role of imaging evaluation of cardiomyopathies (hypertrophic-dilated) · 2017-05-04 · evaluation...
TRANSCRIPT
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ROLE OF IMAGINGEvaluation of cardiomyopathies (hypertrophic-dilated)
2017
Division of Inherited Cardiac DiseasesHeart Center for the Young and Athletes
A’ Dpt. of Cardiology – University of Athens
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• Young man that plays football
• Age: 17 years old
• Asymptomatic
• o/e = Normal
• Personal history (-)
• Family history (-)
HCM
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ESCHCM
GUIDELINES
2014
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MRI IN HCM
• GUIDELINES 2014
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CMR – how to use information
Fibrosis in Hypertrophic Cardiomyopathy– does it have prognostic implications?
In 2/3 of HCM pts there is myocardial fibrosis
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LA >45mm
ESC
GUIDELINES
IN HCM 2014
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HYPERTROPHIC CARDIOMYOPATHY
INTERVENTION IN SYMPTOMATIC CASES
HOCM
DDDR
ABLATION
MYECTOMY
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HCM
SYMPTOMSLVOT gr<50 mmHg
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EXERCISE
ECHO
HCM
2014
PROVOKED LVOT gradient
70% HCM pts
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ECHO-
DOPPLER
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The echocardiographer challenge
First branch Second branch
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LVOTgradientbefore and after the procedure
F/U
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MRBEFORE AND AFTER SEPTAL ABLATION
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3 D TOEMV STRUCTURAL ABNORMALITIES
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TOE
ESCHCM
GUIDELINES
2014
GUIDING THE MYECTOMY
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The Diagnosis of inherited cardiac disease concerns
the Patient and the Family
HYPERTROPHIC CARDIOMYOPATHY
• Cardiology
• PediatricsGenetics
MOLECULAR
CARDIOLOGY
Family Screening
Typical
form
Subclinical
form
Gene
carrier
Follow up
every year
Relatives that
have not been
genotyped
>20 years of age
Follow up
every 3 years
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SUBCLINICAL FORM OF HCM DUE TO EVOLUTION
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Mutation:
Arg286Cys
Q waves
CONCEALED FORM OF HCM DUE TO SUBCLINICAL EXPRESSION
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CMR With Late Gadolinium Enhancement in Genotype Positive–Phenotype Negative Hypertrophic Cardiomyopathy
Ethan J. Rowin et al., JACC, 2012
Ιn G+P- HCM patients, cardiac magnetic resonance (CMR) identified substantial late gadolinium enhancement (LGE) indicative of myocardial fibrosis (structural abnormality)
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LVH
LVOT gr
LA
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ESC
GUIDELINES
IN HCM
2014
Holds for typical hypertrophic cardiomyopathy > 16 years of age and not
for special types of HCM - phenocopies
MRI – Fibrosis
Apical aneurysm
EF < 50%
Double mutation
Abnormal blood
pressure response
Electrophysiological
Test (EPS)
Modifiers
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HCM APICAL ANEURYSMHCM- AHA 2011
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MRI IN HCM
• GUIDELINES 2014
CMR IN HCM 2 STANDAR
DEVIATION TECHNIC
LGE>15-20%SIGNIFICANT
B MARON 2014
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DCM
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EVALUATION OF GLOBAL
BIVENTRICULAR FUNCTION
IS ESSENTIAL FOR ADEQUATE PTS EVALUATION
EF , LV VOLUME , LV MASS
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DD OF LGE AT CARDIAC MRI BY LOCATION
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ACUTE VS CHRONIC INJURIES
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In patients with depressed ejection fraction, lack of a
substantial (five segments or more) viability response to
dobutamine stress echocardiography is invariably associated
with a lack of response to CRT
• In other words, it is unlikely that home comfort
will benefit from a brand-new electric system if
there are no walls and no ceiling left.
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DCM AND SUDDEN DEATH
• Few parameters have been identified as good predictors of SCD in DCM pts
• EF
• Syncope
Keogh et al AJC 1990
Knight et al JACC 1999
Task Force on SCD/ESC 2002
Task Force on SCD- Arrhythmia/ESC 2006
fibrosis
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MRI in DCMFIBROSIS AND SUDDEN DEATH
JAMA
2013
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DCM Clinical Spectrum
Preclinical or Early phase
(Relative of patients with DCM or Hypokinetic Non Dilated CM)
Clinical phase
Dilated CM
(LV Dilation + Hypokinesia)
(DCMD-H)
Hypokinetic Non Dilated CM
(Hypokinesia/no Dilation)
(HNDCM or DCMND-H)
Arrhythmic CM
(Arrhythmias or conduction defect)
^
(DCMND-NH-A/CD,with
or without mut+AHA+ )
IsolatedVentricular Dilation
(Dilation/no
Hypokinesia)*^
(DCMD-NH, with or
without mut+AHA+ )
No cardiac expression
(Mutation carrierand/or AHA positive)
(no LV abn, no arrhythmia)
^(DCMND-NH-Mut+AHA+)
Progressive expression of the phenotype
*Shown by two independent imaging modalities, ^mutation carrier or not; anti-heart autoantibody (AHA) positive or negative
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HYPOKINETIC NON DILATED CARDIOMYOPATHYHNDC
Hypokinetic non-dilated cardiomyopathy
► Left ventricular or biventricular systolic dysfunction
without dilatation (defined as LVEF < 45%), not explained
by abnormal loading conditions or coronary artery disease.
