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Background: Rheumatoid arthritis (RA) is a systemic inflammatory disease in which cardiovascular (CV) diseases are the leading cause of mortality among affected patients. RA primarily affects women between the ages of 35 and 45, a period marked by estrogen decline related to menopause. Previous studies have reported that menopause can trigger changes that heighten the risk of subclinical atherosclerosis and subclinical left ventricular (LV) dysfunction. As a result, postmenopausal women with RA may face a higher susceptibility to major CV events. However, the impact of menopause and its CV risk in this population remains under-studied and, therefore, largely unknown.
Objectives: Compare the prevalence of subclinical CV alterations in post- and pre-menopausal women with RA.
Methods: Cross-sectional and comparative study involving RA women 30 to 75 years old who met the 2010 ACR/EULAR classification criteria. Menopause was defined as the absence of menstrual periods for at least 12 consecutive months. Patients with previous CV disease were excluded. Carotid ultrasound was performed on 281 participants, of whom only 120 underwent transthoracic echocardiography. Carotid plaque (CP) was defined as a diffuse carotid intima-media thickness (cIMT) ≥1.2 mm or focal thickness ≥0.8 mm. The echocardiographic evaluation included left ventricular mass index (LVMI), relative wall thickness (RWT) among others. Subclinical diastolic dysfunction (SDD) was categorized according to the 2016 American Society of Echocardiography, and subclinical systolic dysfunction (SSD) as a global longitudinal strain (GLS) greater than -18%. The Kolmogorov-Smirnov test assessed normality. Comparisons were made using Chi-square, T-test, or Mann-Whitney U test as appropriate. Variables that were significantly related to CP and DDS (p <0.05) were included in a multivariable logistic regression. A p-value ≤0.05 was considered statistically significant.
Results: Among 281 female RA patients who underwent carotid ultrasound (159 post-menopausal, 122 pre-menopausal). Hypertension was more common in post-menopausal women (39.6% vs. 28.6%, p = 0.05) and had a higher prevalence of CP (56.6% vs. 39.2%, p < 0.001). A logistic regression model with significant clinical variables showed age as the only independent factor associated with CP (OR 0.91, 95% CI 0.84 – 0.94, p <0.001). In 120 RA patients who underwent echocardiography, LVMI was higher in post-menopausal women (82.5 vs. 66.1, p = 0.003). Pre-menopausal patients had normal diastolic function (60.8%, p = 0.009) and post-menopausal showed grade I (52.7%, p= 0.03). A logistic regression with significant clinical variables showed age as the only independent factor associated with SDD (OR 0.88, 95% CI 0.84 – 0.94, p <0.001). No differences were found in subclinical systolic dysfunction (Table 2).
Conclusion: Our study identified a higher prevalence of CP, increased LVMI and SDD in postmenopausal RA patients compared to their premenopausal counterparts. This project is the first to directly compare pre- and post-menopausal women with RA, highlighting that menopause appears to be an important CV risk factor even more critical in this population compared with the existing literature reported in healthy postmenopausal women.
REFERENCES: [1] Muka T, et al. Association of Vasomotor and Other Menopausal Symptoms with Risk of Cardiovascular Disease: A Systematic Review and Meta-Analysis. DeAngelis MM, editor. PLoS ONE. 2016 Jun 17;11(6):0157417.
[2] Maiello M, et. al. Early diagnosis of subclinical left ventricular dysfunction in postmenopausal women with rheumatoid arthritis. Clinical Physiology and Functional Imaging. 2023 May 2;43(5):313–7.
Comparison of carotid ultrasound characteristics.
| Variables | Postmenopausal women (n=159) | Pre menopausal women (n=122) | p-value |
|---|---|---|---|
| Age, years, ± SD | 59 ± 7.7 | 50.9 ± 9.7 | <0.001 |
| Diabetes, n (%) | 26 (16.3) | 27 (22.1) | 0.22 |
| Hypertension, n (%) | 63 (39.6) | 35 (28.6) | 0.05 |
| Dislipidemia, n (%) | 71 (44.6) | 41 (33.6) | 0.10 |
| Active smoking, n (%) | 15 (9.4) | 10 (8.1) | 0.06 |
| Time of evolution, years, median (IQR) | 8.0 (3.0-15.2) | 7.0 (3.0-14.3) | 0.59 |
| DAS28-CPR, median (IQR) | 3.3 (2.1-4.4) | 3.3 (2.3-4.5) | 0.31 |
| Methotrexate, n (%) | 113 (71) | 96 (78.6) | 0.13 |
| Glucocorticoids, n (%) | 90 (56.6) | 65 (53.2) | 0.63 |
| bDMARDs, n (%) | 25 (15.7) | 17 (13.9) | 0.69 |
| Carotid plaque, n (%) | 92 (56.6) | 48 (39.2) | <0.001 |
SD, standard deviation; IQR, interquartile range; DAS28-CRP: Disease Activity Score for 28 joints with C-Reactive Protein calculation; bDMARDs, biologic disease-modifying antirheumatic drugs.
Comparison of echocardiography characteristics.
| Variables | Postmenopausal women (n=74) | Premenopausal women (n=46) | p-value |
|---|---|---|---|
| Age, years ± SD | 58 ± 7.3 | 48.8 ± 9.3 | <0.001 |
| Diabetes, n (%) | 14 (18.9) | 7 (15.2) | 0.60 |
| Hypertension, n (%) | 30 (40.5) | 10 (21.7) | 0.03 |
| Dyslipidemia, n (%) | 41 (55.4) | 15 (32.6) | 0.01 |
| Active smoking, n (%) | 2 (2.7) | 5 (10.8) | 0.01 |
| Time of evolution, years, median (IQR) | 5.5 (2.0-12.8) | 7.9 (3.0-13.7) | 0.22 |
| DAS28-ESR, ± SD | 4.0 ± 1.3 | 4.6 ± 2.4 | 0.03 |
| LVMI g/m2, median (IQR) | 82.5 (68.1-111.1) | 66.1 (60.0-82.4) | 0.003 |
| RWT, median (IQR) | 0.41 (0.35-0.47) | 0.40 (0.35-0.47) | 0.94 |
| SDD | |||
| Normal, n (%) | 27 (36.4) | 28 (60.8) | 0.009 |
| Grade I, n (%) | 39 (52.7) | 15 (32.6) | 0.03 |
| Grade II n (%) | 5 (6.7) | 3 (6.5) | 0.96 |
| Grade III, n (%) | 2 (2.7) | 0 (0) | 0.26 |
| SSD | |||
| TAPSE, median (IQR) | 22 (19.5-25) | 22 (21-24) | 0.94 |
| LVEF, mean ± SD | 61.4 ± 4.8 | 60.6 ± 4.6 | 0.34 |
| SLG, mean ± SD | -20.7 ± 2.5 | -20.4 (2.4) | 0.45 |
| SSD, n (%) | 60 (81) | 38 (82.6) | 0.83 |
SD, standard deviation; IQR, interquartile range; DAS28-ESR, Disease Activity Score 28 joints with Erythrocyte Sedimentation Rate; LVMI, left ventricle mass index; RWT, relative wall thickness; TAPSE, tricuspid annular plane systolic excursion; LVEF, left ventricle ejection fraction; SLG, strain longitudinal global; SDD, subclinical diastolic dysfunction; SSD, subclinical systolic dysfunction.
Acknowledgements: NIL.
Disclosure of Interests: None declared.
© The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license (