Neuromodulation Technology at the Neural Interface,
Journal Year:
2022,
Volume and Issue:
25(3), P. 356 - 365
Published: Feb. 19, 2022
The
cardiac
autonomic
nervous
system
(CANS)
plays
an
important
role
in
the
pathophysiology
of
atrial
fibrillation
(AF).
Cardiovascular
disease
can
cause
imbalance
within
CANS,
which
may
contribute
to
initiation
and
maintenance
AF.
Increased
understanding
neuromodulation
CANS
has
resulted
novel
emerging
therapies
treat
arrhythmias
by
targeting
different
circuits
CANS.
Regarding
AF,
vagus
nerve
have
yielded
promising
outcomes.
However,
be
both
pro-arrhythmogenic
anti-arrhythmogenic.
Currently,
these
opposing
effects
stimulation
(VNS)
not
been
clearly
described.
aim
this
review
is
therefore
discuss
anti-arrhythmogenic
VNS
recent
advances
clinical
practice
provide
future
perspectives
for
AF.A
comprehensive
current
literature
on
its
tissue
was
performed.
Both
experimental
studies
are
reviewed
discussed
separately.VNS
exhibits
effects.
anatomical
site
settings
during
play
a
crucial
determining
effect
electrophysiology.
Since
last
decade,
there
accumulating
evidence
from
randomized
that
low-level
(LLVNS),
below
bradycardia
threshold,
effective
treatment
AF.LLVNS
therapeutic
modality
AF
further
research
will
elucidate
underlying
mechanisms,
optimal
settings,
apply
LLVNS.
British Journal of Anaesthesia,
Journal Year:
2024,
Volume and Issue:
132(4), P. 653 - 666
Published: Jan. 22, 2024
Assay-specific
increases
in
circulating
cardiac
troponin
are
observed
20–40%
of
patients
after
noncardiac
surgery,
depending
on
patient
age,
type
and
comorbidities.
Increased
is
consistently
associated
with
excess
morbidity
mortality
surgery.
Despite
these
findings,
the
underlying
mechanisms
unclear.
The
majority
interventional
trials
have
been
designed
premise
that
ischaemic
disease
drives
elevated
perioperative
concentrations.
We
consider
data
showing
surgery
could
be
a
nonspecific
marker
cardiomyocyte
stress.
Elevated
concentrations
reflect
coordinated
pathological
processes
underpinning
organ
injury
not
necessarily
caused
by
ischaemia.
Laboratory
studies
suggest
matching
coronary
artery
autoregulation
myocardial
perfusion–contraction
coupling
limit
impact
systemic
haemodynamic
changes
myocardium,
2
ischaemia
might
likeliest
explanation
for
elevation
period
triggers
multiple
cause
to
cross
sarcolemma.
A
two-hit
model
involving
two
or
more
including
inflammation,
strain,
adrenergic
stress,
autonomic
dysfunction
exacerbate
initiate
acute
directly
absence
cell
death.
Consideration
diverse
pivotal
design
interpretation
trials.
Circulation Research,
Journal Year:
2024,
Volume and Issue:
134(10), P. 1348 - 1378
Published: May 9, 2024
Loss
or
dysregulation
of
the
normally
precise
control
heart
rate
via
autonomic
nervous
system
plays
a
critical
role
during
development
and
progression
cardiovascular
disease-including
ischemic
disease,
failure,
arrhythmias.
While
clinical
significance
regulating
changes
in
rate,
known
as
chronotropic
effect,
is
undeniable,
mechanisms
controlling
these
remain
not
fully
understood.
Heart
acceleration
deceleration
are
mediated
by
increasing
decreasing
spontaneous
firing
pacemaker
cells
sinoatrial
node.
During
transition
from
rest
to
activity,
sympathetic
neurons
stimulate
activating
β-adrenergic
receptors
intracellular
cyclic
adenosine
monophosphate.
The
same
signal
transduction
pathway
targeted
positive
drugs
such
norepinephrine
dobutamine,
which
used
treatment
cardiogenic
shock
severe
failure.
monophosphate-sensitive
hyperpolarization-activated
current
(I
Bioelectronic Medicine,
Journal Year:
2020,
Volume and Issue:
6(1)
Published: Nov. 24, 2020
Abstract
COVID-19
has
left
mankind
desperately
seeking
how
to
manage
dramatically
rising
infection
rates
associated
with
severe
disease
progressions.
courses
range
from
mild
symptoms
up
multiple
organ
failure
and
death,
triggered
by
excessively
high
serum
cytokine
levels
(IL
1β,
IL
6,
TNF
α,
8).
