cardiovascular mr imaging...wall thickening = 100*(ds-dd) / dd basal and middle 6 –6 segments...
TRANSCRIPT
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• University of Pécs, Heart Institute
Cardiovascular
MR Imaging
Tamás Simor MD, PhD, Med Hab
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University of Pécs
1,5 T GE OptimaTM
Diagnostic Center Pécs
1,5 T Siemens Magnetom Avanto
3 T Siemens TRIO
Analysis: MASS 8.1 (MEDIS, NL)
based on short axis movies
Parameters: EDV, ESV, SV, EF, LVM
Cardiovascular MRI
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Cardiovascular MRI
Contrast
injector
Stress pump
(Adenosin)
ECG & SpO2Visual and verbal
communication
Administration of contrastNon Invasive
Blood pressure
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Hystory
• 1946 Principles of Magnetic Resonance ,
Spektroscopy and analytic chemistry
Felix Bloch és Edward Purcell Nobel price (1952)
• 1971 Relaxation times of normal tissue and tumor are
different Raymond Damadian
• 1973 Hounsfield – CTPrinciples of Magnetic rezonance
“back projection” MRI - Paul Lauterbur
• 1975 Introduction of Phase and Frequency encoding and
Fourier transformation - Richard Ernst – basis of
current MRI techniques Nobel price (1991)
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5
• 1980 – Edelstein – first MRI images, based on Ernst principles – 1 image = 5 minutes
EKG triggered cardiac studies in X – Y – Z directions
• 1990 – 1 image = 5 seconds dynamic clinical MRI
• 1990 – ultra-fast/near-real-time imagingtissue tagging-tracking 3-D acquisition and 3-D visualisation
Result: complex analysis of anatomy an function of cardiovascular system.
• Clinical application: delayed due to limitations
• Further development (end of 90s):
Complex cardiovascular MRI profile
Hystory 2
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Gudeline
ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR Appropriateness Criteria for
Cardiac Computed Tomography and Cardiac Magnetic Resonance Imaging
JACC 48, 7, 2006
Score Study Cat.
7-9 Appropriate test for specific indication (test is
generally acceptable and is a reasonable approach
for the indication).
A
4-6 Uncertain for specific indication (test may be
generally acceptable and may be a reasonable
approach for the indication). (Uncertainty also implies
that more research and/or patient information is
needed to classify the indication definitively.)
U
1-3 Inappropriate test for that indication (test is not
generally acceptable and is not a reasonable
approach for the indication).
I
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MRI in ischemic heart disease
• Function
• Viability
• Perfusion
ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR Appropriateness Criteria for
Cardiac Computed Tomography and Cardiac Magnetic Resonance Imaging
JACC 48, 7, 2006
A(8), A(8), A(8), U(6)
A(9), A(9), A(9), A(4), U(4)
A(7), U(6)
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Global left ventricular function
EF=(EDV-ESV)/EDV*100
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Inter-study variability
Pennell, D. Heart 2001;85:581-589
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Parameters to be measured
• Enddiastolic volume (EDV)
• Endsystolic volume (ESV)
• Stroke volume (SV)
• Cardiac output (CO)
• Ejection fraction (EF)
• Left ventricular mass (LVM) and (LVM/BSA)
• Peak ejection rate (PER)
• Peak filling rate (PFR)
and ratios normalizes by EDV.
