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SCIENCE AND INNOVATION INTERNATIONAL SCIENTIFIC JOURNAL VOLUME 4 ISSUE 11 NOVEMBER 2025 ISSN: 2181-3337 | SCIENTISTS.UZ 206 STUDY OF REGIONAL VASCULAR STIFFNESS OF MUSCULAR AND ELASTIC-TYPE ARTERIES IN PATIENTS WITH ARTERIAL HYPERTENSION AND PERIPHERAL ARTERIAL ATHEROSCLEROSIS N.A. Abidova Tashkent State Medical University (TSMU) https://doi.org/10.5281/zenodo.17854780 Abstract. The present study evaluated the regional vascular stiffness of arteries of elastic (aorta) and muscular (brachial, femoral) types in patients with arterial hypertension (AH) and atherosclerotic lesions of peripheral arteries. It was found that 73% of patients exhibited a clinically significant increase in aortic stiffness. The parameters of pulse wave velocity (cfPWV and crPWV) showed significant correlations with intima–media thickness (IMT) and the degree of stenosis of the carotid and femoral arteries. The obtained data confirm the systemic nature of vascular remodeling in the coexistence of hypertension and atherosclerosis and emphasize the necessity of a comprehensive assessment of vascular stiffness for cardiovascular risk stratification. Keywords: hypertension, atherosclerosis, vascular stiffness, cfPWV, crPWV, IMT, stenosis. Introduction. Arterial hypertension (AH) is one of the leading risk factors for the development of cardiovascular diseases and a key predictor of mortality associated with cardiovascular pathologies [7–9]. According to the World Health Organization, approximately 5 million people die prematurely each year from complications associated with arterial hypertension. An increase in vascular rigidity is considered one of the earliest structural and functional changes in the arterial wall that is accessible to non-invasive instrumental monitoring [10]. According to several researchers, the vascular stiffness index is an integral indicator reflecting the risk of cardiovascular events [11]. The main factors contributing to increased vascular stiffness include age, arterial hypertension, diabetes mellitus, dyslipidemia, and others [12–14]. An important area of discussion remains the influence of atherosclerosis on the progression of arterial rigidity. Atherosclerosis and arteriosclerosis, acting through different pathogenetic mechanisms, exert a synergistic negative effect on the vascular wall: atherosclerosis mainly affects the intima, whereas arteriosclerosis involves the medial layer. The study of vascular remodeling features in patients with a combination of arterial hypertension and atherosclerotic lesions of peripheral arteries is a relevant task for clinical practice. Objective of the Study. To assess regional vascular stiffness of muscular and elastic-type arteries in patients with arterial hypertension and atherosclerotic lesions of peripheral vessels. Materials and Methods. The study included 100 patients diagnosed with hypertensive disease (HD), including 55 men and 45 women, with a mean age of 57.2 ± 10.3 years. Distribution by stages of HD: Stage I — 4 patients (4%), Stage II — 36 patients (36%),
SCIENCE AND INNOVATION INTERNATIONAL SCIENTIFIC JOURNAL VOLUME 4 ISSUE 11 NOVEMBER 2025 ISSN: 2181-3337 | SCIENTISTS.UZ 207 Stage III — 60 patients (60%). Distribution by degree of arterial hypertension: Grade 1 — 48 patients (48%), Grade 2 — 29 patients (29%), Grade 3 — 23 patients (23%). The mean duration of the disease was 2.25 years (interquartile range 1.00–7.25). All patients underwent a comprehensive clinical examination with detailed medical history collection. Regional stiffness of elastic arteries was assessed by measuring carotid–femoral pulse wave velocity (cfPWV), and stiffness of muscular arteries, represented by the brachial artery, was determined by carotid–radial pulse wave velocity (crPWV) using the “Neurosoft Poly-SpectrumPWV” device. The methodology was consistent with the recommendations of the European Consensus on Arterial Stiffness and the