Note:
► Strictly decreased LVEF is mandatory in index patient with
HNDC since no combination with dilatation is mandatory for the
diagnosis.
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POST MORTEM DATA
NORMAL STRUCTURALLY HEART
NORMAL CORONARY ARTERIES
SEGMENTAL OR REGIONAL FIBROSIS WITHOUT
SPECIFIC HISTOLOGICAL FINDINGS
UNEXPLAINED OR VAGUE AETIOLOGY
SUDDEN DEATH
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ECG:
3 years ago
PR= 200msec
Ι
ΙΙ
ΙΙΙ
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Ι
ΙΙ
ΙΙΙ
Male, 28 years of age
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HNDC
PLN
ANGIO NORMAL
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+
28y - SCD
AY
76y
Reported normal
Ca
6 brothers
alive60y
CaCa Ca
40d
= Person with indication of cardiomyopathy
= Normal person
+ = Person that was genetically tested and a mutation was identified
= SCD – Rest ECG abnormalities
85y70y
No
cardiac
reason
94y
Arrhythmia
(?)
Dyslipidemia
ΑΥ – 80y>90y 90y
+
-
- = Person that was genetically tested and a mutation was not identified
FAMILY CLINICOGENETIC APPROACH
Disease causative
genetic mutation
p.Arg25Cys
of gene PLN
(phospholabane)
Mild DCMarrhythmogenic
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ACM
Concealed phase
Overt phase
Advanced disease
ARVC ALVC
AFFECTS
LV
FIRST
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ALVC
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PTS CLINICAL PROFILEACM / DCM OR MYOCARDITIS?
• INVERTED T WAVES IN INFERIOR/LATERAL LEADS : MINOR• S-A-ECG (+) MINOR• SD IN THE FAMILY – FATHER : MINOR• HOLTER : 600VE’ S/24 h ARRHYTHMIAS: MINOR
• Mild left ventricular dilation and/or systolic impairment• Early arrhythmogenesis
• PREDOMINANT LV INVOLVEMENT - subepicardial fibrosis
• ACM /ALVC
Sen-Chowdry et al, JACC 2008
FAMILIAL ELEMENTSCD
MYOCARDITIS
ARRHYTHMOGENESIS
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= Unaffected person
= Individual with structural abnormalities – myocardial fibrosis
73y60y
ΑΕΕ
44y
SD 14y
SD 43y
SD – CAD?
35y ago 40y
+ = Mutation positive individual
+
CLINICO – GENETIC APPROACH
++
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2012 2016
2012: 50 VEs/24 h 2016 : 6.000 VEs/24h
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3,4
1,6 1,61,7
1,9
2,3
4,8
3,6
5,9
3,2
4,5
0,10,2
4,7
12,1
10,0
1,2
2,7
1,2
1,7
3,1
0,8
0,6
6,1
5,0
5,3
4,2
0,7
0,9
0,2
0,0 0,0
0,4
1,8
0,8
1,0
1,6
0,4
0,1
1,7
0,8
1,7
0,9
8,7
6,0
0,1 0,0 0,0
0
2
4
6
8
10
12
14
Me
rlo
-14
Gu
lati-1
3
Gu
lati-1
3
Me
rlo
-11
Gri
mm
-03
Me
rlo
-13
He
rma
n-1
2
Pa
so
tti-
08
Va
n R
ijsin
ge
n-1
2
Va
n R
ijsin
ge
n-1
4
Va
n d
er
Zw
aa
g-1
2
Wa
hb
i-1
2
Bh
akta
-11
Co
nn
uck-0
8
Co
nn
uck-0
8
Die
go
li-1
1
HFD-HTx annual rate
SD-ICD annual rate
SD-ICD/HFD-HTx ratio
Large general DCM series,
(non-genotyped)
Sarcomeric LMNA PLN
MD1
Duchenne
Becker
Titin
% per year
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Isolated non ischemic LV LGE with a stria pattern
may be associated with life-threatening arrhythmias
and sudden death in the athlete.
Because of its subepicardial / midmyocardial location, LV
scar is often not detected by echocardiography.
Circ Arrhythm Electrophysiol. 2016
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T1 LGE LGE
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MYOCARDITISINHERITED
CARDIOMYOPATHY
EXERSICE
INDUCED
TRAUMA
GENETICS
CIRCULATION 2016
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TAKE HOME MESSAGEHCM - DCM
IMAGING ESSENTIAL
► Diagnosis ( part of the spectrum)
► Mechanisms of symptoms
► Risk stratification
► Decide how treat symptoms