Frontiers in Cardiovascular Medicine,
Год журнала:
2018,
Номер
5
Опубликована: Май 23, 2018
In
patients
with
aortic
and/or
mitral
valve
disease
the
presence
of
pulmonary
hypertension
(PH)
indicates
a
decompensated
state
left
ventricular
and
atrial
dysfunction
exhausted
compensatory
mechanism,
i.e.,
heart
failure.
Pulmonary
in
this
context
is
consequence
backwards
transmission
elevated
pressure.
form
PH,
vascular
resistance
initially
normal
(isolated
post-capillary
PH).
Depending
on
extent
chronicity
pressure
elevation
additional
remodeling
may
occur
(combined
pre-
Mechanical
interventions
for
correction
often
but
not
always
reduce
pressures.
However,
reduction
pressures
modest,
persistent
PH
these
common
marker
poor
prognosis.
present
review
we
discuss
pathophysiology
clinical
impact
disease,
comprehensive
non-invasive
invasive
diagnostic
approach
required
to
define
treatment
recent
insights
from
mechanistic
studies,
registries
randomized
provide
an
outlook
regarding
gaps
evidence,
future
challenges,
research
opportunities
setting.
European Respiratory Journal,
Год журнала:
2018,
Номер
53(1), С. 1801887 - 1801887
Опубликована: Дек. 13, 2018
Clinical
and
translational
research
has
played
a
major
role
in
advancing
our
understanding
of
pulmonary
hypertension
(PH),
including
arterial
other
forms
PH
with
severe
vascular
remodelling
(e.g.
chronic
thromboembolic
veno-occlusive
disease).
However,
remains
an
incurable
condition
high
mortality
rate,
underscoring
the
need
for
better
transfer
novel
scientific
knowledge
into
healthcare
interventions.
Herein,
we
review
recent
findings
pathology
(with
questioning
strict
morphological
categorisation
various
pre-
or
post-capillary
involvement
vessels)
cellular
mechanisms
contributing
to
onset
progression
associated
PH.
We
also
discuss
ways
improve
management
support
optimise
drug
development
this
field.
Circulation Research,
Год журнала:
2019,
Номер
124(11), С. 1598 - 1617
Опубликована: Май 23, 2019
Approximately
half
of
the
patients
with
signs
and
symptoms
heart
failure
have
a
left
ventricular
ejection
fraction
that
is
not
markedly
abnormal.
Despite
historically
initial
surprise,
heightened
risks
for
specific
major
adverse
events
occur
across
broad
range
fraction,
including
normal.
The
recognition
magnitude
problem
preserved
in
past
20
years
has
spurred
an
explosion
clinical
investigation
growing
intensity
informative
outcome
trials.
This
article
addresses
historic
development
this
component
syndrome,
epidemiology,
pathophysiology,
existing
planned
therapeutic
studies.
Looking
forward,
more
phenotyping
even
genotyping
subpopulations
should
lead
to
improvements
outcomes
from
future
European Respiratory Journal,
Год журнала:
2018,
Номер
53(1), С. 1801897 - 1801897
Опубликована: Дек. 13, 2018
Pulmonary
hypertension
(PH)
is
frequent
in
left
heart
disease
(LHD),
as
a
consequence
of
the
underlying
condition.
Significant
advances
have
occurred
over
past
5
years
since
5th
World
Symposium
on
Hypertension
2013,
leading
to
better
understanding
PH-LHD,
challenges
and
gaps
evidence.
PH
failure
with
preserved
ejection
fraction
represents
most
complex
situation,
it
may
be
misdiagnosed
group
1
PH.
Based
latest
evidence,
we
propose
new
haemodynamic
definition
for
due
LHD
three-step
pragmatic
approach
differential
diagnosis.
This
includes
identification
specific
"left
heart"
phenotype
non-invasive
probability
PH-LHD.
Invasive
confirmation
PH-LHD
based
accurate
measurement
pulmonary
arterial
wedge
pressure
and,
patients
high
probability,
provocative
testing
clarify
Finally,
recent
clinical
trials
did
not
demonstrate
benefit
treating
hypertension-approved
therapies.
New England Journal of Medicine,
Год журнала:
2021,
Номер
385(25), С. 2361 - 2376
Опубликована: Дек. 15, 2021
Without
effective
treatment,
pulmonary
arterial
hypertension
results
in
high
morbidity
and
mortality.
This
review
discusses
the
pathogenesis
of
disorder,
thorough
clinical
evaluation
required
to
establish
diagnosis,
available
therapies,
future
directions.
Circulation,
Год журнала:
2020,
Номер
141(12), С. 1001 - 1026
Опубликована: Март 23, 2020
Heart
failure
with
preserved
ejection
fraction
(HFpEF),
a
major
public
health
problem
that
is
rising
in
prevalence,
associated
high
morbidity
and
mortality
considered
to
be
the
greatest
unmet
need
cardiovascular
medicine
today
because
of
general
lack
effective
treatments.