American Heart Association [1,2]. All patients underwent ultrasound duplex scanning of the brachiocephalic arteries and lower limb arteries using an expertclass device “Samsung Medison EKO7” (Japan). The intima–media thickness (IMT) of the common carotid arteries (CCA), common femoral arteries (CFA), and superficial femoral arteries (SFA) was evaluated. The mean IMT of the CCA (mean CIMT) was calculated using the following formula: Mean CIMT = (CIMT of left CCA + CIMT of right CCA) / 2 An atherosclerotic plaque (ASP) was defined as a focal thickening of the intima–media complex (IMC) exceeding 1.5 mm, or an increase of 0.5 mm or more compared with adjacent segments of the common carotid artery (CCA), or exceeding 50% of the CIMT of neighboring areas [3]. The percentage of stenosis was assessed planimetrically in B-mode, by measuring the vessel diameter in cross-section according to the methodology of the European Carotid Surgery Trial (ECST) [4]. The total carotid stenosis (SumStCA) was calculated as the sum of all stenoses on both sides, as well as the maximum stenosis percentage (MaxStCA) for each patient. The degree of stenosis of the lower limb arteries was assessed planimetrically and using Doppler ultrasound hemodynamic criteria [5,6]. The laboratory study included the determination of levels of total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), glycated hemoglobin (HbA1c), and creatinine with calculation of the glomerular filtration rate (GFR) according to the CKD-EPI formula, as well as the level of highsensitivity C-reactive protein (hsCRP). The clinical characteristics of patients are presented in Table 1. Table 1. Clinical and Demographic Characteristics of the Study Cohort of Patients Parameters Patients (n = 100) Smoking, n (%) 26 (26%) Ischemic heart disease, n (%) 38 (38%) Type 2 diabetes mellitus, n (%) 25 (25%) Chronic heart failure, n (%) 40 (40%) Intermittent claudication, n (%) 8 (8%) Use of RAAS inhibitors, n (%) 66 (66%) Use of antiplatelet agents, n (%) 56 (56%) Use of beta-blockers, n (%) 26 (26%) Use of statins, n (%) 34 (34%)
SCIENCE AND INNOVATION INTERNATIONAL SCIENTIFIC JOURNAL VOLUME 4 ISSUE 11 NOVEMBER 2025 ISSN: 2181-3337 | SCIENTISTS.UZ 208 Total cholesterol, mmol/L 5.06 ± 1.14 LDL-C, mmol/L 2.94 ± 1.19 HDL-C, mmol/L 1.34 ± 0.37 Triglycerides, mmol/L 1.79 ± 1.00 GFR, mL/min/1.73 m² 60.2 ± 14.2 hsCRP, mg/L 3.63 ± 4.20 HbA1c, % 5.30 ± 1.38 Mean CIMT of CCA, mm 0.98 ± 0.19 Mean CIMT of CFA, mm 0.97 ± 0.25 Mean CIMT of SFA, mm 0.75 ± 0.24() Total carotid stenosis (SumStCA), % 28.0 ± 21.8 Maximum carotid stenosis (MaxStCA), % 59.3 ± 59.7 Maximum femoral artery stenosis (MaxStFA), % 21.0 ± 20.8 Statistical data processing was performed using IBM SPSS Statistics, version 22. Quantitative variables were analyzed using the nonparametric Wilcoxon–Mann–Whitney test, while categorical variables were assessed using the chi-square (χ²) test [14]. Correlations between variables were evaluated using Spearman’s correlation analysis with calculation of statistical significance levels and correlation strength. Results and Discussion. According to the data obtained from duplex ultrasound scanning, atherosclerotic plaques (ASP) were detected in the carotid arteries in 71 (71%) patients and in the lower limb arteries in 60 (60%) patients. In 50 (50%) of the examined individuals, atherosclerotic plaques were present simultaneously in both the carotid and lower extremity arterial beds. Vascular stenosis with a lumen narrowing exceeding 50% was diagnosed in 8 (8%) patients. The indicators of vascular stiffness parameters are presented in Table 2. Table 2. Parameters of Vascular Stiffness Sex Carotid–Radial PWV (m/s) Carotid–Femoral PWV (m/s) Men 12,5±3,45 12,0±2,53 Women 11,8±2,93 12,3±3,44 Total 12,2±3,24 12,2±2,96 The proportion of patients with carotid–femoral pulse wave velocity (cfPWV) above 10 m/s, which is considered the threshold value for determining a prognostically significant increase in