Biomedicines,
Journal Year:
2023,
Volume and Issue:
11(8), P. 2239 - 2239
Published: Aug. 9, 2023
The
global
action
against
coronavirus
disease
2019
(COVID-19),
caused
by
SARS-CoV-2
infection,
shed
light
on
endothelial
dysfunction.
Although
primarily
affects
the
pulmonary
system,
multiple
studies
have
documented
pan-vascular
involvement
in
COVID-19.
virus
is
able
to
penetrate
barrier,
damaging
it
directly
or
indirectly
and
causing
endotheliitis
multi-organ
injury.
Several
mechanisms
cooperate
development
of
dysfunction,
including
cell
injury
pyroptosis,
hyperinflammation
cytokine
storm
syndrome,
oxidative
stress
reduced
nitric
oxide
bioavailability,
glycocalyx
disruption,
hypercoagulability,
thrombosis.
After
acute-phase
some
patients
reported
signs
symptoms
a
systemic
disorder
known
as
long
COVID,
which
broad
range
cardiovascular
(CV)
disorders
emerged.
To
date,
exact
pathophysiology
COVID
remains
unclear:
addition
persistence
infection
mechanisms,
specific
pathways
CV
damage
been
postulated,
such
persistent
viral
reservoirs
heart
an
autoimmune
response
cardiac
antigens
through
molecular
mimicry.
aim
this
review
provide
overview
main
patterns
enduring
activation
following
offer
latest
summary
complications
COVID.
COVID-19,
with
persistent
and
new
onset
of
symptoms
such
as
fatigue,
post-exertional
malaise,
cognitive
dysfunction
that
last
for
months
impact
everyday
functioning,
is
referred
to
Long
COVID
under
the
general
category
post-acute
sequelae
SARS-CoV-2
infection
(PASC).
PASC
highly
heterogenous
may
be
associated
multisystem
tissue
damage/dysfunction
including
acute
encephalitis,
cardiopulmonary
syndromes,
fibrosis,
hepatobiliary
damages,
gastrointestinal
dysregulation,
myocardial
infarction,
neuromuscular
neuropsychiatric
disorders,
pulmonary
damage,
renal
failure,
stroke,
vascular
endothelial
dysregulation.
A
better
understanding
pathophysiologic
mechanisms
underlying
essential
guide
prevention
treatment.
This
review
addresses
potential
hypotheses
connect
long-term
health
consequences.
Comparisons
between
other
virus-initiated
chronic
syndromes
myalgic
encephalomyelitis/chronic
fatigue
syndrome
postural
orthostatic
tachycardia
will
addressed.
Aligning
identifying
potentially
regulated
common
underlining
pathways
necessary
true
nature
PASC.
The
discussed
contributors
include
from
injury
one
or
more
organs,
reservoirs
replicating
virus
its
remnants
in
several
tissues,
re-activation
latent
pathogens
Epstein-Barr
herpes
viruses
COVID-19
immune-dysregulated
environment,
interactions
host
microbiome/virome
communities,
clotting/coagulation
dysfunctional
brainstem/vagus
nerve
signaling,
dysautonomia
autonomic
dysfunction,
ongoing
activity
primed
immune
cells,
autoimmunity
due
molecular
mimicry
pathogen
proteins.
individualized
suggests
different
therapeutic
approaches
required
best
manage
specific
patients.
Trends in Endocrinology and Metabolism,
Journal Year:
2023,
Volume and Issue:
34(6), P. 321 - 344
Published: April 19, 2023
Acute
COVID-19
infection
is
followed
by
prolonged
symptoms
in
approximately
one
ten
cases:
known
as
Long
COVID.
The
disease
affects
~65
million
individuals
worldwide.
Many
pathophysiological
processes
appear
to
underlie
COVID,
including
viral
factors
(persistence,
reactivation,
and
bacteriophagic
action
of
SARS
CoV-2);
host
(chronic
inflammation,
metabolic
endocrine
dysregulation,
immune
autoimmunity);
downstream
impacts
(tissue
damage
from
the
initial
infection,
tissue
hypoxia,
dysbiosis,
autonomic
nervous
system
dysfunction).