To
address
this
challenging
syndrome,
National
Heart,
Lung,
Blood
Institute
convened
working
group
made
up
experts
HFpEF
novel
research
methodologies
discuss
gaps
prioritize
directions
over
next
decade.
Here,
we
summarize
discussion
group,
followed
by
key
recommendations
for
future
priorities.
There
was
uniform
recognition
highly
integrated,
multiorgan,
systemic
disorder
requiring
multipronged
investigative
approach
both
humans
animal
models
improve
understanding
mechanisms
treatment
HFpEF.
It
recognized
advances
basic
roles
inflammation,
macrovascular
microvascular
dysfunction,
fibrosis,
tissue
remodeling
are
needed
ideally
would
obtained
from
(1)
improved
models,
including
large
which
incorporate
effects
aging
comorbid
conditions;
(2)
repositories
deeply
phenotyped
physiological
data
human
tissue,
accessible
researchers
enhance
collaboration
advances;
(3)
methods
take
advantage
computational
multiscale
modeling
analysis
complex,
high-density
across
multiple
domains.
The
emphasized
interactions
among
basic,
translational,
clinical,
epidemiological
scientists
organ
systems
cell
types,
leveraging
different
areas
or
focus,
between
centers.
A
network
collaborative
centers
accelerate
clinical
pathobiological
strategies
discussed
as
an
example
strategy
advance
progress.
This
resource
facilitate
comprehensive,
deep
phenotyping
multicenter
patient
cohort
standardized
protocols
robust
biorepository.
priorities
outlined
document
meant
stimulate
scientific
providing
road
map
investigations
diverse
JAMA,
Год журнала:
2023,
Номер
329(10), С. 827 - 827
Опубликована: Март 14, 2023
Heart
failure
with
preserved
ejection
fraction
(HFpEF),
defined
as
HF
an
EF
of
50%
or
higher
at
diagnosis,
affects
approximately
3
million
people
in
the
US
and
up
to
32
worldwide.
Patients
HFpEF
are
hospitalized
1.4
times
per
year
have
annual
mortality
rate
15%.Risk
factors
for
include
older
age,
hypertension,
diabetes,
dyslipidemia,
obesity.
Approximately
65%
patients
present
dyspnea
physical
examination,
chest
radiographic,
echocardiographic,
invasive
hemodynamic
evidence
overt
congestion
(volume
overload)
rest.
35%
"unexplained"
on
exertion,
meaning
they
do
not
clear
physical,
echocardiographic
signs
HF.
These
elevated
atrial
pressures
exercise
measured
stress
testing
estimated
Doppler
echocardiography
testing.
In
unselected
presenting
unexplained
dyspnea,
H2FPEF
score
incorporating
clinical
(age,
obesity,
fibrillation
status)
resting
(estimated
pulmonary
artery
systolic
pressure
left
pressure)
variables
can
assist
diagnosis
(H2FPEF
range,
0-9;
>5
indicates
more
than
95%
probability
HFpEF).
Specific
causes
syndrome
normal
other
should
be
identified
treated,
such
valvular,
infiltrative,
pericardial
disease.
First-line
pharmacologic
therapy
consists
sodium-glucose
cotransporter
type
2
inhibitors,
dapagliflozin
empagliflozin,
which
reduced
hospitalization
cardiovascular
death
by
20%
compared
placebo
randomized
trials.
Compared
usual
care,
training
diet-induced
weight
loss
produced
clinically
meaningful
increases
functional
capacity
quality
life
Diuretics
(typically
loop
diuretics,
furosemide
torsemide)
prescribed
improve
symptoms.
Education
self-care
(eg,
adherence
medications
dietary
restrictions,
monitoring
symptoms
vital
signs)
help
avoid
decompensation.Approximately
HFpEF.
exercise,
self-care,
diuretics
needed
maintain
euvolemia,
obesity
European Heart Journal,
Год журнала:
2018,
Номер
39(30), С. 2780 - 2792
Опубликована: Май 8, 2018
This
review
aims
to
provide
a
translational
perspective
on
recent
developments
in
heart
failure
with
preserved
ejection
fraction
(HFpEF),
linking
mechanistic
insights
potential
therapies.
A
key
concept
this
is
that
HFpEF
haemodynamic
condition
wherein
the
fails
keep
up
circulatory
demands
of
body,
or
does
so
at
expense
raised
left
ventricular
filling
pressures.
We,
therefore,
propose
'final
common
pathway'
for
development
congestion,
i.e.
basic
mechanisms
increased
end-diastolic
pressure,
atrial
hypertension,
pulmonary
venous
and
plasma
volume
expansion,
represents
important
initial
targets
therapy
HFpEF.
Accordingly,
we
group
into
six
translating
therapies
HFpEF:
beginning
three
(left
expansion),
working
backward
molecular
[systemic
microvascular
inflammation,
cardiometabolic
functional
abnormalities,
cellular
(titin)/extracellular
(fibrosis)
structural
abnormalities].