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THE ROLE OF INFLAMMATORY BIOMARKERS AND ENDOTHELIAL
DYSFUNCTION IN THE PATHOPHYSIOLOGY AND MANAGEMENT OF ISCHEMIC
HEART DISEASE
¹Raxmonov Mexroj Akmaljon o‘g‘li
²Razzakova Nozimaxon Olimovna
³Sharipov Shaxbozbek Shavkat o‘g‘li
¹'²'³Samarkand State Medical University DKTF, Department of Internal Medicine, Cardiology
and Functional Diagnostics! Second-year clinical residents
https://doi.org/10.5281/zenodo.15637095
Research objective
Ischemic heart disease (IHD), also known as coronary artery disease (CAD), remains the
leading cause of morbidity and mortality globally. The main objective of this research is to
explore the role of inflammatory biomarkers and endothelial dysfunction in the pathogenesis,
diagnosis, prognosis, and therapeutic strategies of ischemic heart disease. A growing div of
evidence suggests that chronic low-grade inflammation and endothelial dysfunction are central to
the initiation, progression, and clinical outcomes of atherosclerosis—the primary pathological
process underlying IHD. Traditionally, IHD has been attributed primarily to lipid accumulation
and mechanical obstruction of coronary arteries, but contemporary research highlights the
dynamic and complex interactions between immune responses, vascular biology, and metabolic
regulation.
Introduction
: Inflammatory biomarkers such as high-sensitivity C-reactive protein
(hsCRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and soluble adhesion
molecules have been implicated in all stages of atherogenesis, from endothelial activation to
plaque rupture. Among them, hsCRP is the most widely studied and clinically applied
biomarker, independently associated with future cardiovascular events and mortality.
Additionally, elevated levels of IL-6 and TNF-α are strongly correlated with plaque instability
and adverse outcomes post-myocardial infarction. Endothelial dysfunction, characterized by
impaired nitric oxide (NO) bioavailability and increased oxidative stress, plays a pivotal role in
the progression of atherosclerosis. The endothelium is not merely a passive barrier but a dynamic
endocrine organ that modulates vascular tone, hemostasis, inflammation, and angiogenesis.
When endothelial cells are exposed to risk factors such as hypertension, hyperlipidemia,
diabetes, and smoking, they become dysfunctional, losing their vasodilatory and anti-
inflammatory properties. This results in vasoconstriction, leukocyte adhesion, platelet
aggregation, and thrombogenesis, which collectively contribute to ischemic episodes.
Materials and Methods
Endothelial function can be assessed noninvasively by flow-mediated dilation (FMD) of
the brachial artery, peripheral arterial tonometry, and circulating biomarkers such as asymmetric
dimethylarginine (ADMA) and endothelial microparticles. Therapeutic modulation of
endothelial dysfunction and inflammation offers a promising avenue for improving outcomes in
patients with IHD. Statins, beyond their lipid-lowering effects, exert pleiotropic anti-
inflammatory and endothelial-stabilizing actions. Anti-inflammatory agents such as colchicine
and IL-1β inhibitors (e.g., canakinumab) have demonstrated efficacy in reducing cardiovascular
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events, as evidenced by landmark trials like CANTOS and COLCOT. Lifestyle interventions
including smoking cessation, Mediterranean diet, physical activity, and weight loss are critical in
restoring endothelial function and lowering systemic inflammation. Emerging therapies targeting
novel pathways such as NLRP3 inflammasome, TLRs, and gut microbiota-derived metabolites
like trimethylamine-N-oxide (TMAO) are under investigation for their potential cardiovascular
benefits.
Results
Genetic and epigenetic factors also modulate individual susceptibility to inflammation
and endothelial dysfunction, suggesting that personalized approaches may optimize prevention
and treatment strategies. For example, polymorphisms in genes encoding CRP, IL-6, and
endothelial nitric oxide synthase (eNOS) influence disease severity and response to therapy.
Moreover, circulating microRNAs involved in endothelial repair and inflammation have
emerged as potential diagnostic and prognostic biomarkers. Advanced imaging modalities such
as coronary CT angiography with plaque characterization, PET imaging of vascular
inflammation, and cardiac MRI provide insights into the biological activity of atherosclerotic
lesions, complementing functional and biochemical assessments.
Conclusion
In the clinical setting, combining traditional risk scores with inflammatory and
endothelial biomarkers enhances risk stratification and guides therapeutic decision-making.
Integrative models that account for inflammatory burden and vascular health could improve
secondary prevention efforts in post-acute coronary syndrome patients. Despite significant
progress, several challenges persist, including the standardization of biomarker assays, the
translation of mechanistic insights into clinical practice, and the identification of optimal
therapeutic targets with minimal off-target effects. Future research should focus on large-scale,
longitudinal studies to validate biomarker utility, assess cost-effectiveness, and integrate omics-
based approaches for comprehensive cardiovascular risk profiling. In conclusion, understanding
the interplay between inflammation and endothelial dysfunction provides a refined framework
for interpreting ischemic heart disease as a systemic vascular condition rather than a mere
mechanical obstruction. Targeted interventions aimed at restoring endothelial health and
reducing inflammatory burden hold the promise of transforming the prevention and management
of ischemic heart disease in the modern era of precision medicine.
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