Deleted Journal,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 10, 2025
Zusammenfassung
Geschlechterspezifische
Unterschiede
im
Lipidstoffwechsel
sind
vor
allem
hormonell
bedingt.
Frauen
haben
prämenopausal
Vergleich
zu
Männern
tendenziell
günstigere
Lipidwerte,
wie
höhere
Konzentrationen
an
High-Density-Lipoprotein-Cholesterin
(HDL-C)
und
niedrigere
Low-Density-Lipoprotein-Cholesterin
(LDL-C).
Mit
Beginn
der
Menopause
verschlechtern
sich
diese
Werte
jedoch
durch
hormonelle
Veränderungen,
wodurch
bei
das
Risiko
für
atherosklerotische
Herz-Kreislauf-Erkrankungen
erhöht.
Trotz
vergleichbarer
Wirksamkeit
lipidsenkender
Therapien
zeigen
mehrere
Studien
einheitlich,
dass
seltener
die
empfohlenen
LDL-C-Zielwerte
erreichen.
Besonders
in
klinischen
Praxis
bestehen
große
Diskrepanzen
zwischen
Leitlinienempfehlungen
tatsächlicher
Behandlung,
Hochrisikopatientinnen.
Verschiedene
Barrieren
tragen
wesentlich
dazu
bei:
Dazu
gehören
Unterschätzung
des
Risikos
behandelnde
Ärzte,
ein
zurückhaltenderes
Verordnungsverhalten,
eingeschränktes
Bewusstsein
Notwendigkeit
einer
Therapie
Patientinnen
sowie
eine
verminderte
Medikamentenadhärenz.
Letztere
wird
unter
anderem
stärkere
Wahrnehmung
von
Nebenwirkungen
Prävalenz
Statinintoleranz
beeinflusst.
Die
Betreuung
spezialisierten
Lipidzentren
zeigt,
viele
schwer
einstellbare
Patienten,
z.
B.
Patienten
mit
oder
hohen
LDL-C-Ausgangswerten,
gezielter
Nachsorge
erfolgreich
behandelt
werden
können.
Neue
pharmakologische
Ansätze
Kombinationstherapien
ermöglichen
es,
Therapieziele
Dennoch
erreichen
trotz
solcher
Maßnahmen
ihre
LDL-Zielwerte,
was
auf
intensiverer
geschlechtersensibler
Strategien
hinweist.
Eine
wirksame
Lipidtherapie
erfordert
verstärkt
den
Einsatz
Kombinationstherapien,
regelmäßige
Kontrollen
enge
Zusammenarbeit
Patient
Arzt.
ist
es
entscheidend,
Therapieadhärenz
verbessern
mögliche
konsequent
anzugehen,
um
kardiovaskuläre
effektiv
senken.
Biomedicines,
Journal Year:
2024,
Volume and Issue:
12(5), P. 978 - 978
Published: April 29, 2024
Recent
studies
of
Cardiovascular-Kidney-Metabolic
Syndrome
(CKMS)
indicate
that
elevated
concentrations
derivatives
phospholipids
(ceramide,
sphingosine),
oxidized
LDL,
and
lipoproteins
(a,
b)
are
toxic
to
kidney
heart
function.
Energy
production
for
renal
proximal
tubule
resorption
critical
fuels
electrolytes
is
required
homeostasis.
Cardiac
energy
ventricular
contraction/relaxation
preferentially
supplied
by
long
chain
fatty
acids.
Metabolism
acids
accomplished
within
the
cardiomyocyte
cytoplasm
mitochondria
means
glycolytic,
tricarboxylic
acid,
electron
transport
cycles.
Toxic
lipids
excessive
lipid
may
inhibit
cardiac
contraction
requires
calcium
movement
from
sarcoplasmic
reticulum
a
high
low
concentration
at
relatively
cost.
relaxation
involves
return
lower
higher
more
consumption.
Diastolic
dysfunction
occurs
when
conversion
inadequate.
diminished
ATP
availability
in
presence
inadequate
blood
pressure,
glycemia,
or
control
lead
failure.
