Pathogenetic Interrelations Of Inflammation And Dyslipidemia In Atherothrombotic Lesions Of Extracranial Arteries
Nargiza Abdullaeva , Samarkand State Medical University, Uzbekistan Sardorbek Yuldashev , Samarkand State Medical University, UzbekistanAbstract
Atherothrombotic lesions of the extracranial arteries represent one of the main causes of ischemic stroke and are strongly associated with systemic inflammation and dyslipidemia. This study aimed to analyze the pathogenetic interrelations between inflammatory and lipid markers in patients with varying degrees of atherothrombotic extracranial artery stenosis. A total of 128 elderly patients (mean age 67 ± 7.2 years) diagnosed with internal carotid artery (ICA) stenosis were examined between 2022 and 2024. Based on lesion type, patients were divided into three groups: unilateral ICA stenosis (Group I, n = 41), bilateral ICA stenosis (Group II, n = 58), and combined ICA + vertebral artery stenosis (Group III, n = 29), with an additional control group (n = 20).
Biochemical markers such as high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and lipid profile parameters (LDL, HDL, total cholesterol, triglycerides) were measured and statistically analyzed using IBM SPSS 25.0, MedCalc 20.0, and R 4.2.2. The mean hs-CRP and IL-6 values showed a significant progressive increase from Group I to III (p < 0.05), reflecting enhanced systemic inflammation with advancing stenosis. Total cholesterol and LDL levels also increased significantly, while HDL levels showed a nonsignificant downward trend.
These findings demonstrate that chronic inflammation and dyslipidemia act synergistically in promoting atherothrombotic progression and plaque instability. The most severe biochemical alterations were observed in patients with combined ICA and vertebral artery stenosis, indicating a more generalized and aggressive form of vascular pathology. Regular monitoring of inflammatory and lipid markers is recommended for early identification of high-risk patients, better prediction of stroke risk, and optimization of therapeutic strategies.
Keywords
Atherothrombosis, extracranial arteries, inflammation
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