Background: Ultrasonography can measure vascular intimal-medial thickness (IMT) and delineate the degrees of stenosis in Takayasu arteritis (TAK). Further, higher IMT has been reported in patients with active disease, with prospective studies showing changes in carotid IMT with treatment. A cross-sectional study has attempted derivation of a score incorporating IMT values at different arterial sites that correlated with disease activity(2). In this study we measured IMT at multiple vascular sites at enrollment and at six months and tried to correlate IMT with disease activity, hsCRP, and active inflammation assessed by F-18FDG-PET scan. Objectives: 1.To investigate whether arterial IMT in bilateral common carotid, subclavian, brachial, and femoral arteries, is associated with disease activity state in TAK. 2.To assess the correlation of arterial IMT values with clinical disease activity parameters, serological biomarkers and PET-VAS score. 3.To assess if there is a significant change in arterial IMT values at multiple arteries over time (six months follow-up). 4.To assess if change in IMT correlates with change in clinical and serological parameters of disease activity over time. Methods: We prospectively enrolled 47 TAK patients (fulfilling ACR 1993) from May 2022 to December 2023; 24 had active and 23 inactive disease state as per Physician Global assessment (PGA). Arterial IMT was measured at 8 vascular sites (bilateral common carotid, subclavian, brachial, and femoral arteries) using ultrasonography (Esaote MyLab50) by two different observers. Observers were blinded between each other and towards the clinical details. For each vascular site, mean of three highest values obtained from fixed segments was obtained. Thickness was measured in the far wall with uniform frequency, angle of insonation and depth. Disease activity was evaluated using Indian Takayasu Arteritis Activity Score (ITAS 2010), hsCRP, and PET VAS score. PGA was considered the gold standard measure for classifying active and inactive disease. Patients were followed-up and their arterial IMT and disease activity parameters were reassessed at 6 months. Results: Median age was 31 years and 87.20% were females. Thirty patients(63.80%) were new disease (diagnosed < 1 year). Most patients(68.08%) had an Ishikawa type V disease. Interobserver agreement was adequate. Total IMT of 8 arteries was numerically higher in the active group but did not reach statistical significance (Table 1). However, total IMT of both carotid arteries was significantly associated with active disease. IMT measurements, particularly in both carotid arteries, showed significant correlation with disease activity markers including total PET-VAS scores, ITAS-CRP, and PGA. The strongest correlation was observed between Left Common Carotid IMT and PGA (Spearman's rho =0.584, p < 0.001). Disease activity state had significant association with IMT values, independent of age, gender, BMI, hypertension and dyslipidemia, in linear regression analysis. Area under the curve for Total IMT and Total carotid IMT as markers for active disease were 0.658(p=0.064; 95% CI: 0.498-0.817) and 0.673(p=0.042; 95% CI: 0.517-0.829). Twenty five patients were reassessed at 6-months follow-up. Mean total IMT was significantly lower at 6-months and similar changes were reflected in IMT values of left common carotid, left subclavian and femoral arteries. Change in total IMT correlated positively with a change in disease activity status. Positive correlations were observed also between change in carotid IMT and ITAS-CRP (Table 2). Change in IMT over 6 months was significantly higher in patients who had active disease at recruitment and nearly 60% among them were recently diagnosed cases. Conclusion: Ultrasonographic measurement of IMT at multiple arterial sites, particularly carotid arteries, is a promising tool for evaluating TAK disease activity. Measurement of total carotid IMT alone may be a sufficient marker for disease activity in supradiaphragmatic disease. There is significant change in IMT over 6 months especially in the group with active disease, suggesting a window of opportunity for disease modification. REFERENCES: NIL. Acknowledgements: The author has received a research grant for this project from Indian Rheumatology Association. Disclosure of Interests: None declared.
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