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Regional left ventricular function
Wall thickening = 100*(Ds-Dd) / Dd
Basal
and
Middle
6 – 6 segments
inferoseptal
anteroseptal
anterior
anterolateral
Inferolateral
Inferior
Left ventricular mass= LV muscle volume * 1,05
Apical 4 segments
Septal
Anterior
Lateral
Inferior
Left ventricle: 17 segment
Apex 1 segment
LAD
CXRCA
Cerqueira et al AHA Scientific Statement, Circulation 2002;105:539-542
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Cerqueira et al AHA Scientific Statement, Circulation 2002;105:539-542
Bull’s eye diagram
Basal
Middle
Apical
Regional left ventricular function
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Dobutamin-Stressz MRI: 4 CH view
rest Stress
20 µg/kg/min
Stress
40 µg/kg/min
Stress
30 µg/kg/min
Nagel E et al, Circulation 1999
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MR Contrastinjection
time
Normal myocardium Infarcted myocardium
First passLate enhancement
Perfusion MRI andLate enhancement contrast
Scar tissue
10 – 20 minutes
< 10 sec
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Late enhancement Contrast MRI
• In vivo
• 10 – 20 min. post Gd DTPA
• Inversion recovery
FLASH or True-FISP
• “Bright is dead”
• Normal, stunned, hibernating
myocardium is dark
• Ex-vivo
• TTC staining
Kim R et al, Circulation 1999
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Coronary heart disease Myocardial infarction
⚫ Detection of Infarct and it’s extent
⚫ Detection of Infarct Transmurality, Viabilty
Pennell et al. Eur Heart J.2004; 25: 1940-1965.
Cardiovascular MRI
A (9)
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Myocardial infarct - intramural thrombus
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4 chamber SSFP movie
Aneurym resection MRI
pre post norm
EDV (ml) 1423 167 77-195
EF (%) 3 54 56-78
Selvanayagam J et al, Circulation 2003
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• University of Pécs, Heart Institute
Myocardial infarct „remodeling”
3rd day 180th day
Heart function – T2/T1 weighted SSFP – short axis
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Myocardial infarct „remodeling”
3rd day 180th day
Oedema in heart muscle– T2 acquisition – short axis
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Myocardial infarct „remodeling”
3rd day 180th day
Viability– T1 wighted acquisition – short axis
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50 y, I, aVL, ST elevation – Cx occlusion - PCI
Peak CK: 5912; MB: 792 – Q AMI
MRI: 2 weeks after acute MI
lateral wall> akinetic
transmural late enhancement
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50 y – LAD D1 occlusion - PCI
Peak CK: 560; MB: 62 – non Q AMI
MRI: 1 week after acute MI
normal wall motion
late enhancement in small extent
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Chronic Q AMI
MRI: wall motion, focal thinning in wall thickness
with transmural late enhancemement
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Chronic non Q AMI
MRI: normal wall thickening
subendocardial late enhancement
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Relationship between transmural extent of HE before
bypass surgery and likelihood of increased contractility
after surgery
Transmural Extent of Hyperenhancement (%)
Impro
ved c
ontr
actilit
y (
%)
0
20
40
60
80
100
All Dysfunctional Segments
Selvanayagam J et al Circulation 2004
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Revascularisation
Kim, R J et al. Heart 2004;90:137-140
Before
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Kim, R J et al. Heart 2004;90:137-140
Revascularisation
before after
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1 Zurich, Switzerland, 2 Würzburg, Germany, 3 Gainesville/Jacksonville, US 4 Berlin Germany, 5 Munich, Germany, GEHC, 6 Pecs, Hungary
• 33 centres, 1.5 Tesla, 465 patients
• Patients with chest pain undergoing coronary angiography
• CAD defined as >50% diameter stenosis in at least one vessel with at
least 2mm diameter
MR IMPACT II(Magnetic Resonance Imaging for Myocardial Perfusion Assessment in Coronary artery disease Trial)
A phase III multicenter, multivendor trial comparing perfusion cardiac magnetic resonance versus
single photon emission computed tomography for the detection of coronary artery disease.
