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LINKING IMMUNE ACTIVATION TO ACUTE EVENTS IN CHRONIC HEART FAILURE
PATIENTS
Khasanova
Zarnigor
Kurbanovna
Bukhara
Branch
of
the
Republican
Scientific
Center
for
Emergency
Medical
Care
Rakhimov Tokhirjon Ganievich
Fergana Medical Institute of Public Health, Fergana, Uzbekistan
Eminov Ravshanjon Ikromjon Ugli
Fergana Medical Institute of Public Health, Fergana, Uzbekistan
Abstract:
This
study
investigates
the
role
of
inflammatory
cytokines
in
the
acute
decompensation
of
chronic
heart
failure
(CHF).
A
total
of
56
patients
were
observed
over
three
years
at
the
Bukhara
Branch
of
the
Republican
Scientific
Center
for
Emergency
Medical
Care.
Cytokine
profiling
showed
significantly
elevated
levels
of
TNF-α,
IL-6,
and
IL-1β
in
acutely
decompensated
CHF
patients
compared
to
stable
ones.
These
levels
correlated
with
worsened
clinical
status,
including
higher
NYHA
class
and
NT-proBNP.
The
results
suggest
that
cytokine
activation
is
closely
associated
with
myocardial
stress
and
can
serve
as
a
marker
for
early
decompensation.
Targeted
anti-inflammatory
therapies,
particularly
IL-1
inhibitors,
may
improve
outcomes.
Cytokine
profiling,
therefore,
holds
promise
as
both
a
diagnostic
and
therapeutic
tool
in
CHF
management.
Keywords:
cytokines,
heart
failure,
inflammation,
IL-6,
TNF-α
Introduction
Inflammatory
biomarkers
play
a
crucial
role
in
predicting
acute
decompensation
in
chronic
heart
failure
(CHF)
patients,
offering
significant
implications
for
personalized
treatment
strategies.
These
biomarkers,
including
high-sensitivity
C-reactive
protein
(hsCRP),
soluble
ST2
(sST2),
galectin-3,
interleukin-6
(IL-6),
and
growth
differentiation
factor-15
(GDF-15),
are
associated
with
the
pathogenesis
and
progression
of
heart
failure
(HF)
and
have
been
linked
to
adverse
outcomes
in
both
chronic
and
acute
settings[1]
[6].
In
particular,
sST2
and
galectin-3
are
recommended
for
clinical
use
due
to
their
ability
to
track
treatment
responses
and
predict
mortality
in
HF
patients[1].
The
pan-
immune
inflammation
value
(PIV),
a
composite
score
based
on
blood
counts,
has
emerged
as
a
potent
predictor
of
in-hospital
mortality
in
acute
heart
failure
(AHF)
patients,
outperforming
other
inflammatory
markers[7]
[10].
This
suggests
that
PIV
could
be
integrated
into
clinical
models
to
enhance
prognostic
accuracy
and
guide
therapeutic
decisions.
Furthermore,
the
CRP/albumin
ratio
has
been
shown
to
predict
hospitalization
risk
for
HF
decompensation,
highlighting
the
potential
of
inflammatory
markers
in
risk
stratification[5].
The
integration
of
these
biomarkers
into
clinical
practice
could
facilitate
the
development
of
personalized
treatment
strategies,
allowing
for
targeted
anti-inflammatory
therapies
that
address
specific
pathophysiological
defects
in
HF
patients[2]
[3].
Despite
the
promising
role
of
inflammatory
biomarkers,
further
research
is
needed
to
fully
understand
their
causal
associations
with
HF
and
to
optimize
their
use
in
routine
clinical
practice[1]
[9].
Overall,
the
use
of
inflammatory
biomarkers
in
predicting
acute
decompensation
in
CHF
patients
underscores
the
potential
for
personalized
treatment
approaches
that
could
improve
patient
outcomes
and
quality
of
life.
Relevance
of
the
Topic:
Understanding
the
immune-inflammatory
mechanisms
involved
in
acute
decompensation
of
CHF
is
critical
for
developing
novel
biomarkers
and
anti-inflammatory
treatment
strategies.
Identifying
cytokine
patterns
may
offer
clinicians
predictive
tools
and
therapeutic
targets
to
reduce
hospitalizations
and
improve
survival
in
heart
failure
patients.
