession (A and B) and delayed enhancement (C and D) images of the basal left ventricular septum show full-thickness infarction. The area of delayed enhancement (C and D) is well remodeled with marked thinning of the involved septum. This remodeling creates a greater cross-sectional dimension of the LVOT and reduces gradients in this region.

 


Figure 29
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  		Fig. 10D —52-year-old man with hypertrophic cardiomyopathy and left ventricular outflow tract (LVOT) obstruction treated with alcohol septal ablation. Steady-state free precession (A and B) and delayed enhancement (C and D) images of the basal left ventricular septum show full-thickness infarction. The area of delayed enhancement (C and D) is well remodeled with marked thinning of the involved septum. This remodeling creates a greater cross-sectional dimension of the LVOT and reduces gradients in this region.

 
Septal Myomectomy
Septal myomectomy is considered the gold standard of septal reduction techniques currently in use [2, 42]. This procedure, performed through an aortotomy, creates a rectangular trough in the myocardium via two parallel longitudinal incisions in the basal septum. Incisions are connected proximally below the aortic valve and are extended distally just beyond the level of mitral valve–septum contact and subaortic obstruction (Fig. 9A) or, in some patients, are extended to the base of the papillary muscles (extended myomectomy) [43].

Mortality at expert centers is approximately 1–1.5% for myomectomy alone and 1–5% for combined myomectomy and coronary artery bypass grafting [2, 44]. Complications such as complete heart block, requiring insertion of a permanent pacemaker, and iatrogenic ventricular septal perforation have become uncommon (≤ 1–2%) as surgical techniques have improved. Partial or complete left bundle branch block is a common consequence of the muscular resection and is not associated with adverse sequelae [37].

Septal Alcohol Ablation
Septal alcohol ablation involves iatrogenic infarction of the basal interventricular septum. Initially, a coronary angiogram is obtained, followed by placement of a balloon catheter into the first major septal perforator (Fig. 9B). A temporary pacing catheter is positioned in the right ventricle. After the balloon is inflated, another angiogram is obtained to verify the position of the balloon and to ensure that no alcohol will leak into the left anterior descending coronary artery or the coronary venous system. Contrast-enhanced echocardiography is used to define the perfusion territory of the targeted septal perforator before alcohol embolization [2]. ECG is used to closely monitor for signs of bradycardia or heart block [45, 46].

Postprocedure MRI with delayed contrast-enhanced imaging reliably shows the area of infarcted septal myocardium [47] (Fig. 10A, 10B, 10C, 10D). For visualization of the LVOT diameter, MRI is best performed 3 months after the procedure because remodeling may not yet be complete before this time. In addition, LVOT gradients may continue to decrease for up to 1 year after surgical ablation because of left ventricular septal remodeling over time [2]. Having said this, delayed contrast-enhanced imaging performed less than 3 months after the procedure will adequately show the extent of infarction and any areas of microvascular obstruction [47, 48].

Postprocedure complications of septal alcohol ablation include ventricular septal defect formation, heart block (5–30%), and coronary artery dissection [2]. Current modifications to the procedure, which use a slower injection of alcohol and contrast-enhanced transesophageal echocardiography, have shown a reduction in occurrence of complete heart block from 22% before modifying the procedure to 8.6% after modification. This lower occurrence is still high compared with that of myomectomy in which complete heart block occurs in approximately 1–2% [46]. Not surprisingly, there is a reported higher incidence of permanent pacemaker implantation after alcohol septal ablation than after myomectomy—on the order of 14–25% [49].

The long-term arrhythmogenic potential of scarred myocardium is not yet clear, but short-term results show no increase in arrhythmogenesis.

LVOT gradients, septal thickness, left atrial dimensions, mitral regurgitation, and patient symptoms have been shown to decrease after ablation [47, 50]. Some studies show no significant differences in functional outcome between alcohol septal ablation and surgical myomectomy when considering resting LVOT gradients, LVEDV, LVESV, and left ventricular mass. Other reports however show greater reductions in LVOT gradients and reduction in systolic anterior motion (both resting and provocable) in patients who have undergone myomectomy [51].

