Download The Heart of the Matter: Cardiac Imaging of Sarcoidosis

The Heart of the Matter: Cardiac Imaging of Sarcoidosis
Society of Thoracic Radiology (STR)
March 13‐16, 2016
Lea Azour, Adam H. Jacobi, Matthew D. Cham
The Icahn School of Medicine at Mount Sinai, New York, NY
Disclosures
• The authors have no financial relationships with the manufacturers of any commercial product and/or providers of commercial services in relation to this exhibit.
Cardiac Sarcoidosis
I.
II.
Background Diagnostic Imaging Modalities
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•
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III.
MR Imaging Features
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•
•
•
IV.
Late gadolinium enhancement pattern
T2 signal features
T1 mapping
Cine imaging
Differential Diagnosis for Late Gadolinium Enhancement (LGE)
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•
•
•
•
•
V.
Gallium‐67 scintigraphy
Myocardial perfusion imaging
18F‐FDG PET Scan
Cardiac MRI
Myocarditis
Fabry Disease
Amyloidosis
Eosinophilic Granulomatosis with Polyangiitis
Endomyocardial Fibrosis (EMF)
Arrhythmogenic Right Ventricular Dysplasia (ARVD)
Management and Prognosis
I. Background
• Sarcoidosis is a multi‐organ disease of unknown etiology most commonly affecting the lungs
• Incidence is greatest between 20‐39 years of age1
• 2:1 female to male preponderance • Annual incidence in African Americans 3x that of Caucasians
• Prevalence greatest in northern European countries
• Cardiac involvement is reported in 2‐7% of patients with systemic sarcoidosis1, 3
• On autopsy, cardiac involvement is found to be higher, in 25‐78% of individuals with sarcoidosis1, 2
• Imaging is contributing to the increased detection of cardiac sarcoidosis3
I. Background
• Cardiac sarcoidosis is associated with a poor prognosis, with multiple disease manifestations1, 3, 4 :
•
•
•
•
Clinically silent myocardial granulomas
Cardiomyopathy with arrhythmias (12‐32%)
Heart failure (25‐75%)
Sudden cardiac death (25‐65%)
• 5 year mortality associated with cardiac sarcoidosis is reported to range from 25‐66% 5
• Cardiac imaging may allow for the early detection of cardiac sarcoidosis (CS) and/or the direction of endomyocardial biopsy
I. Background: Diagnostic Guidelines for Cardiac Sarcoidosis
Japanese Ministry of Health & Welfare (2006)
Endomyocardial biopsy showing noncaseating epithelioid cell granulomas in the setting of extra‐cardiac sarcoidosis
Histologic Diagnosis
Major Criteria
Clinical Diagnosis
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Gallium‐67 scintigraphy: positive uptake
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Advanced atrioventricular block
Basal thinning of interventricular septum
Left ventricular ejection fraction <50%
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Gadolinium‐enhanced MRI: delayed myocardial enhancement
Myocardial perfusion imaging: perfusion defect
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2 Major Criteria
OR
1 Major + 2 Minor
Minor Criteria
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Endomyocardial biopsy: interstitial fibrosis or monocyte infiltration
Abnormal ECG (ventricular arrhythmias, bundle branch block, axis deviation, or abnormal Q wave)
Abnormal echocardiography
II. Diagnostic Imaging Modalities
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•
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Gallium‐67 Scintigraphy
18F‐FDG PET Scan
Myocardial Perfusion Imaging (MPI)
Cardiac Magnetic Resonance Imaging (CMR)
II. Diagnostic Imaging Modalities: Gallium Scan
• Abnormal accumulation of Gallium‐67 corresponds to areas of active inflammation
• For example, mildly INCREASED UPTAKE IN THE HEART is compatible with cardiac sarcoidosis
• PANDA SIGN: symmetric uptake in the nasopharynx, lacrimal and parotid glands
• Present in 75% of patients with sarcoidosis
• LAMBDA SIGN: uptake in right paratracheal and bilateral hilar lymph nodes in pulmonary sarcoidosis
•
•
•
•
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Advantages
Highly specific
Can assess treatment response
Identification of extra‐thoracic uptake
Disadvantages
Low sensitivity (as low as 15%)
Radiation exposure
Panda Sign
Lambda Sign
II. Diagnostic Imaging Modalities: PET Scan
18‐FDG PET
MDE CT
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node
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TREATMENT RESPONSE
PRE
•
POST
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Patient preparation:
• Low carbohydrate diet for 8‐24 hours; 4‐18 hour fast to diminish physiologic uptake
Myocardial uptake corresponds to macrophage‐
dense areas of active inflammation
RV uptake a significant predictor of adverse cardiac events, controlling for LVEF and clinical factors6
RV uptake associated with 3x higher adverse event rate6
PET may be used to assess treatment response
II. Diagnostic Imaging Modalities: Myocardial Perfusion Imaging
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•
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Radiopharmaceutical Agents:
• Thallium‐201
• 99mTc‐MIBI
Mechanism: • Agents accumulate in normal myocardial cells • Regional distribution of myocardial blood perfusion is then estimated non‐invasively
Findings in cardiac sarcoidosis:
• Resting images may show segmental areas of decreased perfusion in the ventricular myocardium
• Decreased perfusion corresponds to areas of fibrogranulomatous replacement
• REVERSE DISTRIBUTION: resting focal perfusion defects decrease or disappear during stress
Reverse ischemia pattern: Lateral and anterolateral wall defects are seen, with rest defect (middle column) greater than stress defect (leftmost column).