J. Schwitter, 1 C. Wacker, 2 N. Wilke, 3
N. Al-Saadi, 4 N. Hoebel, 5 T. Simor 6
CardioVascularMR Center Zurich
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Stress MR – CORON -SPECT
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VENTRICULAR DIASTOLIC FUNCTION
EF=(EDV-ESV)/EDV*100
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LV FUNCTION and Wall thickness
HCM
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Correlation of Wall thickness / thickening
WT %= -6.8285 x WT + 167.5
R2 = 0.4845
-20
20
60
100
140
180
220
5 10 15 20 25 30
falvastagság (WT mm)
falvastagodás
(WT %)
n=289
Wall thickening
Wall thickness
HCM
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Peak filling rate
NORMAL PFR
REDUCED PFR
Indian Heart J (2017), http://dx.doi.org/10.1016/j.ihj.2016.12.021
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HCM
ARVD/C
Mitokondriális miopátiák
Ioncsatorna betegségek
LVNC
Primer kardiomiopátiák1
1AHA Scientific Statement, Circulation, 2006;113:1807-1816
DCM
RCM
Gyulladásos
Tako-tsubo
Peripartum
Tahikardia indukálta
IDM
Genetikus Kevert Szerzett
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DCM Hossztengelyi movie
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Késői típusú kontraszt vizsgálat
Egyenletesen fekete az izomzat
Nem ischaemias eredet
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Midmyocardiális kontraszt halmozásRossz prognózis
Késői típusú kontraszt
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Nem egyenletesen fekete az izomzat - ischaemias eredet
Késői típusú kontraszt
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HF DCM SA movie
BTSZB Jelentősen csökkent EF jelentős aszinkronia
Revascularizáció ?Gyógyszeres th.?PM th. ?
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Lipid infiltration /Connective tissueRight ventricle
Double IR
Late enhancement
Triangle dysplasiaOutflow tract Free wall apex
Movie
aneurysm
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Major Minor
Global or regional dysfunction and structural alterations
MRI
Regional RV akinesia, or dyskinesia, or dyssynchronous RV contraction
and 1 of the following➢ Ratio of RV EDV to BSA
>100 ml/m2 (female) >110 ml/m2 (male)
➢ or RV EF < 40%
Regional RV akinesia, or dyskinesia, or dyssynchronous RV contraction
and 1 of the following➢ Ratio of RV EDV to BSA
90 - 100 ml/m2 (female)100 - 110 ml/m2 (male)
or RV EF 40 - 45%
ECHO Regional RV akinesia, dyskinesia, or aneurysmand 1 of the following (end diastole):➢ PLAX RVOT ≥32 mm (corrected
for body size [PLAX/BSA] ≥19 mm/m2)
➢ PSAX RVOT ≥36 mm (corrected for body size [PSAX/BSA] ≥21 mm/m
➢ or fractional area change ≤33%
Regional RV akinesia, dyskinesia
and 1 of the following (end diastole) :➢ PLAX RVOT ≥29 to <32 mm
(corrected for body size [PLAX/BSA] ≥16 to 19 mm/m2)
➢ PSAX RVOT ≥32 to 36 mm (corrected for body size [PSAX/BSA] ≥18 to 21 mm/m2
➢ or fractional area change >33 to ≤40%
Angiography RV aneurysm, akinesia, dyskinesia
ARVD Diagnostic criteria
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ARVD
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T2* fits in heart and liver
HEART
LIVER
T2* (ms)
14.3
14.1
5.4
6.0
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T2* MRI: New Standard for Cardiac Iron
Photos courtesy of Dr. M. D. Cappellini. Anderson LJ, et al. Eur Heart J. 2001;22:2171.
LV
EF
(%
)
0
50
70
40
30
20
10
60
80
90
0 20 40 60 9080 10010 30 50 70
Heart T2* (ms)
Cardiac T2* value of
37 in a normal heart
Cardiac T2* value of
4 in a significantly
iron overloaded
heart
Relationship between myocardial T2* values and left ventricular ejection
fraction (LVEF). Below a myocardial T2* of 20 ms, there was a progressive
and significant decline in LVEF (R = 0.61, P < .0001)
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Myocarditis• Incidencia 8-10/100.000
• Posztmortem vizsgálatok: myocarditis a fiataloknál fellépő hirtelen halál egyik gyakori oka: 8,6-11% (Fabre et al. Heart, 2006; Papadakis et al. Europace, 2009)
• Ismeretlen etiológiájú DCM: 10-40% (Nugent et al. N Engl J Med, 2003)
• Infektív
vírus: Adeno, Coxsackie A, B, EBV, CMV, HHV6, ParvoB19, Influenza A, B, Hepatitis B, C, HIV
baktériumok, gombák, egyéb
• Immun
vasculitis-kötőszöveti betegségek: SLE, RA, sarcoidosis, Sjögren-sy. gyulladásos bélbetegségek: Crohn, colitis ulcerosa
• Posztirradiációs
• Gyógyszer indukálta
szulfonamidok, metildopa, antraciklinek, kokain
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Myocarditis okok
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• University of Pécs, Heart Institute
Case of the week – 08-13: Viral Myocarditis by CMRHistory: A 22-year-old college student noted chest pain one week after
recovering from flu-like symptoms. His ECG revealed inferolateral ST-
elevation and his cardiac biomarkers were elevated.