Whether alcohol septal ablation can create a permanent arrhythmogenic substrate in the form of a healed intramyocardial septal scar is controversial. This issue is particularly relevant because many patients with HCM already possess an unstable electrophysiologic substrate as part of their underlying disease. Reports however suggest that there is no evidence that septal ablation increases the incidence of ventricular arrhythmias, the incidence of sudden cardiac death, or the rate of discharge of implantable cardioverter-defibrillators [42, 52, 53].


Screening for HCM
Top
 Abstract
 Introduction
 Differential Diagnosis
 Sudden Cardiac Death and...
 Treatment of HCM
 Screening for HCM
Summary
 References
 
Screening programs for HCM in the past have considered a normal imaging study and ECG as proof that an adult is genetically unaffected. However, certain genotypes of HCM have been shown to exhibit age-related penetrance and delayed appearance of LVH—that is, in midlife or later [54, 55].

The American College of Cardiology/European Society of Cardiology clinical expert consensus document on HCM suggests that relatives of affected individuals be screened yearly by means of echocardiography and that relatives who are 12–18 years old undergo ECG examinations. Because of the possibility of delayed adult-onset LVH, they also recommend that adult relatives with normal echocardiograms who are 18 years old or older undergo subsequent clinical studies every 5 years. This document also suggests that affected patients identified through family screening or otherwise be evaluated every 12–18 months [37].


Summary
Top
 Abstract
 Introduction
 Differential Diagnosis
 Sudden Cardiac Death and...
 Treatment of HCM
 Screening for HCM
 Summary
References
 
Cardiovascular MRI is a useful imaging tool for the diagnosis of HCM and follow-up of patients after either surgical myomectomy or septal ablation therapy. In addition, MRI can help to discriminate HCM from the differential diagnoses of other cardiomyopathies and cardiac disorders.

The strengths of MRI include accuracy and reproducibility when measuring left ventricular mass, volumes, and function and its ability to identify macroscopic areas of abnormal myocardium with delayed gadolinium-enhanced imaging.

Current research studies comparing traditional clinical indicators for predicting sudden cardiac death with cardiovascular MRI findings and delayed enhancement imaging highlight MRI's future potential in moving toward patient risk stratification in HCM. Further research in this area is necessary, however, to determine how best to manage this subset of patients with delayed enhancement and the impact of management on reducing the incidence of sudden cardiac death.

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  		APPENDIX 1: Classic Predictors of Sudden Cardiac Death in Patients with Hypertrophic Cardiomyopathy

 


References
Top
 Abstract
 Introduction
 Differential Diagnosis
 Sudden Cardiac Death and...
 Treatment of HCM
 Screening for HCM
 Summary
 References
 