The
vagally
driven
cholinergic
anti-inflammatory
pathway
(CAP)
stops
the
action
of
nuclear
factor
κB
(NF-κB),
transcriptional
pro-inflammatory
cytokines.
Thus,
well-balanced
release
depends
on
adequate
vagal
signaling.
Coronaviruses
replicate
using
NF-κB
as
well.
By
degrading
cytoplasmatic
inhibitor
subunits
(IκB),
coronaviruses
induce
unrestricted
expression
accelerating
both,
virus
replication
transcription.
We
hypothesize
that
CAP
detriment
due
depressed
tone
critically
determines
severity
COVID-19.
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(23), P. 9005 - 9005
Published: Nov. 27, 2020
Cardiac
autonomic
neuropathy
(CAN)
is
one
of
the
earliest
complications
type
2
diabetes
(T2D),
presenting
a
silent
cause
cardiovascular
morbidity
and
mortality.
Recent
research
relates
pathogenesis
disease
in
T2D
to
an
ensuing
chronic,
low-grade
proinflammatory
pro-oxidative
environment,
being
hallmark
metabolic
syndrome.
Metabolic
inflammation
emerges
as
adipose
tissue
inflammatory
changes
extending
systemically,
on
advent
hyperglycemia,
reach
central
regions
brain.
In
light
glucose
insulin
homeostasis,
dysbiosis
or
alteration
gut
microbiome
(GM)
emerges,
further
contributing
processes
through
increased
blood–brain
barrier
permeability.
Interestingly,
studies
reveal
that
determinants
oxidative
stress
progression
exist
at
crossroad
CAN
manifestations,
dictating
their
evolution
along
natural
course
development.
Indeed,
sympathetic
parasympathetic
deterioration
was
shown
correlate
with
markers
adipose,
vascular,
systemic
inflammation.
Additionally,
evidence
points
out
could
promote
sympatho-excitatory
state
differentially
affecting
secretion
hormones
neuromodulators,
such
norepinephrine,
serotonin,
γ-aminobutyric
acid,
acting
renin–angiotensin–aldosterone
axis.
Emerging
neuronal
concomitant
autophagic
defects
brainstem
nuclei
were
described
possible
underlying
mechanisms
experimental
models
syndrome
T2D.
Drugs
anti-inflammatory
characteristics
provide
potential
avenues
for
targeting
pathways
involved
initiation
progression.
The
aim
this
review
delineate
etiology
context
disorder
characterized
by
elevated
load.
Neuromodulation Technology at the Neural Interface,
Journal Year:
2022,
Volume and Issue:
25(3), P. 356 - 365
Published: Feb. 19, 2022
The
cardiac
autonomic
nervous
system
(CANS)
plays
an
important
role
in
the
pathophysiology
of
atrial
fibrillation
(AF).
Cardiovascular
disease
can
cause
imbalance
within
CANS,
which
may
contribute
to
initiation
and
maintenance
AF.
Increased
understanding
neuromodulation
CANS
has
resulted
novel
emerging
therapies
treat
arrhythmias
by
targeting
different
circuits
CANS.
Regarding
AF,
vagus
nerve
have
yielded
promising
outcomes.
However,
be
both
pro-arrhythmogenic
anti-arrhythmogenic.
Currently,
these
opposing
effects
stimulation
(VNS)
not
been
clearly
described.
aim
this
review
is
therefore
discuss
anti-arrhythmogenic
VNS
recent
advances
clinical
practice
provide
future
perspectives
for
AF.A
comprehensive
current
literature
on
its
tissue
was
performed.
Both
experimental
studies
are
reviewed
discussed
separately.VNS
exhibits
effects.
anatomical
site
settings
during
play
a
crucial
determining
effect
electrophysiology.
Since
last
decade,
there
accumulating
evidence
from
randomized
that
low-level
(LLVNS),
below
bradycardia
threshold,
effective
treatment
AF.LLVNS
therapeutic
modality
AF
further
research
will
elucidate
underlying
mechanisms,
optimal
settings,
apply
LLVNS.