These
mechanisms
culminate
long-term
persistence
disorder
characterized
a
thrombotic
endothelialitis,
endothelial
hyperactivated
platelets,
fibrinaloid
microclots.
abnormalities
blood
vessels
coagulation
affect
every
organ
represent
unifying
pathway
for
various
Pathology - Research and Practice,
Journal Year:
2023,
Volume and Issue:
246, P. 154497 - 154497
Published: May 3, 2023
Worldwide
there
have
been
over
760
million
confirmed
coronavirus
disease
2019
(COVID-19)
cases,
and
13
billion
COVID-19
vaccine
doses
administered
as
of
April
2023,
according
to
the
World
Health
Organization.
An
infection
with
severe
acute
respiratory
syndrome
2
(SARS-CoV-2)
can
lead
an
disease,
i.e.
COVID-19,
but
also
a
post-acute
(PACS,
"long
COVID").
Currently,
side
effects
vaccines
are
increasingly
being
noted
studied.
Here,
we
summarise
currently
available
indications
discuss
our
conclusions
that
(i)
these
specific
similarities
differences
PACS,
(ii)
new
term
should
be
used
refer
(post-COVID-19
vaccination
syndrome,
PCVS,
colloquially
"post-COVIDvac-syndrome"),
(iii)
is
need
distinguish
between
(ACVS)
(PACVS)
-
in
analogy
PACS
("long
Moreover,
address
mixed
forms
caused
by
natural
SARS-CoV-2
vaccination.
We
explain
why
it
important
for
medical
diagnosis,
care
research
use
terms
(PCVS,
ACVS
PACVS)
order
avoid
confusion
misinterpretation
underlying
causes
enable
optimal
therapy.
do
not
recommend
"Post-Vac-Syndrome"
imprecise.
The
article
serves
current
problem
"medical
gaslighting"
relation
PCVS
raising
awareness
among
professionals
supplying
appropriate
terminology
disease.
Reviews in Medical Virology,
Journal Year:
2023,
Volume and Issue:
33(2)
Published: Jan. 27, 2023
Abstract
Severe
acute
respiratory
syndrome
coronavirus
2
may
inflict
a
post‐viral
condition
known
as
post‐COVID‐19
(PCS)
or
long‐COVID.
Studies
measuring
levels
of
inflammatory
and
vascular
biomarkers
in
blood,
serum,
plasma
COVID‐19
survivors
with
PCS
versus
non‐PCS
controls
have
produced
mixed
findings.
Our
review
sought
to
meta‐analyse
those
studies.
A
systematic
literature
search
was
performed
across
five
databases
until
25
June
2022,
an
updated
on
1
November
2022.
Data
analyses
were
Review
Manager
R
Studio
statistical
software.
Twenty‐four
from
23
studies
meta‐analysed.
Higher
C‐reactive
protein
(Standardized
mean
difference
(SMD)
=
0.20;
95%
CI:
0.02–0.39),
D‐dimer
(SMD
0.27;
0.09–0.46),
lactate
dehydrogenase
0.30;
0.05–0.54),
leukocytes
0.34;
0.02–0.66)
found
than
without
PCS.
After
sensitivity
analyses,
lymphocytes
0.12–0.48)
interleukin‐6
0.12–0.49)
also
significantly
higher
cases.
No
significant
differences
noted
the
remaining
investigated
(e.g.,
ferritin,
platelets,
troponin,
fibrinogen).
Subgroup
suggested
biomarker
changes
mainly
driven
by
cases
diagnosed
via
manifestation
organ
abnormalities
rather
symptomatic
persistence,
well
duration
<6
≥6
months.
In
conclusion,
our
pinpointed
certain
associated
PCS,
which
shed
light
potential
new
approaches
understanding,
diagnosing,
treating
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: March 4, 2024
The
coronavirus
disease
2019
(COVID-19)
pandemic
caused
by
SARS-CoV-2
has
been
defined
as
the
greatest
global
health
and
socioeconomic
crisis
of
modern
times.
While
most
people
recover
after
being
infected
with
virus,
a
significant
proportion
them
continue
to
experience
issues
weeks,
months
even
years
acute
infection
SARS-CoV-2.