  1. Hansen MW, Merchant N. MRI of hypertrophic cardiomyopathy: part 1, MRI appearances. AJR 2007;189 :1335 –1343[Abstract/Free Full Text]
  2. Elliott P, McKenna WJ. Hypertrophic cardiomyopathy. Lancet 2004; 363:1881 –1891[CrossRef][Medline]
  3. Hughes SE. The pathology of hypertrophic cardiomyopathy. Histopathology 2004;44 : 412–427[CrossRef][Medline]
  4. Fattori R, Rocchi G, Celletti F, Bertaccini P, Rapezzi C, Gavelli G. Contribution of magnetic resonance imaging in the differential diagnosis of cardiac amyloidosis and symmetric hypertrophic cardiomyopathy. Am Heart J 1998; 136:824 –830[CrossRef][Medline]
  5. Prasad K, Atherton J, Smith GC, McKenna WJ, Frenneaux MP, Nihoyannopoulos P. Echocardiographic pitfalls in the diagnosis of hypertrophic cardiomyopathy. Heart 1999;82 [suppl 3]:III8 –III15[Medline]
  6. Maceira AM, Joshi J, Prasad SK, et al. Cardiovascular magnetic resonance in cardiac amyloidosis. Circulation2005; 111:186 –193[Abstract/Free Full Text]
  7. Mahrholdt H, Wagner A, Judd RM, Sechtem U, Kim RJ. Delayed enhancement cardiovascular magnetic resonance assessment of non-ischaemic cardiomyopathies. Eur Heart J 2005;26 :1461 –1474[Abstract/Free Full Text]
  8. Beckerman J, Wang P, Hlatky M. Cardiovascular screening of athletes. Clin J Sport Med 2004;14 : 127–133[CrossRef][Medline]
  9. Maron BJ. Sudden death in young athletes. N Engl J Med 2003; 349:1064 –1075[Free Full Text]
  10. Pelliccia A, Maron BJ, Culasso F, Spataro A, Caselli G. Athlete's heart in women: echocardiographic characterization of highly trained elite female athletes. JAMA 1996;276 : 211–215[Abstract/Free Full Text]
  11. Pelliccia A, Maron BJ, De Luca R, Di Paolo FM, Spataro A, Culasso F. Remodeling of left ventricular hypertrophy in elite athletes after long-term deconditioning. Circulation2002; 105:944 –949[Abstract/Free Full Text]
  12. Petersen SE, Selvanayagam JB, Francis JM, et al. Differentiation of athlete's heart from pathological forms of cardiac hypertrophy by means of geometric indices derived from cardiovascular magnetic resonance. J Cardiovasc Magn Reson 2005;7 : 551–558[Medline]
  13. Sachdev B, Takenaka T, Teraguchi H, et al. Prevalence of Anderson-Fabry disease in male patients with late onset hypertrophic cardiomyopathy. Circulation 2002;105 :1407 –1411[Abstract/Free Full Text]
  14. Chimenti C, Pieroni M, Morgante E, et al. Prevalence of Fabry disease in female patients with late-onset hypertrophic cardiomyopathy. Circulation 2004;110 :1047 –1053[Abstract/Free Full Text]
  15. Goldman ME, Cantor R, Schwartz MF, Baker M, Desnick RJ. Echocardiographic abnormalities and disease severity in Fabry's disease. J Am Coll Cardiol 1986;7 : 1157–1161[Abstract]
  16. Linhart A, Palecek T, Bultas J, et al. New insights in cardiac structural changes in patients with Fabry's disease. Am Heart J 2000; 139:1101 –1108[CrossRef][Medline]
  17. Moon JC, Sachdev B, Elkington AG, et al. Gadolinium enhanced cardiovascular magnetic resonance in Anderson-Fabry disease: evidence for a disease specific abnormality of the myocardial interstitium. Eur Heart J 2003; 24:2151 –2155[Abstract/Free Full Text]
  18. Sperling RT, Parker JA, Manning WJ, Danias PG. Apical hypertrophic cardiomyopathy: clinical, electrocardiographic, scintigraphic, echocardiographic, and magnetic resonance imaging findings of a case. J Cardiovasc Magn Reson 2002;4 : 291–295[CrossRef][Medline]
  19. Dijkmans PA, Visser CA, Kamp O. An abnormal ECG with inverted T waves in the precordial leads: confirming the diagnosis with contrast enhanced echocardiography. Heart 2005;91 : 913[Free Full Text]
  20. Anderson KR, Sutton MG, Lie JT. Histopathological types of cardiac fibrosis in myocardial disease. J Pathol1979; 128:79 –85[CrossRef][Medline]