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Purpose of the Study: To evaluate laboratory cytokine profiles in patients with CHF during stable and
acutely decompensated phases and assess their association with clinical severity and comorbidities.
Materials and Methods: This retrospective cohort study was conducted at the Bukhara Branch of the
Republican Scientific Center for Emergency Medical Care over a three-year period (2022–2025).
Fifty-six patients with diagnosed CHF were divided into two groups: stable CHF (n=28) and acutely
decompensated CHF (ADCHF) (n=28). Laboratory assessment included TNF-α, IL-6, and IL-1β levels
measured via ELISA. Clinical data, NYHA class, BNP/NT-proBNP, CRP, and ESR levels were also
collected. Statistical analysis was performed using SPSS v25.0, with p < 0.05 considered significant.
Results: The ADCHF group showed significantly elevated cytokine levels compared to the stable
group. TNF-α was 14.2 ± 4.1 pg/mL in ADCHF vs. 6.5 ± 2.2 pg/mL (p<0.01), IL-6 was 12.6 ± 3.7
pg/mL vs. 5.8 ± 2.0 pg/mL (p<0.01), and IL-1β was 9.8 ± 2.6 pg/mL vs. 4.2 ± 1.3 pg/mL (p<0.05).
These increases correlated with elevated NYHA class, NT-proBNP, CRP, and ESR levels.
Figure 1.
Comparision of cytokine levels in stable CHF vs ADCHF
A positive correlation was observed between IL-6 and NT-proBNP (r = 0.67, p<0.01), suggesting a
link between inflammation and myocardial stress. The most common comorbidities included
hypertension (75%), ischemic heart disease (64%), and diabetes mellitus (39%).
Discussion: This study supports current evidence linking cytokine activation to acute heart failure
episodes. Elevated TNF-α contributes to cardiomyocyte apoptosis and contractile dysfunction, IL-6 is
associated with disease severity and fibrotic remodeling, while IL-1β exacerbates endothelial damage
and hypotension [1]. Emerging biomarkers like soluble ST2 (sST2) further enhance risk prediction,
and therapies targeting IL-1 show promise in reducing inflammatory burden [2,3]. Our findings
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reinforce the value of cytokine profiling for clinical assessment and personalized care in heart failure
patients.
This study supports current evidence linking cytokine activation to acute heart failure episodes.
Elevated TNF-α contributes to cardiomyocyte apoptosis and contractile dysfunction, IL-6 is associated
with disease severity and fibrotic remodeling, while IL-1β exacerbates endothelial damage and
hypotension [1]. Emerging biomarkers like soluble ST2 (sST2) further enhance risk prediction, and
therapies targeting IL-1 show promise in reducing inflammatory burden [2,3]. Our findings reinforce
the value of cytokine profiling for clinical assessment and personalized care in heart failure patients.
Recent clinical trials support the therapeutic potential of interleukin-1 (IL-1) inhibition in heart failure
management. A randomized controlled trial by Van Tassell et al. demonstrated that administration of
anakinra—an IL-1 receptor antagonist—reduced systemic inflammation and improved exercise
tolerance in patients with acute decompensated heart failure [2]. In another study focused on heart
failure with preserved ejection fraction (HFpEF), IL-1 blockade led to a significant reduction in CRP
and improved cardiorespiratory fitness, suggesting a direct link between cytokine suppression and
myocardial performance [2]. These findings suggest that IL-1 plays a pathogenic role in both systolic
and diastolic dysfunction.
Furthermore, sST2, a biomarker of myocardial stress and inflammation, has gained attention as a
predictor of outcomes in CHF. sST2 acts as a decoy receptor for IL-33, interrupting its protective
signaling and facilitating myocardial fibrosis and remodeling [3]. Studies show that combining sST2
with NT-proBNP enhances prognostic accuracy and improves patient risk stratification beyond
traditional markers [3]. Therefore, incorporating inflammatory biomarkers like sST2 alongside
cytokine profiling may refine diagnostic and therapeutic strategies in managing acute decompensated
CHF.
Conclusion:
Elevated inflammatory cytokines are closely associated with acute decompensation in CHF and reflect
both disease severity and inflammatory activity. Cytokine profiling could improve prognostication and
guide targeted interventions, offering a potential breakthrough in heart failure management strategies.
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