Similar
disruption
tubular
fuels/electrolytes
has
been
found
be
associated
with
phospholipid
(sphingolipid)
accumulation.
Elevated
tissue
low-density
lipoprotein
cholesterols
loss
filtration
efficiency
level
glomerular
podocyte.
Macroscopically
deposits
epicardial
intra-nephric
adipose
vascular
pathology,
fibrosis,
inhibition
essential
functions
both
kidney.
Chronic
triglyceride
accumulation
fibrosis
liver,
structures.
Successful
kidney,
allograft
these
vital
organs
does
not
eliminate
risk
toxicity.
Lipid
lowering
therapy
assist
protecting
organ
function
before
after
transplantation.
European Heart Journal Open,
Journal Year:
2024,
Volume and Issue:
4(5)
Published: Aug. 31, 2024
Abstract
Aims
Lipoprotein(a)
[Lp(a)]
levels
are
predominantly
genetically
determined
and
repeat
measurements
generally
considered
unlikely
to
be
clinically
useful.
However,
the
temporal
variation
of
Lp(a)
is
not
well
characterized.
Our
aim
was
determine
intra-individual
variability
whether
a
repeated
measure
reclassified
Lp(a)-specific
cardiovascular
risk
using
European
Atherosclerosis
Society
(EAS)
consensus
statement
categories.
Methods
results
This
retrospective
cohort
study
analysed
initial
serum
measured
same
methodology
from
609
individuals
in
Nashville
Biosciences
database,
de-identified
electronic
medical
records
database.
Baseline
follow-up
paired
values
were
significantly
different
(P
<
0.05),
with
an
absolute
change
≥10
mg/dL
38.1%
[95%
CI
34.2–42%]
>25%
40.5%
36.6–44.3%]
individuals.
Although
categories
those
whose
EAS
low-risk
high-risk
did
change,
53%
intermediate
‘grey-zone’
category
transitioned
either
(20%)
or
(33%)
category.
Black
exhibited
greater
than
White
women
men.
There
positive
correlation
between
baseline
changes
Lp(a),
(r
=
0.59,
P
0.01).
Conclusion
Temporal-related
present
many
A
may
allow
more
precise
prediction
for
value
EAS-defined
should
included
calculating
expected
effect
sizes
future
clinical
research
studies
targeting
Lp(a).
Journal of Atherosclerosis and Thrombosis,
Journal Year:
2024,
Volume and Issue:
31(6), P. 854 - 860
Published: April 12, 2024
Atherosclerosis
begins
with
the
infiltration
of
cholesterol-containing
lipoproteins
into
arterial
wall.
White
blood
cell
(WBC)-associated
inflammation
follows.
Despite
decades
research
using
genetic
and
pharmacologic
methods
to
alter
WBC
function,
in
humans,
most
effective
method
prevent
initiation
progression
disease
remains
low-density
lipoprotein
(LDL)
reduction.
However,
additional
approaches
reducing
cardiovascular
would
be
useful
as
residual
risk
events
continues
even
currently
LDL-reducing
treatments.
Some
this
may
due
vascular
toxicity
triglyceride-rich
(TRLs).
Another
option
is
that
LDL
transcytosis
continues,
albeit
at
reduced
rates
lower
circulating
levels
lipoprotein.
This
review
will
address
these
two
topics.
The
evidence
TRLs
promote
atherosclerosis
processes
allow
taken
up
by
endothelial
cells
leading
their
accumulation
subendothelial
space.
European Journal of Preventive Cardiology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: July 20, 2024
Abstract
Recent
trends
indicate
a
concerning
increase
in
early-onset
atherosclerotic
cardiovascular
disease
(ASCVD)
among
younger
individuals
(men
aged
<55
years
women
<65
years).
These
findings
highlight
the
pathobiology
of
ASCVD
as
process
that
begins
early
life
and
underscores
need
for
more
tailored
screening
methods
preventive
strategies.
Increasing
attention
has
been
placed
on
growing
burden
traditional
cardiometabolic
risk
factors
young
while
also
recognizing
unique
mediate
pre-mature
atherosclerosis
this
demographic
such
substance
use,
socioeconomic
disparities,
adverse
pregnancy
outcomes,
chronic
inflammatory
states
contribute
to
increasing
incidence
ASCVD.