aortic stiffness, was 73%. The mean values of carotid–radial pulse wave velocity (crPWV) also exceeded 10 m/s; however, generally accepted reference standards for this parameter have not been established. In patients with atherosclerotic changes in the brachiocephalic arteries and visualized atherosclerotic plaques (AP) detected by duplex scanning, a statistically significant increase in cfPWV was observed compared to the group without AP — 12.5 ± 2.86 m/s versus 11.3 ± 3.08 m/s (p = 0.017). Differences in crPWV values between these groups did not reach statistical significance — 12.3 ± 2.69 m/s and 11.9 ± 4.34 m/s, respectively (p = 0.07). Among patients with atherosclerotic lesions of the lower limb arteries, the mean cfPWV value was 12.8 ± 2.81 m/s, whereas in subjects without AP in this vascular basin it was 11.2 ± 2.96 m/s (p = 0.001). The crPWV indices in patients with lower limb arterial atherosclerosis were also significantly higher — 12.5 ± 2.54 m/s compared to 11.8 ± 4.05 m/s in those without lesions (p =
SCIENCE AND INNOVATION INTERNATIONAL SCIENTIFIC JOURNAL VOLUME 4 ISSUE 11 NOVEMBER 2025 ISSN: 2181-3337 | SCIENTISTS.UZ 209 0.021). In a subgroup of 50 patients with AP in both vascular basins, the mean cfPWV and crPWV values were 12.8 ± 2.62 m/s and 12.5 ± 2.39 m/s, respectively. These values were significantly higher than those in 50 patients with isolated lesions of a single vascular basin or without AP — cfPWV 11.4 ± 3.13 m/s (p = 0.002) and crPWV 11.9 ± 3.89 m/s (p = 0.029). The obtained data are consistent with the findings of study [15], which also reported an increase in cfPWV among patients with atherosclerotic involvement of different vascular basins (coronary, cerebral, and lower limb arteries) compared to the control group. To identify correlations between vascular stiffness parameters and ultrasound markers of the severity of atherosclerotic lesions, a correlation analysis was performed. The results are presented in Table 3. Table 3. Correlations Between Vascular Stiffness Parameters and Markers of Atherosclerotic Vascular Lesions. Parameter cfPWV crPWV IMT of Common Carotid Artery (CCA) r = 0.306 p = 0.002 r = 0.280 p = 0.005 Maximum Carotid Artery Stenosis (MaxStCA) r = 0.273 p = 0.006 r = 0.218 p = 0.029 Total Carotid Artery Stenosis (SumStCA) r = 0.232 p = 0.020 r = 0.202 p = 0.044 IMT of Common Femoral Artery (CFA) r = 0.318 p = 0.001 r = 0.244 p = 0.015 IMT of Superficial Femoral Artery (SFA) r = 0.250 p = 0.012 r = 0.276 p = 0.006 Maximum Femoral Artery Stenosis (MaxStFA) r = 0.280 p = 0.005 r = 0.255 p = 0.011 IMT CCA — indicator of intima–media thickness in the common carotid arteries; IMT CFA — indicator of intima–media thickness in the common femoral arteries; IMT SFA — indicator of intima–media thickness in the superficial femoral arteries; MaxStCA — maximum degree of carotid artery stenosis; MaxStFA — maximum degree of femoral artery stenosis; SumStCA — total percentage of carotid artery stenosis. Results and Discussion. Analysis of the results presented in Table 3 revealed statistically significant positive correlations between carotid–femoral pulse wave velocity (cfPWV), reflecting the stiffness of large elastic arteries, and several ultrasound markers of atherosclerotic involvement of peripheral vessels. In particular, a significant association was established between cfPWV and intima–media thickness (IMT) of the common carotid arteries (CCA), the maximum and total percentage of carotid artery stenosis, IMT of the common femoral arteries (CFA), IMT of the superficial femoral arteries (SFA), as well as the maximum degree of femoral artery stenosis. This indicates that an increase in elastic artery stiffness is closely related to the severity of structural vascular wall changes caused by atherosclerosis and to the degree of vessel narrowing in the carotid and femoral regions. Similarly, parameters of regional stiffness of muscular-type arteries, measured using carotid–radial pulse wave velocity (crPWV), also demonstrated statistically significant correlations with the same ultrasound parameters — IMT and stenosis degree of carotid and femoral arteries. These correlations suggest that, in addition to elastic vessels, muscular-type