Image courtesy of Dr. Josef Machac
Patient with no defect on MPI
REST
MPI
STRESS
II. Diagnostic Imaging Modalities: Combined MPI/PET
FDG‐PET
PET +
Perfusion at Rest
FDG Metabolism
Pathology
Normal
normal normal
normal
Early Sarcoid
normal HIGH
Active inflammation
Advanced Sarcoid
LOW
HIGH
Severe inflammation +/‐ scar
End Stage Sarcoid
LOW
normal
Myocardial scar
II. Diagnostic Imaging Modalities: Nuclear Imaging versus CMR
MPI
Finding: Segmental perfusion defect at rest
67Gallium
Sensitivity Specificit
y Radiation
Advantages
Limitations
35‐46% 8, 9
(Th‐201)
‐‐
‐18mSv (Th‐
201)
‐pattern distinct
from that of ischemia
‐reverse distribution not specific to CS
65% 7 (Tc‐
99m)
‐‐
‐12mSv (Tc‐
99m)
0‐36% 10, 11
80‐100%10, 11
9mSv
‐whole body imaging
‐may assess Rx response
‐low spatial resolution
‐low sensitivity
89‐100% 11‐14
38‐97%11‐14
7mSv
‐whole body imaging
‐may assess Rx response
‐cumbersome patient preparation 100% 14, 15
78%14, 15
None
‐high spatial resolution
‐high sensitivity
‐renal function
‐metallic devices
7
scintigraphy
Finding: increased myocardial uptake
18F‐FDG PET
Finding: increased myocardial uptake
CMR
Finding: High intensity lesions; ventricular thinning
III. MR Imaging of CS
A.
B.
C.
D.
E.
Sites of cardiac involvement
LGE pattern
T2 signal features
T1 mapping
Cine imaging
III. MR Imaging of CS:
Sites of Cardiac Involvement
1. Interventricular septum
3. RV free wall
RV
LV
4. Atria
2. LV free wall
5. Pericardium
LA
Left ventricular outflow tract view with preferred sites of involvement in descending order16
• Noncaseating myocardial granulomas are most commonly found in the interventricular septum and left ventricular free wall1, 16
• Common clinical manifestations include heart block (septal involvement), mitral regurgitation (LV free wall involvement), and ventricular aneurysm7
III. MR Imaging of CS:
LGE Pattern
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Abnormal myocardium with fibrogranulomatous infiltration/scar will demonstrate LGE
• Typically subEPIcardial or mid‐
myocardial, may be subendocardial or transmural
• RV septal fibrosis  characteristic AV block due to Purkinje fiber involvement
LGE is associated with 9x greater adverse cardiac event rate, and 11.5x higher rate of sudden death17
An increased number of cardiac segments demonstrate LGE with increasing duration of extra‐cardiac sarcoidosis18
Distinguishing Features of Cardiac Sarcoidosis:
Enhancement at RV aspect of septum very specific
Corollary imaging findings on nuclear medicine studies
History of extracardiac sarcoidosis
III. MR Imaging of CS:
T2 Signal Features
• T2W image (left) shows increased signal in the mid‐inferior wall. • Accompanying LGE image (right) shows subepicardial and midmyocardial enhancement of the same region. Granulomas are also noted in the spleen.
• Focal high T2 signal represents myocardial edema associated with granulomatous inflammation
• May have corresponding delayed enhancement or wall motion abnormality
• Increased T2 signal is not specific to CS, and may be seen in the setting of myocarditis, infiltrative and ischemic cardiomyopathy
•
•
T2 black blood image demonstrates hyperintensity at the basal anteroseptum and RV free wall.
Delayed post contrast sequence (right) shows multiple areas of mid‐myocardial, subepicardial and transmural LGE in the LV and RV. Subendocardial enhancement is seen at the basal septum.