Transthoracic echocardiography: regional left ventricular dysfunction with
focal hypokinesis of the mid inferior and inferolateral walls (E).
CMR: Coronary MR imaging demonstrated unobstructed proximal coronary
arteries (images A,B).T2 weighted fast spin echo demonstrated increase
inferolateral and lateral signal intensity (arrow, image C). Mid zone and
epimyocardial LGE was present in the mid-inferior and lateral walls (arrow,
image D). Cine CMR confirmed the finding of regional left ventricular
dysfunction with hypokinesis of the inferior, inferolateral, and lateral walls (E). (1,2)
Discussion: These images, in concert with the clinical presentation, support
a diagnosis of focal myocarditis following viral illness.
1.Laissy JP, Hyafil F, Feldman LJ, et al. Differentiating acute myocardial infarction from myocarditis: diagnostic
value of early- and delayed-perfusion cardiac MR imaging. Radiology 2005;237:75-82.
Gregory Piazza and Warren J. Manning, Beth Israel Deaconess Medical Center, Boston Mass. USAGregory
Piazza and Warren J. Manning, Beth Israel Deaconess Medical Center, Boston Mass. USA
E F
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VENTRICULAR FUNCTION IN HCM
EF=(EDV-ESV)/EDV*100
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LV FUNCTION and Wall thickness in HCM
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Correlation of Wall thickness / thickening
WT %= -6.8285 x WT + 167.5
R2 = 0.4845
-20
20
60
100
140
180
220
5 10 15 20 25 30
falvastagság (WT mm)
falvastagodás
(WT %)
n=289
Wall thickening
Wall thickness
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Diverse patterns of LVH in HCM
A. involving ventricular septum (VS), but sparing the LV free
wall (FW);
B. hypertrophy of the basal anterior free wall and a portion of
the contiguous anterior septum, representing the most
common area of LV wall thickening in HCM;
C. massive hypertrophy (wall thickness, 33 mm) limited to basal
posterior ventricular septumJ Am Coll Cardiol 2009, 54:220-8.
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Diverse patterns of LVH in HCM
D. focal area sharply confined to basal anterior septum;
E. localized to LV apex;
F. segmental LV hypertrophy of the basal anterior septum and anterolateral
wall, separated by regions of normal LV thickness .
J Am Coll Cardiol 2009, 54:220-8.
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Diverse patterns of LVH in HCM
G. increased wall thickness in the superior segment (thin arrow) and extreme hypertrophy of
the inferior segment (thick arrow) of the RV wall;
H. medium-sized LV apical aneurysm (arrowheads) and maximal LV wall thickening at mid-
ventricular level wit h muscular apposition of septum and LV free wall producing distinct
proximal (P) and distal chambers;
I. anomalous insertion of papillary muscle (thin arrows) directly into the anterior leaflet of
the mitral valve (thick arrow) (in the absence of chordae tendinae) producing obstruction to
blood flow from the apposition of the papillary muscle and basal ventricular septum;
JACC 2009, 54:220-8.
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Diverse patterns of LVH in HCM
J. extraordinarily long anterior mitral valve leaflet measuring 33 mm; PML is of
normal length (although not well visualized in this frame);
K. multiple accessory papillary muscles, 4 in number (arrows);
L. 7-year-old asymptomatic genotype positive/phenotype negative HCM girl with
3 deep myocardial crypts in the basal (posterior) inferior LV free wall.
