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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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Copyright © 2007 by the American Roentgen Ray Society.