Additionally,
mounting
evidence
pointed
out
significant
disparities
diagnosis
management
outcomes
based
sex
race.
Moving
towards
personalized
approach,
emerging
data
technological
developments
using
diverse
tools
polygenic
scores
coronary
artery
calcium
scans
have
shown
potential
earlier
detection
risk.
Thus,
we
review
current
causal
drive
improve
assessment
individuals.
Circulation,
Journal Year:
2025,
Volume and Issue:
151(6), P. 400 - 415
Published: Feb. 10, 2025
Atherosclerotic
cardiovascular
disease
is
a
major
health
concern
worldwide
and
requires
effective
preventive
measures.
Lp(a)
(lipoprotein
[a])
has
recently
garnered
attention
as
an
independent
risk
factor
for
astherosclerotic
disease,
with
proinflammatory
prothrombotic
mechanisms
contributing
to
its
atherogenicity.
On
equimolar
basis,
~5
6
times
more
atherogenic
than
particles
that
have
been
widely
associated
adverse
outcomes,
such
LDL
(low-density
lipoprotein).
can
enter
the
vessel
wall,
leading
accumulation
of
oxidized
phospholipids
in
arterial
intima,
which
are
crucial
initiating
plaque
inflammation
triggering
vascular
progression.
In
addition,
may
cause
atherothrombosis
through
interactions
between
apoA
(apolipoprotein
A)
platelet
PAR-1
(protease-activated
receptor
1)
receptor,
well
competitive
inhibition
plasminogen.
Because
mostly
determined
on
genetic
bases,
1-time
assessment
lifetime
suffice
identify
patients
elevated
levels.
Mendelian
randomization
studies
post
hoc
analyses
randomized
trials
cholesterol–lowering
drugs
showed
causal
link
concentrations
therapeutic
reduction
expected
contribute
estimated
mitigation.
Many
Lp(a)-lowering
drugs,
including
monoclonal
antibodies,
small
interfering
ribonucleic
acids,
antisense
oligonucleotides,
molecules,
gene
editing
compounds,
at
different
stages
clinical
investigation
show
promise
use.
particular,
increased
testing
treatment
substantial
impact
population
level,
enabling
identification
high-risk
individuals
subsequent
prevention
large
number
events.
Ongoing
phase
3
will
further
elucidate
benefits
over
long
term,
offering
potential
avenues
targeted
interventions
improved
outcomes.
American Journal of Preventive Cardiology,
Journal Year:
2025,
Volume and Issue:
21, P. 100945 - 100945
Published: Feb. 14, 2025
Lipoprotein(a)
[Lp(a)]
is
a
genetically
inherited,
independent
risk
factor
for
cardiovascular
disease
(CVD),
affecting
approximately
20-25%
of
the
global
population.
Elevated
Lp(a)
levels
are
associated
with
2-3-fold
increased
myocardial
infarction
and
aortic
valve
stenosis,
comparable
to
seen
in
individuals
familial
hypercholesterolemia.
Despite
its
clinical
relevance,
integration
screening
into
routine
practice
has
been
limited
by
inconsistent
measurement
techniques
lack
targeted
treatments.
Recent
advancements,
including
improved
assays
development
potential
Lp(a)-lowering
therapies,
have
renewed
focus
on
importance
screening.
This
review
aims
clarify
role
health
examining
current
evidence
who
should
be
screened,
when
occur,
most
accurate
methods
measuring
Lp(a).
Key
recommendations
include
universal,
one-time
adults,
selective
high-risk
pediatric
patients,
special
considerations
conditions
such
as
hypercholesterolemia
chronic
kidney
disease.
Advances
assay
technology
now
allow
more
precise
measurement,
supporting
better
stratification.
Additionally,
emerging
therapies
that
specifically
target
elevated
could
lead
personalized
management
CVD
risk.
Our
findings
support
assessment,
highlighting
improve
early
detection
prevention
strategies
across
diverse
patient
populations.