role of imaging in lv hypertrophy · osman n jhu choi ey et al. eur heart j 2013 mesa n=1768 fu=10...
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![Page 1: ROLE OF IMAGING IN LV HYPERTROPHY · Osman N JHU Choi EY et al. Eur Heart J 2013 MESA N=1768 FU=10 years. Whole Heart Strain Imaging Evin M. et al. JMRI 2015 Lamy J. PhD LIB-15-10-5](https://reader034.vdocuments.us/reader034/viewer/2022052106/60412dcf72226c10253d995a/html5/thumbnails/1.jpg)
ROLE OF IMAGING INLV HYPERTROPHY
FOCUS ON HYPERTENSION AND
OTHER NON SPECIFIC CAUSES
Alban REDHEUIL Professor of Radiology, Cardiovascular Imaging Department
Institute of Cardiologie, La Pitié Salpêtrière, Paris
Laboratoire d’Imagerie Biomédicale LIB-INSERM-CNRS
ICAN Imaging Core Lab
SFICV journées scientifiquesVichy, juin 2019
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Hypertension
• #1 cardiovascular disease in the world (prevalence) and increasing / age• Main risk factor for mortality and cardiovascular events (MI, stroke, PAD) in a real-life setting
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Myocardial Hypertrophy
• Cardiomyocytes are terminally differentiated after birth
• AGING : physiological LVH maintaning cardiac efficiency over time
• PATHOLOGICAL LVH: adverse CV events, HF, arrhythmia, death
Normal Hypertrophie
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Etiologies of LVH
Hypertension (BP)
Aortic StiffnessArterial Stiffness
Aortic valve stenosis
Pressure overload
X
Myocardial DiseaseFINITE CARDIOMYOCYTE
CAPITAL
ADAPTIVE RESPONSE TO WORKLOAD
PATHOLOGICAL
HYPERTROPHY
HEART FAILURE
Cardiomyocyte hypertrophy-Inherited: HCM-Myocardial hypoxia
- Obesity- Diabetes- Aging- MI- Obs. Pulmonary Dis.- Anemia
Extracellular matrix storage-Fibrosis-Amyloid-Fabry-EdemaLV WALL STRESS WS
Volume overload
Valvular regurgitationCKD
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Tissue Characterization
PerfusionMicrovesselsCoronary arteries
Adipose tissueSteatosis
Extra Cellular MatrixCollagen fibers
Myocardium
CardiomyocyteContractile Cell
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LV Geometry and Events
MESA n=5000FU= 4 years
Definition of thresholds of risk
Bluemke et al. JACC 2008
LV massCumulative events
LV massCumulative events
CHDCHD
StrokeStroke
M/VM/V
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Which heart is hypertrophic ?
Maximal thickness = 15 mmMass index = 80 g/m2
EDV index = 67 ml/m2
M/V=1.2
Maximal thickness = 6 mmMass index = 105 g/m2
EDV index = 210 ml/m2
M/V=0.5
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Diastole SystoleIRMIRM
VentriculographieVentriculographie
d’après Netter
EchocardiographieEchocardiographie
Etude de la contraction myocardique en IRM:
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CMR vs. Echo
Armstrong et al. iJACC 2012
No study directly compared the methods for the ability to predict events, agreement in hypertrophy classification, or performance in cardiovascular risk reclassification
ECHOCMR
Reproducibility –Availability ++Data on events ++
Reproducibility ++Availability +/-Data on events +
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Cardiac Remodelingimportance of precision imaging and reproducibility
Grothues F. et al. Am J Cardiol
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Altérations géométriques : remodelage ventriculaire
Atteinte du VG
Remodelage excentrique•Dilatation VG
•Amincissement parois VG
•Hypertrophie (masse)
Dilatation OG
Atteinte VD•Dilatation VD
•Dilatation OD/VCI/VSH
Volumes, masse, épaisseurs 4 cavités
Volumes, masse, épaisseurs 4 cavités
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Ventricular Remodeling in VHD
Normal Pressure overload Volume overload
ConcentricHypertrophy
EccentricHypertrophy
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Etude de la contraction myocardique en IRM:•Approche multiphase-multicoupe synchronisée au cycle cardiaque => anatomie•Pondération T1/T2•Résolution temporelle: 1 image toutes les 30 à 60 ms
diastole systole
apex
médio-ventriculaire
base
coupe transverse