Circulation 2011, 124:40-7. Am J Cardiol 2008, 101:668-73.
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kollagén disarray
3%
32%
50%
50%
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A. Extensive transmural LGE in the anterior wall (small arrows) with smaller
focal area in the inferior wall (small arrows);
B. mid-myocardial LGE in the lateral wall (small arrows) and diffuse LGE in
the ventricular septum which extends into the RV wall (large arrows) in a 26
year-old man with “end-stage” phase of HCM with an ejection fraction of
40%;
C. LGE confined to the LV apex (arrows)
Recommendations Class Level Ref.
In the absence of contraindications, CMR with LGE should be
considered in patients fulfilling diagnostic criteria for HCM, to
assess cardiac anatomy, ventricular function, and the presence
and extent of myocardial fibrosis.
IIa B
124,126,
127,130
136,138–
143
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D. LGE localized to the insertion area of the RV wall into the anterior (large
arrow) and posterior ventricular septum (small arrow);
E. Transmural LGE involving the majority of the ventricular septum (large
arrow) and lateral wall (small arrow).
F. Basal short-axis image with transmural LGE located predominantly in the
ventricular septum (arrows).
Recommendations Class Level Ref.
In the absence of contraindications, CMR with LGE should be
considered in patients fulfilling diagnostic criteria for HCM, to
assess cardiac anatomy, ventricular function, and the presence
and extent of myocardial fibrosis.
IIa B
124,126,
127,130
136,138–
143
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Recommendations Class Level Ref.
CMR with LGE imaging should be considered in patients with
suspected apical hypertrophy or aneurysm. IIa C
127,129
MovieAkinesis in the apex
LEIn the apex
PerfusionDeficit in the apex
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HOCM –
Before
PTSMA
After
PTSMA
Recommendations Class Level Ref.
In the absence of contraindications, CMR with LGE should be
considered in patients fulfilling diagnostic criteria for HCM, to
assess cardiac anatomy, ventricular function, and the presence
and extent of myocardial fibrosis.
IIa B
124,126,
127,130
136,138–
143
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Recommendations Class Level Ref.
CMR with LGE may be considered before septal alcohol
ablation or myectomy, to assess the extent and distribution of
hypertrophy and myocardial fibrosis.cIIb C
150,151
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• .
SA LATE ENHANCEMENT
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LVOT Late enhancement and movie
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Optimization and validation of a fully‐integrated pulse sequence for modified look‐locker inversion‐recovery (MOLLI) T1 mapping of the heart
Journal of Magnetic Resonance Imaging
Volume 26, Issue 4, pages 1081-1086, 25 SEP 2007
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Precontrast LVOT
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POSTcontrast LVOT
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T1 fitting - precontrast
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T1 fitting - postcontrast
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Generated T1 images
T1 image precontrastMyocardium: 850-1200 ms
HCM: 850 – 1000 ms
Blood: 1500 ms
T1 image postcontrastRemote Myocardium : 480-550 ms
Myocardium with HCM: 220-300 ms
Blood: 380 ms
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Extracellular volume fraction in the Myocardial tissue
T1 preGd T1 postGd ECV image
ECV=λ * (1–Hct)
λ=ΔR1myocardium / ΔR1bloodΔR1=1/T1postGd – 1/T1preGd
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CM, no LGE = cardiomyopathy without visually evident LGE, CM, +LGE = cardiomyopathy with
visually evident LGE.
Radiology: Volume 265: N3, 2012
Myocardial T1 time according to disease category.
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The main finding of the study was that patients with heart failure had increased ECV as compared
to control subjects with the highest ECV in the cohort with SHF.
Similarly, peak- filling rates (PFR) were significantly reduced in SHF and reduced to a lesser extent
in patients with HF-PEF.
Interestingly, ECV was correlated with PFR in the HF-PEF group, but not in the control subjects or
those with SHF.
