360 research outputs found
A model based on clinical parameters to identify myocardial late gadolinium enhancement by magnetic resonance in patients with aortic stenosis: An observational study
Objective With increasing age, the prevalence of aortic stenosis grows exponentially, increasing left heart pressures and potentially leading to myocardial hypertrophy, myocardial fibrosis and adverse outcomes. To identify patients who are at greatest risk, an outpatient model for risk stratification would be of value to better direct patient imaging, frequency of monitoring and expeditious management of aortic stenosis with possible earlier surgical intervention. In this study, a relatively simple model is proposed to identify myocardial fibrosis in patients with a diagnosis of moderate or severe aortic stenosis. Design Patients with moderate to severe aortic stenosis were enrolled into the study; patient characteristics, blood work, medications as well as transthoracic echocardiography and cardiovascular magnetic resonance were used to determine potential identifiers of myocardial fibrosis. Setting The Royal Brompton Hospital, London, UK Participants One hundred and thirteen patients in derivation cohort and 26 patients in validation cohort. Main outcome measures Identification of myocardial fibrosis. Results Three blood biomarkers (serum platelets, serum urea, N-terminal pro-B-type natriuretic peptide) and left ventricular ejection fraction were shown to be capable of identifying myocardial fibrosis. The model was validated in a separate cohort of 26 patients. Conclusions Although further external validation of the model is necessary prior to its use in clinical practice, the proposed clinical model may direct patient care with respect to earlier magnetic resonance imagining, frequency of monitoring and may help in risk stratification for surgical intervention for myocardial fibrosis in patients with aortic stenosis
Aortic valve stenosis-multimodality assessment with PET/CT and PET/MRI
Aortic valve disease is the most common form of heart valve disease in developed countries and a growing healthcare burden with an ageing population. Transthoracic and transoesophageal echocardiography remains central to the diagnosis and surveillance of patients with aortic stenosis, providing gold standard assessments of valve haemodynamics and myocardial performance. However, other multimodality imaging techniques are being explored for the assessment of aortic stenosis, including combined PET/CT and PET/MR. Both approaches provide unique information with respect to disease activity in the valve alongside more conventional anatomic assessments of the valve and myocardium in this condition. This review investigates the emerging use of PET/CT and PET/MR to assess patients with aortic stenosis, examining how the complementary data provided by each modality may be used for research applications and potentially in future clinical practice
Assessment of aortic stenosis using modern non-invasive imaging techniques
Introduction.
Aortic
stenosis
is
characterised
both
by
progressive
narrowing
of
the
valve
and
the
hypertrophic
response
of
the
left
ventricle.
The
purpose
of
this
thesis
was
to
study
the
contribution
of
inflammation
and
calcification
to
valve
narrowing
using
Positron
Emission
and
Computed
Tomography
(PET/CT)
and
to
investigate
the
hypertrophic
response
using
cardiovascular
magnetic
resonance
(CMR).
Methods.
PET/CT
studies.
Patients
with
aortic
sclerosis
and
mild,
moderate
and
severe
stenosis
were
prospectively
compared
to
matched
control
subjects.
Aortic
valve
severity
was
determined
by
echocardiography.
Calcification
and
inflammation
in
the
aortic
valve
and
coronary
arteries
were
assessed
by
sodium
18-Ââfluoride
(18F-ÂâNaF)
and
18-Ââfluorodeoxyglucose
(18F-ÂâFDG)
uptake
using
PET.
CMR
studies.
Consecutive
patients
with
moderate
or
severe
aortic
stenosis
undergoing
CMR
were
enrolled
into
a
registry.
Patients
who
received
gadolinium
contrast
were
categorised
into
absent,
mid-Ââ
wall
or
infarct
patterns
of
late
gadolinium
enhancement
(LGE)
by
blinded
independent
observers.
Patients
follow-Ââup
was
completed
using
patient
questionnaires,
source
record
data
and
the
National
Strategic
Tracing
Scheme.
After
excluding
those
patients
with
concomitant
triggers
to
LV
remodeling,
the
extent
and
patterns
of
hypertrophy
were
investigated
based
upon
measurements
of
indexed
LV
mass,
indexed
LV
volume
and
the
relative
wall
mass.
Results.
PET/CT
studies.
121
subjects
(20
controls;
20
aortic
sclerosis;
25
mild,
33
moderate
and
23
severe
aortic
stenosis)
were
studied.
Quantification
of
tracer
uptake
within
the
valve
demonstrated
excellent
inter-Ââobserver
reproducibility
with
no
biases
and
limits
of
agreement
of
±0.21
(18F-ÂâNaF)
and
±0.13
(18F-ÂâFDG)
for
maximum
tissue-Ââto-Ââbackground
ratios
(TBR).
Activity
of
both
tracers
was
higher
in
patients
with
aortic
stenosis
than
control
subjects
(18F-ÂâNaF:
2.87±0.82
vs
1.55±0.17;
18F-Ââ
FDG:
1.58±0.21
vs
1.30±0.13;
both
P<0.001).
18F-ÂâNaF
uptake
displayed
a
progressive
rise
with
valve
severity
(r2=0.540,
P<0.001)
with
a
more
modest
increase
observed
for
18F-ÂâFDG
(r2=0.218;
P<0.001).
Amongst
patients
with
aortic
stenosis,
91%
had
increased
18F-ÂâNaF
(>1.97)
and
35%
increased
18F-Ââ
FDG
(>1.63)
uptake.
Increased
18F-ÂâNaF
uptake
was
also
observed
in
the
coronary
arteries
in
a
subset
of
patients
with
atherosclerosis.
These
patients
(n=40)
had
higher
rates
of
prior
cardiovascular
events
(p=0.016)
and
angina
(p=0.023),
and
higher
Framingham
risk
scores
(p=0.011).
CMR
studies.
143
patients
(aged
68±14
years;
97
male)
were
followed
up
for
2.0±1.4
years
and
27
died.
Compared
to
those
with
no
LGE
(n=49),
univariate
analysis
revealed
that
patients
with
mid-Ââwall
fibrosis
(n=54)
had
an
eight-Ââfold
increase
in
all-Ââcause
mortality
despite
similar
aortic
stenosis
severity
and
coronary
artery
disease
burden.
Patients
with
an
infarct
pattern
(n=40)
had
a
six-Ââfold
increase.
Mid-Ââwall
fibrosis
(HR
5.35
[95%
CI
1.16-Ââ24.56];
P=0.03)
emerged
as
an
independent
predictor
of
all
cause
mortality
by
multivariate
analysis.
The
pattern
of
LV
remodelling
was
studied
in
91
patients
(61±21
years;
57
male)
and
displayed
wide
variation
comprising
normal
ventricular
geometry
(n=11),
concentric
remodelling
(n=11),
asymmetric
remodelling
(n=11),
concentric
hypertrophy
(n=34),
asymmetric
hypertrophy
(n=14)
and
LV
decompensation
(n=10).
The
magnitude
of
the
hypertrophic
response
was
unrelated
to
the
severity
of
aortic
valve
narrowing.
Conclusions. Modern imaging techniques have provided important insights in to the pathology underlying aortic stenosis and suggest that valvular calcification and myocardial fibrosis have a key role. Both represent important potential targets for future therapeutic interventions
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