cardiovascular mr imaging...wall thickening = 100*(ds-dd) / dd basal and middle 6 –6 segments...

• University of Pécs, Heart Institute

Cardiovascular

MR Imaging

Tamás Simor MD, PhD, Med Hab

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

Cardiovascular MRI

Contrast

injector

Stress pump

(Adenosin)

ECG & SpO2Visual and verbal

communication

Administration of contrastNon Invasive

Blood pressure

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)

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

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

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)

Global left ventricular function

EF=(EDV-ESV)/EDV*100

Inter-study variability

Pennell, D. Heart 2001;85:581-589

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.

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

Cerqueira et al AHA Scientific Statement, Circulation 2002;105:539-542

Bull’s eye diagram

Basal

Middle

Apical

Regional left ventricular function

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

MR Contrastinjection

time

Normal myocardium Infarcted myocardium

First passLate enhancement

Perfusion MRI andLate enhancement contrast

Scar tissue

10 – 20 minutes

< 10 sec

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

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)

Myocardial infarct - intramural thrombus

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


Myocardial infarct „remodeling”

3rd day 180th day

Heart function – T2/T1 weighted SSFP – short axis


3rd day 180th day

Oedema in heart muscle– T2 acquisition – short axis


3rd day 180th day

Viability– T1 wighted acquisition – short axis

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

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

Chronic Q AMI

MRI: wall motion, focal thinning in wall thickness

with transmural late enhancemement

Chronic non Q AMI

MRI: normal wall thickening

subendocardial late enhancement

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

Revascularisation

Kim, R J et al. Heart 2004;90:137-140

Before

Kim, R J et al. Heart 2004;90:137-140

Revascularisation

before after

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

Stress MR – CORON -SPECT

VENTRICULAR DIASTOLIC FUNCTION


LV FUNCTION and Wall thickness

HCM

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

Peak filling rate

NORMAL PFR

REDUCED PFR

Indian Heart J (2017), http://dx.doi.org/10.1016/j.ihj.2016.12.021

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

DCM Hossztengelyi movie

Késői típusú kontraszt vizsgálat

Egyenletesen fekete az izomzat

Nem ischaemias eredet

Midmyocardiális kontraszt halmozásRossz prognózis

Késői típusú kontraszt

Nem egyenletesen fekete az izomzat - ischaemias eredet

Késői típusú kontraszt

HF DCM SA movie

BTSZB Jelentősen csökkent EF jelentős aszinkronia

Revascularizáció ?Gyógyszeres th.?PM th. ?

Lipid infiltration /Connective tissueRight ventricle

Double IR

Late enhancement

Triangle dysplasiaOutflow tract Free wall apex

Movie

aneurysm

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

T2* fits in heart and liver

HEART

LIVER

T2* (ms)

14.3

14.1

5.4

6.0

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)

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

Myocarditis okok


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

http://radiology.rsnajnls.org/cgi/content/full/237/1/75

VENTRICULAR FUNCTION IN HCM


LV FUNCTION and Wall thickness in HCM

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

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.


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.


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.


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.

kollagén disarray

3%

32%

50%

50%

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

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).






IIa B

124,126,

127,130

136,138–

143


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

HOCM –

Before

PTSMA

After

PTSMA






IIa B

124,126,

127,130

136,138–

143


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

• .

SA LATE ENHANCEMENT

LVOT Late enhancement and movie

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

http://onlinelibrary.wiley.com/doi/10.1002/jmri.v26:4/issuetoc

Precontrast LVOT

POSTcontrast LVOT

T1 fitting - precontrast

T1 fitting - postcontrast

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

Extracellular volume fraction in the Myocardial tissue

T1 preGd T1 postGd ECV image

ECV=λ * (1–Hct)

λ=ΔR1myocardium / ΔR1bloodΔR1=1/T1postGd – 1/T1preGd

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.

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.

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

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

Amyloidosishypertrophy and biventricular subendocardial late enhancement

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)

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

Thanks!

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


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


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



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



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



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


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

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

cardiovascular mr imaging...wall thickening = 100*(ds-dd) / dd basal and middle 6 –6 segments...

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