  21. Andy JJ. Aetiology of endomyocardial fibrosis (EMF). West Afr J Med 2001;20 : 199–207[Medline]
  22. Felice PV, Sawicki J, Anto J. Endomyocardial disease and eosinophilia. Angiology 1993;44 : 869–874[Medline]
  23. Hassan WM, Fawzy ME, Al Helaly S, Hegazy H, Malik S. Pitfalls in diagnosis and clinical, echocardiographic, and hemodynamic findings in endomyocardial fibrosis: a 25-year experience. Chest2005; 128:3985 –3992[CrossRef][Medline]
  24. Puvaneswary M, Joshua F, Ratnarajah S. Idiopathic hypereosinophilic syndrome: magnetic resonance imaging findings in endomyocardial fibrosis. Australas Radiol 2001;45 : 524–527[CrossRef][Medline]
  25. Mayet J, Kanagaratnam P, Lincoln C, Oldershaw P. Hypereosinophilic syndrome: endomyocardial fibrosis. Heart1997; 77:391[Free Full Text]
  26. Pitt M, Davies MK, Brady AJ. Hypereosinophilic syndrome: endomyocardial fibrosis. Heart 1996;76 : 377–378[Free Full Text]
  27. Salanitri GC. Endomyocardial fibrosis and intracardiac thrombus occurring in idiopathic hypereosinophilic syndrome. AJR 2005; 184:1432 –1433[Free Full Text]
  28. Alter P, Maisch B. Endomyocardial fibrosis in Churg-Strauss syndrome assessed by cardiac magnetic resonance imaging. Int J Cardiol 2006; 108:112 –113[CrossRef][Medline]
  29. Silverman KJ, Hutchins GM, Bulkley BH. Cardiac sarcoid: a clinicopathologic study of 84 unselected patients with systemic sarcoidosis. Circulation 1978;58 :1204 –1211[Abstract/Free Full Text]
  30. Stauder NI, Bader B, Fenchel M, Kramer U, Kühlkamp V, Miller S. Images in cardiovascular medicine: follow-up of cardiac sarcoidosis by magnetic resonance imaging. Circulation2005; 111:e158 –e160[Free Full Text]
  31. Sharma OP. Cardiac and neurologic dysfunction in sarcoidosis. Clin Chest Med 1997;18 : 813–825[CrossRef][Medline]
  32. Vignaux O. Cardiac sarcoidosis: spectrum of MRI features. AJR 2005; 184:249 –254[Free Full Text]
  33. Dubrey SW, Grocott-Mason R, Mittal TK. Images in cardiology: cardiac sarcoidosis with delayed enhanced MRI. Heart2005; 91:1185[Free Full Text]
  34. Kiuchi S, Teraoka K, Koizumi K, Takazawa K, Yamashita A. Usefulness of late gadolinium enhancement combined with MRI and 67-Ga scintigraphy in the diagnosis of cardiac sarcoidosis and disease activity evaluation. Int J Cardiovasc Imaging 2007;23 : 237–241[CrossRef][Medline]
  35. Smedema JP, Snoep G, van Kroonenburgh MP, et al. Evaluation of the accuracy of gadolinium-enhanced cardiovascular magnetic resonance in the diagnosis of cardiac sarcoidosis. J Am Coll Cardiol2005; 45:1683 –1690[Abstract/Free Full Text]
  36. Tadamura E, Yamamuro M, Kubo S, et al. Effectiveness of delayed enhanced MRI for identification of cardiac sarcoidosis: comparison with radionuclide imaging. AJR 2005;185 : 110–115[Abstract/Free Full Text]
  37. Maron BJ, McKenna WJ, Danielson GK, et al. American College of Cardiology/European Society of Cardiology clinical expert consensus document on hypertrophic cardiomyopathy. A report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines. J Am Coll Cardiol 2003; 42:1687 –1713[Free Full Text]
  38. Teraoka K, Hirano M, Ookubo H, et al. Delayed contrast enhancement of MRI in hypertrophic cardiomyopathy. Magn Reson Imaging 2004; 22:155 –161 [Erratum in Magn Reson Imaging 2004; 22:901][CrossRef][Medline]
  39. Moon JC, Mogensen J, Elliott PM, et al. Myocardial late gadolinium enhancement cardiovascular magnetic resonance in hypertrophic cardiomyopathy caused by mutations in troponin I. Heart2005; 91:1036 –1040[Abstract/Free Full Text]
  40. Moon JC, McKenna WJ, McCrohon JA, Elliott PM, Smith GC, Pennell DJ. Toward clinical risk assessment in hypertrophic cardiomyopathy with gadolinium cardiovascular magnetic resonance. J Am Coll Cardiol2003; 41:1561 –1567[Abstract/Free Full Text]