The pre-contrast T1 time (Native T1) was not significantly different between the groups. This is not
entirely unexpected as native T1 is sensitive to water in both the intracellular and extracellular
compartments of the myocardium.
Post-contrast T1 times were shortest in SHF followed by HF-PEF and the longest in the normal
subjects, which is explained by the accumulation of Gd-DTPA in the extracellular space.
A reduction in post contrast T1 times has also been in HF-PEF and was associated with either heart
failure hospitalization or cardiac death.
Increasing ECV was associated with reduction in EF, and a decrease in the PFR.
This suggests that ECV is sensitive to subtle changes in systolic and diastolic function, as fibrosis
likely contributes to both of these components of cardiac function in HF-PEF.
Seeing the Unseen Fibrosis in Heart Failure with
Preserved Ejection Fraction
JACC Cardiovasc Imaging. 2014 October ; 7(10): 998–1000.
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Bos JM1, Will ML, Gersh BJ, Kruisselbrink TM, Ommen SR, Ackerman MJ.
Characterization of a phenotype-based genetic test prediction score for unrelated
patients with hypertrophic cardiomyopathy.
Mayo Clin Proc. 2014 Jun;89(6):727-37.
Mayo HCM Genotype Predictor
Positive predictors:
age diagnosis <45 years,
MLVWT ≥ 20mm,
family history of HCM,
family history of SCD, and
reversed septal contour
Negative predictor mild concomitant hypertension
80% positive genetic test = 5 positive predictor
1053 patients with the clinical diagnosis of HCM (60% male; mean ± SD age at diagnosis,
44.4 ± 19 years) had HCM genetic testing for the 9 HCM-associated myofilament genes
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Contrast Long-Axis CMR Compared to Necroscopy Long-axis contrast CMRI (Left) patient #2 (TI = 230 ms).
(Right) necropsy sample of a different patient diagnosed with cardiac amyloidosis. Interestingly, the pattern of
diffuse LGE originating from the subendocardium nicely matches the pattern of pale subendocardial amyloid
deposits indicated by white arrowheads in the necropsy sample.
Holger Vogelsberg , Heiko Mahrholdt , Claudia C. Deluigi , Ali Yilmaz , Eva M. Kispert , Simon Greulich , Karin K...
Cardiovascular Magnetic Resonance in Clinically Suspected Cardiac Amyloidosis : Noninvasive Imaging Compared to
Endomyocardial Biopsy
Journal of the American College of Cardiology, Volume 51, Issue 10, 2008, 1022 - 1030
Amyloidosishypertrophy and biventricular subendocardial late enhancement
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Amyloidosishypertrophy and biventricular subendocardial late enhancement
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KARDIOVASZKULÁRIS MR VIZSGÁLAT
STRUKTÚRA ÉS FUNKCIÓ
IndikációMedián
pontszám
Kamra és billentyű funkció vizsgálata†
17Komplex kongenitális szívbetegségek vizsgálata, beleértve a koronária keringés, nagy
erek, szívüregek és billentyűk anomáliáitA(9)
18Jobb kamrai aritmogén kardiomiopátia vizsgálata (ARVC/D) syncope vagy kamrai
aritmia jelentkezése eseténA(9)
19Bal kamra funkció vizsgálata miokardiális infarktust követően vagy szívelégtelenségben
echokardiográfiával technikailag korlátozottan megítélhető esetekbenA(8)
20Bal kamra funkció megítélése
korábbi vizsgálatok alapján ellentmondásos eredményekA(8)
21Specifikus kardiomiopátiák vizsgálata (infiltratív [amiloidosis, sarcoidosis], HCM,
kardiotoxikus terápia okozta) A(8)
22Szívbillentyűk és billentyű protézisek vizsgálata, beleértve a stenosis és regurgitáció
quantifikálását A(8)
23Miokarditis vagy normál koronáriák mellett kialakuló miokardiális infarktus vizsgálata
nekro-enzim emelkedés angiográfiás eltérés nélkül A(8)
24Bal kamra funkció megítélése miokardiális infarktust követően vagy
szívelégtelenségben U(6)
Intra- és extrakardiális struktúrák vizsgálata
Kardiális terimék megítélése (tumor vagy trombus gyanú)
Kontrasztanyag használata a perfúzió és halmozás vizsgálataA(9)
25 Aorta-dissectio vizsgálata A(8)
26Véna pulmonálisok megítélése pitvarfibrilláció radiofrekvenciás ablációját
megelőzőenbal pitvari és véna pulmonalis anatómiaA(8)
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Tissue characterisation using
native T1 and extracellular volume
fraction (ECV). Absolute values for
native T1 depend greatly on field
strength (1.5 T or 3 T), pulse
sequence (MOLLI or ShMOLLI),
scanner manufacturer and rules of
measurements.