calcul de la fraction d’éjection globale et régionale
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MRI Strain Imaging to predict Heart Failure in Asymptomatic Individuals
Osman N JHU
Choi EY et al. Eur Heart J 2013
MESA N=1768FU=10 years
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Whole Heart Strain Imaging
Evin M. et al. JMRI 2015Lamy J. PhD LIB
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-15
-10
-5
0
5
10
15
0 300 600 900
- cm/s
- 5
- 10
- - 10
- - 5
- - 15
Time(ms)
Max
imal lo
ng
itud
ina
l m
yo
card
ial v
elo
citie
s (cm
/s)
Doppler echocardiography
E’
-500
-300
-100
100
300
500
0 300 600 900
Transmitral f low
Aortic Flow
Tra
ns
mitra
l fl
ow
rate
(m
l/s)
Time(ms)
-m/s
- 0.2
- 0.4
- 0.6
- - 0.4
- - 0.2
Young male (35 years)
Transmitral
Aortic
DTIVRT
Ef
Af
Bollache & Kachenoura . JCMR, 2010Ashrafpoor & Kachenoura, ESC, 2012, revision in JACC CVi
Mitral annulus longitudinal velocity
Transmitral flow
Fonction diastolique
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Diagnostics différentiels
• H43
• HTA
• 5xTt
CoA native
HTA sujet âgé
Parois:AS=12-13mmANT=10mmLAT=8mmINF=9mm
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Diagnostic d’HVG
F34SportivePas ATCDAsympto
ETT:15mm
LV volumesEDV=107ml=68ml/m2
ESV=36ml=23ml/m2
LVEF=66%CO=4.7l/min
LV Mass90g=57g/m2
Wall Thickness AS=10mmANT=8mmLAT=6mmINF=8mm
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BG, 36 y/o male
Wall thickness = 12-15 mmMass index = 80 g/m2
EDV index = 67 ml/m2
M/V=1.2LVEF=68%Normal RWM
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BG, 36 y/o male
LGE
T1 pre
T1 post
T2
Diastolic Function
E’ A’
E ANon specific junctional LGE Normal T2=46ms
Ashrafpoor et al. Eur Radiol 2014
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BG, 36 y/o male
• American football player• Headaches and fatigue, android obesity
(115kg/186cm=BMI: 33)• No personal or family history of HTN• Severe hypertension: SBP=200mmHg• ECG=LVH, incomplete LBBB• Therapy x4: Sartan+CaI+BB+diuretic followed R
• Renal function normal, Cortisol + Aldosterone normal• Renal arteries and absominal aorta normal in US +CT • Adrenal glands = normal CT• Femoral and carotid US normal• Normal exercise test and Holter (ECG)• TTE = septum=17mm => addressed for suspicion of
HCM
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Role of cMRI in the case of BG
• Precise measurement of LV wall thickness, volumes and mass
– Increased thickness (15mm not 17mm in TTE), not LV mass
– Concentric remodeling
• Etiology
– Normal mitral apparatus, normal RV
– No fibrosis within hypertrophied myocardium
– No edema, signs of amyloid, iron or PAG deposits
– No aortic coarctation
• Complications
– No myocardial infarction
– Normal systolic and diastolic function
Subsequent results and evolution
– Genetics negative for HCM
– Control of BP with sartan
MRI PROTOCOL IN HTN•LV cine LA+SA•Native and Post-Gd T1 mapping•T2 mapping•LGE
•Aortic valve cine•Aortic valve and ascending aorta V-ENC imaging•3D aorta
•Renal arteries: 3D MRA•Adrenal imaging: T1w, T2w, Dixon (VIBE pre/post Gd)
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Longitudinal changes in LV structure and EF in cMRI
N=2935 participants with baseline and follow-up cardiac MRI in the MESA
Eng et al. Radiology 2015
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Issues with defining normal LV mass values
• Geographic / cultural / ethnic differences– In MESA (Eng et al.) BMI=27.7 vs. 24.4 in
UK biobank (Petersen et al. 2017)
• Methods– In Kawel et al. JCMR 2015 the 3 studies
included papillary muscles in LV mass vs. exclusion in UK biobank (Petersen et al. 2017)
• Other determinants: HTN, Diabetes, CKD
• MRI strengths– Reproducibility
– Precision: internal check = systole=diastolePetersen et al. JCMR 2017
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Normal values for LV mass and geometry
Kawel Boehm N. et al. JCMR 2015 Petersen. et al. JCMR 2017
MEN
WOMEN
LV mass index upper limitMen: 85 vs. 72 g/m2
Women: 81 vs. 55 g/m2
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Which heart is hypertrophic ?