  41. Elliott PM, Gimeno Blanes JR, Mahon NG, Poloniecki JD, McKenna WJ. Relation between severity of left-ventricular hypertrophy and prognosis in patients with hypertrophic cardiomyopathy. Lancet2001; 357:420 –424[CrossRef][Medline]
  42. Kovacic JC, Muller D. Hypertrophic cardiomyopathy: state-of-the-art review, with focus on the management of outflow obstruction. Intern Med J 2003; 33:521 –529[CrossRef][Medline]
  43. Ommen SR, Maron BJ, Olivotto I, et al. Long-term effects of surgical septal myectomy on survival in patients with obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol 2005;46 : 470–476[Abstract/Free Full Text]
  44. Woo A, Williams WG, Choi R, et al. Clinical and echocardiographic determinants of long-term survival after surgical myectomy in obstructive hypertrophic cardiomyopathy. Circulation2005; 111:2033 –2041[Abstract/Free Full Text]
  45. Faber L, Seggewiss H, Gleichmann U. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: results with respect to intraprocedural myocardial contrast echocardiography. Circulation 1998;98 :2415 –2421[Abstract/Free Full Text]
  46. Nagueh SF, Ommen SR, Lakkis NM, et al. Comparison of ethanol septal reduction therapy with surgical myectomy for the treatment of hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol2001; 38:1701 –1706[Abstract/Free Full Text]
  47. Amano Y, Takayama M, Amano M, Kumazaki T. MRI of cardiac morphology and function after percutaneous transluminal septal myocardial ablation for hypertrophic obstructive cardiomyopathy. AJR2004; 182:523 –527[Abstract/Free Full Text]
  48. Schulz-Menger J, Strohm O, Waigand J, Uhlich F, Dietz R, Friedrich MG. The value of magnetic resonance imaging of the left ventricular outflow tract in patients with hypertrophic obstructive cardiomyopathy after septal artery embolization. Circulation 2000;101 :1764 –1766[Abstract/Free Full Text]
  49. Chang SM, Nagueh SF, Spencer WH 3rd, Lakkis NM. Complete heart block: determinants and clinical impact in patients with hypertrophic obstructive cardiomyopathy undergoing nonsurgical septal reduction therapy. J Am Coll Cardiol 2003;42 : 296–300[Abstract/Free Full Text]
  50. Mazur W, Nagueh SF, Lakkis NM, et al. Regression of left ventricular hypertrophy after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. Circulation2001; 103:1492 –1496[Abstract/Free Full Text]
  51. Ralph-Edwards A, Woo A, McCrindle BW, et al. Hypertrophic obstructive cardiomyopathy: comparison of outcomes after myectomy or alcohol ablation adjusted by propensity score. J Thorac Cardiovasc Surg 2005; 129:351 –358[Abstract/Free Full Text]
  52. Gietzen FH, Leuner CJ, Raute-Kreinsen U, et al. Acute and long-term results after transcoronary ablation of septal hypertrophy (TASH): catheter interventional treatment for hypertrophic obstructive cardiomyopathy. Eur Heart J 1999;20 :1342 –1354[Abstract/Free Full Text]
  53. Lawrenz T, Obergassel L, Lieder F, et al. Transcoronary ablation of septal hypertrophy does not alter ICD intervention rates in high risk patients with hypertrophic obstructive cardiomyopathy. Pacing Clin Electrophysiol 2005; 28:295 –300[CrossRef][Medline]
  54. Maron BJ, Niimura H, Casey SA, et al. Development of left ventricular hypertrophy in adults in hypertrophic cardiomyopathy caused by cardiac myosin-binding protein C gene mutations. J Am Coll Cardiol 2001; 38:315 –321[Abstract/Free Full Text]
  55. Niimura H, Bachinski LL, Sangwatanaroj S, et al. Mutations in the gene for cardiac myosin-binding protein C and late-onset familial hypertrophic cardiomyopathy. N Engl J Med 1998;338 :1248 –1257[Abstract/Free Full Text]

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