SCIENCE AND INNOVATION INTERNATIONAL SCIENTIFIC JOURNAL VOLUME 4 ISSUE 11 NOVEMBER 2025 ISSN: 2181-3337 | SCIENTISTS.UZ 210 arteries are also subject to remodeling and stiffness development in response to atherosclerotic processes and arterial hypertension. This supports the hypothesis of a systemic nature of vascular alterations in these pathologies, involving various types of arteries. Despite the significance of the identified correlations, the current scientific literature demonstrates limited focus on the study of muscular artery stiffness in patients with arterial hypertension. Available publications contain only isolated reports indicating elevated crPWV levels in individuals with hypertension [16]. However, systematic studies assessing correlations between crPWV and quantitative ultrasound markers of atherosclerotic lesion severity in peripheral arteries — including carotid and lower limb arteries, as well as IMT parameters — are practically absent. This creates a gap in understanding the mechanisms of vascular remodeling specifically in muscular-type arteries and highlights the necessity for further research in this field. Thus, the obtained data emphasize the importance of a comprehensive assessment of both elastic and muscular artery stiffness in the management of patients with arterial hypertension and atherosclerotic lesions. A deeper investigation of the interrelations between structural and functional vascular wall changes will improve the accuracy of cardiovascular risk prediction and help optimize therapeutic strategies. Conclusions. In the studied cohort of patients with arterial hypertension (AH) and atherosclerotic lesions of peripheral arteries, the majority (73%) demonstrated a prognostically unfavorable increase in aortic stiffness. This indicates a high degree of functional and structural alterations of the aortic wall, underscoring the importance of early detection and monitoring of vascular rigidity in this patient group. Regardless of the localization of the atherosclerotic process — whether in the carotid region or the arteries of the lower limbs — patients showed a significant increase in stiffness of both elastic-type arteries (e.g., the aorta) and muscular-type arteries (e.g., brachial and femoral arteries). These findings confirm the systemic nature of vascular remodeling in the coexistence of hypertension and peripheral atherosclerosis. Increased aortic stiffness, measured by carotid–femoral pulse wave velocity (cfPWV), is closely correlated with morphological signs of atherosclerotic lesions — pronounced intima– media thickening (IMT) in the common carotid, common femoral, and superficial femoral arteries, as well as with the degree of stenosis of these vessels. This reflects the relationship between structural changes in the vascular wall and functional deterioration of large arterial elasticity. The stiffness of muscular-type arteries, assessed by carotid–radial pulse wave velocity (crPWV), is also associated with increased IMT of carotid and femoral arteries and with the severity of stenotic changes in these vessels. Thus, crPWV may serve as an additional marker of structural and functional alterations in muscular-type arteries in patients with hypertension and atherosclerosis. The obtained findings highlight the necessity for an integrated assessment of vascular stiffness and morphological parameters of peripheral arteries in the diagnosis and follow-up of patients with hypertension and atherosclerosis. A comprehensive approach allows for more precise evaluation of vascular damage severity, improved cardiovascular event risk prediction, and optimization of therapeutic management. REFERENCES 1. Laurent S.L., Cockcroft J., Van Bortel L., Boutouyrie P., Giannattasio C., Hayoz D., Pannier B., Vlachopoulos C., Wilkinson I., Struijker-Boudier H.; European Network for Non-invasive