III. MR Imaging of CS:
LGE and T2
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TOP ROW: Delayed post‐contrast imaging shows multiple areas of intramyocardial scar in the basal anterolateral, basal anterior, basal anteroseptal, basal inferior, mid anteroseptal, mid inferoseptal and mid inferolateral segments in this patient with pulmonary sarcoidosis.
BOTTOM ROW: T2 weighted imaging shows increased signal intensity compatible with myocardial edema in multiple corresponding segments.
Findings consistent with active myocardial sarcoidosis.
III. MR Imaging of CS:
T1 Mapping
•
•
Emerging CMR technique to differentiate non‐involved from diseased myocardium
Method: Quantification of intrinsic T1 relaxation time of tissue by measuring myocardial extracellular volume fraction
– T1 mapping sequences include look locker (LL), modified LL inversion recovery (MOLLI), and shortened MOLLI (shMOLLI)
•
Findings:
– SHORTENED POST‐CONTRAST myocardial T1 time correlates with diffuse fibrosis, edema and amyloid19 (increased extracellular volume fraction) found in heart failure,20 hypertrophic cardiomyopathy,21 infarct,22 and muscular dystrophy23
– SHORTENED PRE‐CONTRAST myocardial T1 time correlates with lipid (Fabry disease)24, 25 and iron deposition24
•
Improved diagnostic value: – Potentially more sensitive than LGE in diffuse disease processes
– Detects significantly more areas of myocardial involvement in myocarditis as compared to T2 and LGE sequences26
– Prognostic implications have been reported in patients with heart failure, amyloidosis
III. MR Imaging of CS:
Cine Imaging
Diastole
Systole
•
•
T2
LGE
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Cine imaging provides a functional assessment of the left and right ventricles
Focal areas of wall thinning/ motion abnormality most often found in the basal anteroseptum or left lateral wall
Wall motion may remain normal until a significant portion of the myocardium is involved, rendering CMR of superior sensitivity in comparison to echocardiography
Bright blood images in diastole and systole show thinning, hypokinesis, and absence of thickening in the mid inferolateral segment (top row). There is no myocardial edema on T2 weighted sequence (bottom left). On delayed imaging, there is near transmural enhancement of the mid inferolateral segment (bottom right).
IV: LGE Differential Diagnosis
Myocarditis
Fabry disease
Amyloidosis
Endomyocardial fibrosis
Eosinophilic granulomatosis with polyangiitis
• Arrhythmogenic right ventricular dysplasia (ARVD)
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•
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•
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LGE is classified by myocardial distribution:
Sub
Epicardial
Sub
Mid‐
Transmural
Myocardial Endocardial
LGE is classified by myocardial location:
IV. LGE Differential Diagnosis:
Myocarditis
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Etiology: Most commonly viral; also autoimmune, toxic/ischemic, drug, post‐
transplant etiologies
Lake Louise consensus criteria—presence of 2/3 findings compatible with myocarditis27:
1. T2 myocardial to skeletal muscle signal ratio >1.9
2. T1 global relative enhancement >4
3. SubEPIcardial or transmural LGE
Cine‐CMR: Global LV systolic dysfunction
LGE: • Typically subEPIcardial or midmyocardial
• Preference for lateral free wall
Differentiating features from CS: Clinical history
Lake Louise consensus criteria
Signs including pericarditis, pulmonary edema
• Circumferential subepicardial enhancement throughout the LV. The patient reported preceding GI illness.
• Small pericardial effusion also seen.
IV. LGE Differential Diagnosis:
Fabry Disease
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•
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Etiology: X‐linked lysosomal storage disease due to α‐galactosidase A deficiency  intracellular accumulation of glycosphingolipid
Cine‐CMR: • Left ventricular hypertrophy (LVH)
LGE (may precede LVH): • Midmyocardial or subepicardial
• Focal at basal inferolateral wall
• Positive association between LV mass and LGE28
Differentiating features from CS: LGE characteristically at basal inferolateral wall
Left ventricular hypertrophy
Extra‐cardiac disease—kidneys, nervous system
Positive family history
Focal mid‐
myocardial and subepicardial enhancement at the basal inferolateral segment. Biventricular dilatation noted on 4‐
chamber view.