Maximal thickness = 15 mm ABNORMAL US/UKMass index = 80 g/m2 NORMAL US/ ABNORMAL UKEDV index = 67 ml/m2 NORMAL US/UKM/V=1.2 ABNORMAL US/UK
Maximal thickness = 6 mmMass index = 105 g/m2 ABNORMAL US/UKEDV index = 210 ml/m2 ABNORMAL US/UKM/V=0.5 NORMAL UK (NA US)
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Hypothesis & expected results in Hypertension
Control group Treatment normalized hypertension
Grade 1 or 2 hypertension
Grade 3 hypertension
Heart-LV shape-Fibrosis- Systolic and Diastolic Function
Aorta-Stiffness indexes-Thickness-Curvature
Retinal arteries- Wall to lumen ratio
? ?
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Controlled HypertensionTesting the limits of cMRI
• Treibel et al. JCMR • N=40 HTN with N=26 no LVH and 14 with
LVH• T1 native and ECV increase in HTN only in
the presence of LVH. No significant change in ECV (p=0.06)
• Increment is small• Determinants = LV mass, LV thickness
• Non ischemic pattern LGE = 28% (junction, papillary, mid-patchy)
• Note: 13 % of patients had new diagnoses of hypertrophic cardiomyopathy or silent infarction
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Discriminating HTN cardiomyopathy vs. HCM
• HCM, n=95; hypertension, n=69
• Native T1 = best predictor of HCM vs. HTN
• Association with increased LV mass, thickness, LGE presence and extension
• Major drawback = cutoff
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Increased ECV and T1 associated with altered contraction in HTN only if LVH is present
Kuruvilla et al. JACC imaging 2015
Systolic Function
Systolic Function
Diastolic Function
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Aortic distensibility concentric remodelingAltered Strain increased LV mass
Biomarkers of sequential effects of increased afterload?
Concentric remodeling and LVH in Hypertension are most associated with LV dysfunction and Aortic Stiffness
Rodrigues JCL, et al. Heart 2016
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Cardiovascular effects of Aldosterone
AldosteroneAldosterone AortaAorta
MyocardiumMyocardium
HypertensionHypertension
Structure
Hypertrophy
Structure
Hypertrophy
CompositionFibrosis
Volume overload
CompositionFibrosis
Volume overload
Biology/Cell
Oxidative stressApoptosis
Inflammation
Biology/Cell
Oxidative stressApoptosis
Inflammation
Cardiovascular morbidity and mortalityHeart Failure
Arrhythmias, Sudden death
Cardiovascular morbidity and mortalityHeart Failure
Arrhythmias, Sudden death
FibrosisInflammationStiffness
Regulationof extra cellular matrix
= IMAGING TARGET
Regulationof extra cellular matrix
= IMAGING TARGET
Increased afterload is related to increased
cardiomyocyte volume
Increased aldosterone is independently related to
increased ECM
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Spironolactone prevents fibrosis and cellular hypertrophy in mice
Coehlo-Filho et al. JAHA 2016
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COEURALDO Study
• Hypothesis: the respective effects of aldosterone and hypertension on intra and extracellular myocardial mass beyond the degree of global hypertrophy be characterized and quantified by imaging in humans
• Design: double case-controlled study enrolling 80 asymptomatic participants in 4 groups of 20
– Healthy volunteers– Bartter-Gitelman syndrome– Essential hypertension – Primary hyperaldosteronism
• Exclusion criteria included: diabetes, any preexisting cardiomyopathy, treatment interfering with RAAS
• Main measures: clinical, ECG, Biology, Tonometry, MRI
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Interaction between HTN and ALDO to promote myocardial fibrosis
0
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PAHTNGS HS
Extr
acellu
lar
mass in
dex,
g/m
2
tota
l an
d In
tracellu
lar m
ass in
dex, g
/m2
Redheuil A., Blanchard A. Kachenoura, N,Azizi M, Mousseaux E. et al. submitted
