Assessment of subclinical atherosclerosis with carotid intima-media thickness in patients with scleroderma
Abstract
Aim: Inflammation has an important role in the development of atherosclerosis. The risk of atherosclerosis and its complications is higher for patients with diseases such as systemic lupus erythematosus and rheumatoid arthritis in whom inflammatory activity is high than for healthy individuals. However, several studies have shown conflicting results in patients with scleroderma. In this study, carotid intima-media thickness (CIMT) was compared in patients with scleroderma and a control group.
Methods: Thirty patients diagnosed with scleroderma (mean age 51.3 ± 11.8 years) and 30 healthy volunteers were included in the study. The groups were similar regarding age, gender, and risk factors for atherosclerosis.
Results: There was no statistically significant difference between the groups regarding age, gender, lipid level, hypertension, and diabetes mellitus prevalence (p>0.05). The mean CIMT (scleroderma group: 0.070±0.011, control group: 0.048±0.008, p<0.001) and the maximum CIMT (scleroderma group: 0.076±0.013, control group: 0.054±0.009, p<0.001) were statistically significantly higher in the patients with scleroderma. There was a statistically significant correlation between the mean CIMT and hsCRP (r=0.48, p<0.001); and the mean CIMT and the erythrocyte sedimentation rate (r=0.50, p=0.007) in the scleroderma group. The maximum CIMT and the mean CIMT were significantly higher in patients with diffuse type scleroderma compared to the patients with localized scleroderma (p values 0.001 and 0.011, respectively).
Conclusion: Our results show that CIMT is higher in patients with scleroderma compared to the control group, and this is associated with increased inflammatory activity.
Keywords
atherosclerosis, carotid intima-media thickness, inflammation, scleroderma
Supporting Institution
Destekleyen kurum bulunmamaktadır.
References
- 1. Mallika V, Goswami B, Rajappa M. Atherosclerosis pathophysiology and the role of novel risk factors: a clinicobiochemical perspective. Angiology 2007;58:513-22.
- 2. Ridker PM, Cannon CP, Morrow D, et al. C-Reactive protein levels and outcomes after statin therapy. N Engl J Med 2005; 352: 20–8.
- 3. Fathi R, Marwick TH. Noninvasive tests of vascular function and structure: why and how to perform them. Am Heart J 2001;141:694–703.
- 4. Corretti MC, Anderson TJ, Benjamin EJ, et al. International Brachial Artery Reactivity Task Force. Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilation of the brachial artery: a report of the International Brachial Artery Reactivity Task Force. J Am Coll Cardiol 2002; 39: 257–65.
- 5. Chambless LE, Heiss G, Folsom AR, et al. Association of coronary heart disease incidence with carotid arterial wall thickness and major risk factors: the Atherosclerosis Risk in Communities (ARIC) Study, 1987–1993. Am J Epidemiol 1997;146:483–94.
- 6. Davis PH, Dawson JD, Riley WA, Lauer RM. Carotid intimal-medial thickness is related to cardiovascular risk factors measured from childhood through middle age. The Muscatine Study. Circulation 2001;104:2815–9.
- 7. Salonen JT, Salonen R. Ultrasonographically assessed carotid morphology and the risk of coronary heart disease. Arterioscler Thromb 1991;11:1245–9.
- 8. O'Leary DH, Polak JF, Kronmal RA, et al. Carotid-artery intima and media thickness as a risk factor for myocardial infarction and stroke in older adults. Cardiovascular Health Study Collaborative Research Group. N Engl J Med 1999; 340:14–22.
- 9. Soubrier M, Mathieu S, Dubost JJ. Atheroma and systemic lupus erythematosus. Joint Bone Spine 2007; 74:566-70.
- 10. Grover S, Sinha RP, Singh U, et al. Subclinical atherosclerosis in rheumatoid arthritis in India. J Rheumatol 2006; 33:244-7.