IV. LGE Differential Diagnosis:
Amyloidosis
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•
•
Etiology: Extracellular amyloid deposition
Cine‐CMR: • Biventricular myocardial hypertrophy LGE: • Diffuse; may also demonstrate atrial LGE
• Circumferential • Typically subENDOcardial; severe may be transmural
• Altered gadolinium kinetics: increased blood pool clearance + inability to adequately suppress myocardial signal 
small difference in T1 relaxation between blood and myocardium
Differentiating features from CS: •
•
•
Diffuse cardiac involvement may include both atria and ventricles
Altered gadolinium kinetics with similar LGE signal in myocardium and blood pool
Circumferential, subendocardial LGE pattern
p
• Diffuse subendocardial ventricular and atrial enhancement (arrows) on four‐chamber post‐
contrast view (top right). • A “zebra” pattern of enhancement on MDE, with dark blood pool, bright subendocardium, and dark mid‐myocardium in another patient (bottom right). • Short axis SSFP images show LVH. IV. LGE Differential Diagnosis:
Eosinophilic Granulomatosis with Polyangiitis
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•
•
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Formerly Churg‐Strauss Syndrome
Etiology: Vasculitis of small and medium size arteries
LGE: • Predominately subendocardial
• Often not confined to one coronary territory29
Additional findings: pericardial effusion common; valvular insufficiency; heart failure
Differentiating features from CS:
Subendocardial pattern of LGE
Additional diagnostic criteria30 (≥4): asthma; eosinophilia >10%; mono/polyneuritis; transient pulmonary opacities; paranasal sinus abnormality; extravascular eosinophils
*
*
•
•
•
Diffuse subendocardial enhancement/fibrosis on 4 chamber and 2 chamber views (top row).
Small pericardial effusion (*). Bilateral upper lobe opacities and pleural effusion on axial black blood image, and again on coronal localizer (bottom).
IV. LGE Differential Diagnosis:
Endomyocardial Fibrosis (EMF)
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•
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Synonyms: Davies disease, Loffler endocarditis, restrictive obliterative cardiomyopathy
LGE & Distribution:
• 45% biventricular; 40% right ventricle; 5% left ventricle • Endomyocardial fibrosis with destruction of the ventricular apex +/‐ thrombus
Clinical manifestation: severe (right) heart failure with normal/small ventricles and accompanying atrial enlargement
Differentiating features from CS:
Subendocardial pattern of LGE
Most cases biventricular or right ventricular
Atrial enlargement in the setting of an often‐normal heart size
RV
RA
LV
•
•
Vertical and horizontal long axis delayed post‐contrast images show biventricular endomyocardial enhancement, prominent apically, with a shrunken RV and enlarged RA (top left and right). Also seen is a small pericardial effusion.
Companion case shows delayed subendocardial LV enhancement on short axis view (bottom left). IV. LGE Differential Diagnosis:
Arrhythmogenic Right Ventricular Dysplasia
•
•
•
•
•
•
Etiology: Cardiomyopathy secondary to desmosomal protein gene mutations 
fibrofatty myocardial replacement
Diagnostic criteria31: clinical, pathologic, electrophysiological and imaging • Imaging—global/regional dysfunction and structural alterations (dilatation, aneurysms,  RVEF)—may only satisfy one criterion
Distribution: predominantly right ventricular free wall and RV outflow tract (both often dilated)
Associated with arrhythmias, sudden cardiac death
Differentiating features from CS:
Predominantly RV free wall involvement
Presence of multiple diagnostic criteria such as family history, arrhythmias, conduction abnormalities, and pathology
• Bright blood four chamber cine shows scalloping along the anterior right ventricular free wall compatible with numerous microaneurysms (top).
• There is near transmural LGE in the RV wall, and predominantly subepicardial LGE in the LV, in another patient (bottom).
IV: LGE Differential Diagnosis: Summary
Subendocardial
Transmural
Subendocardial
Mid‐myocardial
Ischemic
Subepicardial
Circumferential
Non‐
Ischemic
 Differential considerations reviewed in this exhibit
 Eosinophilic granulomatosis with polyangiitis
 Endomyocardial Fibrosis



•
•
Sarcoidosis
Myocarditis
Fabry disease
Chagas disease
Dilated cardiomyopathy



•
Sarcoidosis
Myocarditis
Fabry disease
Chagas disease
 Amyloidosis
• Systemic Sclerosis
• Cardiac Transplant
V. Management and Prognosis
 Cardiac sarcoidosis is an indication for treatment given increased risk of sudden death3
 Cardiac sarcoidosis demonstrates characteristic findings on Gallium scintigraphy, MPI, PET and CMR—setting it apart from numerous LGE mimics
 Imaging provides an essential opportunity for diagnosis, and multiple possible interventions:
 Corticosteroids
 Immunosuppressive agents: methotrexate, azathioprine, cyclophosphamide
 Pacemaker/implantable defibrillator
 Cardiac transplant: for end‐stage disease refractory to medical therapy
 Early intervention may mitigate morbidity and mortality
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Correspondence
Lea Azour, M.D.
Icahn School of Medicine at Mount Sinai
Department of Radiology, Box 1234
One Gustave L. Levy Place
New York, NY 10029
[email protected]