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Cardiac Remodeling in Obesity
Aurigemma G P et al. Circ Cardiovasc Imaging. 2013
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Obesity, Epicardial Fat and CAC
N=573 healthy post menopausal womenDe Vos et al. EHJ 2008
N=4093 healthy individualsMahabadi et al. JACC 2013
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LV Geometry in obesity in MESA
Turkbey et al. JACC imaging 2010
N=5098 multiethnic multicenter general US population study
LV massLV mass LV volumeLV volume
M/VM/V
BMIBMI Fat massFat mass
LV massLV mass LV volumeLV volume
M/VM/V
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Cardiac Remodeling in Obesity
Aurigemma G P et al. Circ Cardiovasc Imaging. 2013
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Effect of Bariatric Surgery in CMR
Gaborit, Clément et al. JACC
LV MassLV Mass Cardiac outputCardiac output E/AE/A LA areaLA area
Epicardial fatEpicardial fat Visceral abdominal fatVisceral abdominal fat Myocardial TG (%)Myocardial TG (%)
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Unrecognized MI detected by CMR
• N=936 ICELAND MI Study in older adults
• Diagnosis and prognosis CMR > ECG
• Metabolic rather than atherosclerotic profile
Schelbert et al. JAMA 2012
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Detecting myocardial scar in Diabetes
• EDIC Study: type I DM
• N=749 with CMR
• Scar = 4.3%
• Correlates:
– Age, HTN, male
– LV mass, EDV
– HbA1c, macroalbuminuria
Turkbey E B et al. Circulation. 2011;124:1737-1746
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Prognosis of unrecognized scar in diabetes
Kwong R Y et al. Circulation. 2008;118:1011-1020
N=187
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T1 mapping in diabetes
• 50 diabetic patients with normal LV ejection fraction (EF) and no underlying coronary artery disease or regional macroscopic scar on MRI delayed enhancement
Ng. et al. Circulation cvi 2011
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ECV in diabetes for prognosis ?
• N=1176• ECV increased in diabetes = ECM expansion• Independent of inducible ischemia or chronic MI• Reversible with RAAS inhibition
• Detectable and treatable phenotype?
Schelbert et al. EHJ 2013
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Cortisol and cardiac remodeling and dysfunction
JCEM 2014
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T1 mapping in Cushing’s DiseaseA Pilot Longitudinal Study
Native T1Native T1
LVEFLVEF
LV massLV mass M/VM/V
Roux C, Kachenoura N, Redheuil A. JMRI 2016
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Unexplained LVH detected by MRI in the general population
Massera et al. JAHA 2019
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Phenotypical Heterogeneity in HFpEF
LVHLVH
LA dilationLA dilation
Diastolic DysfunctionDiastolic Dysfunction
Lewis et al. JACC 2017
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New Imaging Biomarkers for HFpEF
• N=112 (62 with HFpEF, 22 HTN, and 28 healthy controls)
• Echo GLS and MRI ECV were the only variables able to independently stratify among the 3 groups of patients.
• ECV was the best technique for differentiation between HTN and HFpEF (ECV AUC: 0.88; GLS AUC: 0.78; p <
0.001). • ECV cutoff of 31% gave 100% sensitivity
and 75% specificity. • ECV was significantly higher and GLS was
significantly reduced in subjects with reduced exercise capacity (lower peak oxygen consumption and higher minute ventilation–carbon dioxide production) (p < 0.001 for both ECV and GLS)
Ify R. Mord JACC cvi 2018
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Myocardial Microstructural Dynamics by In Vivo Diffusion Tensor MRI
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Challenge in LVH = Classify Disease and Stratify Risk
• Physiological or pathological?
• Imaging ?
• Proteomics ?
• Metabolomics ?
• Genetics ?
• New targets for therapy