SCIENCE AND INNOVATION INTERNATIONAL SCIENTIFIC JOURNAL VOLUME 4 ISSUE 11 NOVEMBER 2025 ISSN: 2181-3337 | SCIENTISTS.UZ 211 Investigation of Large Arteries. Expert consensus document on arterial stiffness: methodological issues and clinical applications. Eur Heart J. 2006; 27(21):2588–2605. 2. Townsend R.R., Wilkinson I.B., Schiffrin E.L., Avolio A.P., Chirinos J.A., Cockcroft J.R., Heffernan K.S., Lakatta E.G., McEniery C.M., Mitchell G.F., Najjar S.S., Nichols W.W., Urbina E.M., Weber T.; American Heart Association Council on Hypertension. Recommendations for improving and standardizing vascular research on arterial stiffness: A scientific statement from the American Heart Association. Hypertension. 2015; 66(3):698– 722. 3. Touboul P.J., Hennerici M.G., Meairs S., Adams H., Amarenco P., Bornstein N., Csiba L., Desvarieux M., Ebrahim S., Hernandez R., Jaff M., Kownator S., Naqvi T., Prati P., Rundek T., Sitzer M., Schminke U., Tardif J.C., Taylor A., Vicaut E., Woo K.S. Mannheim carotid intima-media thickness and plaque consensus (2004–2011): Update on behalf of the advisory board of the 3rd–5th “Watching the Risk” symposia. Cerebrovasc Dis. 2012; 34(4):290–296. 4. European Carotid Surgery Trialists' Collaborative Group. Randomized trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial (ECST). Lancet. 1998; 351(9113):1379–1387. 5. Jager K.A., Phillips D.J., Martin R.L., Hanson C., Roederer G.O., Langlois Y.E., Ricketts H.J., Strandness D.E. Jr. Noninvasive mapping of lower limb arterial lesions. Ultrasound Med Biol. 1985; 11(3):515–521. 6. Kulikov V.P. Fundamentals of Ultrasonic Vascular Examination. Moscow: Vidar-M; 2015. 392 p. 7. Lewington S., Clarke R., Qizilbash N., Peto R., Collins R. Age-specific relevance of usual blood pressure to vascular mortality: A meta-analysis of individual data for one million adults in 61 prospective studies. Lancet. 2002; 360:1903–1913. 8. Britton K.A., Gaziano J.M., Djousse L. Normal systolic blood pressure and risk of heart failure in US male physicians. Eur J Heart Fail. 2009; 11:1129–1134. 9. Tu K., Chen Z., Lipscombe L.L.; Canadian Hypertension Education Program Outcomes Research Taskforce. Mortality among patients with hypertension from 1995 to 2005: A population-based study. CMAJ. 2008; 178(11):1436–1440. 10. Cavalcante J.L., Lima J.A., Redheuil A., Al-Mallah M.H. Aortic stiffness: current understanding and future directions. J Am Coll Cardiol. 2011; 57(14):1511–1522. 11. Orlova Ya.A., Ageev F.T. Arterial stiffness as an integral indicator of cardiovascular risk: physiology, assessment methods, and pharmacological correction. Heart (Serdtse). 2006; 5(2):65–69. 12. Albu A., Fodor D., Bondor C., et al. Arterial stiffness, carotid atherosclerosis, and left ventricular diastolic dysfunction in postmenopausal women. Eur J Intern Med. 2013; 24:250– 254. 13. Doonan R.J., Hausvater A., Scallan C., Mikhailidis D.P., Pilote L., Daskalopoulou S.S. The effect of smoking on arterial stiffness. Hypertens Res. 2010; 33(5):398–410. 14. Strasser B., Arvandi M., Pasha E.P., Haley A.P., Stanforth P., Tanaka H. Abdominal obesity is associated with arterial stiffness in middle-aged adults. Nutr Metab Cardiovasc Dis. 2015; 25(5):495–502. 15. Tsuchikura S., Shoji T., Kimoto E., Shinohara K., Hatsuda S., Koyama H., Emoto M., Nishizawa Y. Central versus peripheral arterial stiffness in association with coronary, cerebral, and peripheral arterial disease. Atherosclerosis. 2010; 211(2):480–485.
SCIENCE AND INNOVATION INTERNATIONAL SCIENTIFIC JOURNAL VOLUME 4 ISSUE 11 NOVEMBER 2025 ISSN: 2181-3337 | SCIENTISTS.UZ 212 16. Hua Q., Tan J., Liu D.X., Wen J., Xing X.R. The changes and impact factors of carotid– femoral and carotid–radial pulse wave velocity in patients with essential hypertension. Zhonghua Xin Xue Guan Bing Za Zhi. 2005; 33(12):1088–1091.