This
persistence
clinical
symptoms
in
individuals
for
at
least
three
onset
or
emergence
new
lasting
more
than
two
months,
without
any
other
explanation
alternative
diagnosis
have
named
long
COVID,
long-haul
post-COVID-19
conditions,
chronic
post-acute
sequelae
(PASC).
Long
COVID
characterized
constellation
disorders
that
vary
widely
their
manifestations.
Further,
mechanisms
underlying
are
not
fully
understood,
which
hamper
efficient
treatment
options.
review
describes
predictors
common
related
COVID's
effects
on
central
peripheral
nervous
system
organs
tissues.
Furthermore,
transcriptional
markers,
molecular
signaling
pathways
risk
factors
such
sex,
age,
pre-existing
condition,
hospitalization
during
phase
COVID-19,
vaccination,
lifestyle
presented.
Finally,
recommendations
patient
rehabilitation
management,
well
therapeutical
approaches
discussed.
Understanding
complexity
this
disease,
its
across
multiple
organ
systems
overlapping
pathologies
possible
paramount
developing
diagnostic
tools
treatments.
Cardiovascular Diabetology,
Journal Year:
2024,
Volume and Issue:
23(1)
Published: Feb. 20, 2024
Abstract
Early
since
the
onset
of
COVID-19
pandemic,
medical
and
scientific
community
were
aware
extra
respiratory
actions
SARS-CoV-2
infection.
Endothelitis,
hypercoagulation,
hypofibrinolysis
identified
in
patients
as
subsequent
responses
endothelial
dysfunction.
Activation
barrier
may
increase
severity
disease
contribute
to
long-COVID
syndrome
post-COVID
sequelae.
Besides,
it
cause
alterations
primary,
secondary,
tertiary
hemostasis.
Importantly,
these
have
been
highly
decisive
evolution
infected
also
diagnosed
with
diabetes
mellitus
(DM),
who
showed
previous
In
this
review,
we
provide
an
overview
potential
triggers
activation
related
under
diabetic
milieu.
Several
mechanisms
are
induced
by
both
viral
particle
itself
immune-defensive
response
(i.e.,
NF-κB/NLRP3
inflammasome
pathway,
vasoactive
peptides,
cytokine
storm,
NETosis,
complement
system).
Alterations
coagulation
mediators
such
factor
VIII,
fibrin,
tissue
factor,
von
Willebrand
factor:
ADAMST-13
ratio,
kallikrein-kinin
or
plasminogen-plasmin
systems
reported.
Moreover,
imbalance
thrombotic
thrombolytic
(tPA,
PAI-I,
fibrinogen)
factors
favors
hypercoagulation
hypofibrinolysis.
context
DM,
can
be
exacerbated
leading
higher
loss
However,
a
series
therapeutic
strategies
targeting
activated
endothelium
specific
antibodies
inhibitors
against
thrombin,
key
cytokines,
X,
system,
system
might
represent
new
opportunities
address
hypercoagulable
state
present
DM.
Antidiabetics
ameliorate
dysfunction,
inflammation,
platelet
aggregation.
By
improving
microvascular
pathology
subjects,
associated
comorbidities
risk
mortality
could
reduced.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Feb. 28, 2024
The
COVID-19
pandemic
continues
to
cause
severe
global
disruption,
resulting
in
significant
excess
mortality,
overwhelming
healthcare
systems,
and
imposing
substantial
social
economic
burdens
on
nations.
While
most
of
the
attention
therapeutic
efforts
have
concentrated
acute
phase
disease,
a
notable
proportion
survivors
experience
persistent
symptoms
post-infection
clearance.
This
diverse
set
symptoms,
loosely
categorized
as
long
COVID,
presents
potential
additional
public
health
crisis.
It
is
estimated
that
1
5
exhibit
clinical
manifestations
consistent
with
COVID.
Despite
this
prevalence,
mechanisms
pathophysiology
COVID
remain
poorly
understood.
Alarmingly,
evidence
suggests
cases
within
condition
develop
debilitating
or
disabling
symptoms.
Hence,
urgent
priority
should
be
given
further
studies
equip
systems
for
its
management.
review
provides
an
overview
available
information
emerging
condition,
focusing
affected
individuals’
epidemiology,
pathophysiological
mechanisms,
immunological
inflammatory
profiles.