Cardiac T1 Mapping and Extracellular Volume (ECV) in clinical
practice: a comprehensive review
Philip Haaf et al Journal of Cardiovascular Magnetic Resonance 2016 18:89
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Thanks!
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Diastolés bal kamra funkció - MRI
LV time-volume relation (c) determined by planimetry from a multislice cine short-axis
dataset (b), planned perpendicular to the long-axis of the LV (a). From the time-volume
relation, early peak filling rate (EPFR) is determined from the steepest gradient in the volume
curve in the early filling phase. Atrial filling fraction (AFF) is determined in the atrial filling
phase Curr Cardiovasc Imaging Rep. 2011 Apr; 4(2): 149–158
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Diastolés bal kamra funkció - MRI
Left atrial size is determined by biplane Simpson’s rule on the atrial areas determined in four-
chamber (a) and two-chamber (b) view
Curr Cardiovasc Imaging Rep. 2011 Apr; 4(2): 149–158
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Diastolés bal kamra funkció - MRI
At the moment of end-systole, an acquisition plane is positioned at the mitral valve (a).
Through-plane one-directional velocity-encoded MRI (magnitude and velocity image in b)
results in a time-flow rate graph (c), which is used for wave form analysis. Early (E) and atrial
(A) peak filling rate can be determined, as well as the deceleration time (DT) of the E-peak
Curr Cardiovasc Imaging Rep. 2011 Apr; 4(2): 149–158
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Diastolés bal kamra funkció - MRI
Three-dimensional three-directional velocity-encoded MRI at the aorta and mitral valve (a)
results in velocity images reconstructed at the ascending aorta (b) and the mitral valve (d).
From the velocity images, time-flow rate graphs (c and e) are obtained from which the
isovolumic relaxation time (IVRT) can be determined
Curr Cardiovasc Imaging Rep. 2011 Apr; 4(2): 149–158
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Diastolés bal kamra funkció - MRI
In-plane one-directional velocity-encoded MRI in four-chamber orientation (magnitude image
in a and velocity image in b). Velocity sampling at the pulmonary vein (arrow) results in a
time-velocity graph (c), from which peak systolic velocity (S), peak anterograde diastolic
velocity (D), and peak atrial reversal velocity (Ar) can be determined
Curr Cardiovasc Imaging Rep. 2011 Apr; 4(2): 149–158
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Diastolés bal kamra funkció - MRI
One-directional velocity-encoded MRI (a) of the longitudinal annular velocity in four-
chamber orientation, sampled at the septum (arrow), results in time-velocity graph (b), from
which early peak annular velocity (E′) can be determined
Curr Cardiovasc Imaging Rep. 2011 Apr; 4(2): 149–158
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Hypertrophic
Cardiomyopathy
Protocol1.Anatomy module
2.LV function module
3.LVOT cines (2 orthogonal views)
4.Velocity encoding module in and through LVOT planes
5.LV tagging (3 SA slices, 4ch) optional
6.LGE module
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Hypertrophic
Cardiomyopathy
Report1. Dimensions, mass (corrected for BSA) and
function EDV, ESV, SV, EF and mass
2. Thickening and function of myocardial segments
3. Presence of LVOT obstruction at rest
4. Presence of systolic anterior motion (SAM)
5. Presence and extent of fibrosis