Abstract
Rheumatoid joint pain is an on-going incendiary infection with articular and extra articular signs. In rheumatoid arthritis increased mortality is observed due to cardiovascular diseases due to accelerated atherosclerotic process. CIMT can be used as a biomarker to evaluate subclinical atherosclerosis. This systematic study aims at correlating the coronary artery intimo medial thickness in rheumatoid joint pain patients to evaluate the seriousness of atherosclerosis in same patients. A prospective single-center study was conducted with a study group of 12 patients with RA and 12 stable, age and sex-matched controls. After applying inclusion and exclusion criteria and separating the patients into three gatherings dependent on term of the illness, the USG directed CIMT thickness was calculated and the findings were compared between different groups. There was a clear association between the duration of rheumatoid arthritis and intimo medial carotid artery thickness. There was no substantial association between disease occurrence and CIMT in cases of rheumatoid arthritis. An increase in CIMT should be promptly taken into consideration and appropriate preventive therapies on instituting can prevent and decrease the incidence of cardiovascular and cerebral events in rheumatoid arthritis.
Full text article
References
Alkaabi, J.K. 2003. Rheumatoid arthritis and macrovascular disease. Rheumatology, 42(2):292–297.
Delrincon, et al. 2005. Relative contribution of cardiovascular risk factors and rheumatoid arthritis clinical manifestation to atherosclerosis. Arthritis rheum, 52:3413–3436.
Gonzalez-Juanatey, C., Llorca, J., Testa, A., Revuelta, J., Garcia-Porrua, C., Gonzalez-Gay, M.A. 2003. Increased Prevalence of Severe Subclinical Atherosclerotic Findings in Long-Term Treated Rheumatoid Arthritis Patients Without Clinically Evident Atherosclerotic Disease. Medicine, 82(6):407–413.
Haagsma, C.J., Blom, H.J., van Riel, P.L. C.M., van’t Hof, M.A., Giesendorf, B.A.J., van Oppenraaij Emmerzaal, D., van de Putte, L. B. A. 1999. Influence of sulphasalazine, methotrexate, and the combination of both on plasma homocysteine concentrations in patients with rheumatoid arthritis. Annals of the Rheumatic Diseases, 58(2):79–84.
Jonsson, S.W., Backman, C., Johnson, O., Karp, K., Lundström, E., Sundqvist, K.G., Dahlqvist, S.R. 2001. Increased prevalence of atherosclerosis in patients with medium term rheumatoid arthritis. The Journal of Rheumatology, 28(12):2597–2602.
Landewe, R.B., van den Borne, B.E., Breedveld, F.C., Dijkmans, B.A. 2000. Methotrexate effects in patients with rheumatoid arthritis with cardiovascular comorbidity. The Lancet, 355(9215):1616– 1617.
Lorenz, M.W., Markus, H.S., Bots, M.L., Rosvall, M., Sitzer, M. 2007. Prediction of Clinical Cardiovascular Events with Carotid Intima Media Thickness. Circulation, 115(4):459–467.
Mahajan, V., Handa, R., Kumar, U., Sharma, S., Gulati, G., Pandey, R.M., Lakshmy, R. 2008. Assessment of atherosclerosis by carotid intimomedial thickness in patients with rheumatoid arthritis. The Journal of the Association of Physicians of India, 56:587– 590.
McEntegart, A. 2001. Cardiovascular risk factors, including thrombotic variables, in a population with rheumatoid arthritis. Rheumatology, 40(6):640–644.
Minaur, N.J., Jacoby, R.K., Cosh, J.A., Taylor, G., Rasker, J.J. 2004. Outcome after 40 years with rheumatoid arthritis: a prospective study of function, disease activity, and mortality. The Journal of Rheumatology. Supplement, 69:3–8.
Paredes, S., Girona, J., Hurt-Camejo, E., Vallvé, J.C., Olivé, S., Heras, M., Benito, P., Masana, L. 2002. Antioxidant vitamins and lipid peroxidation in patients with rheumatoid arthritis: association with inflammatory markers. The Journal of Rheumatology, 29(11):2271–2277.
Ralston, S.H., McInnes, I.B. 2014. Rheumatology and bone disease. In Davidson’s Principles and Practice of Medicine. Davidson’s Principles and Practice of Medicine. 22nd ed. Philadelphia, PA: Elsevier Churchill Livingstone.
Ridker, P.M., Cushman, M., Stampfer, M.J., Tracy, R.P., Hennekens, C.H. 1997. Inflammation, Aspirin, and the Risk of Cardiovascular Disease in Apparently Healthy Men. New England Journal of Medicine, 336(14):973–979.
Schulte-Altedorneburg, G., Droste, D.W., Felszeghy, S., Kellermann, M., Popa, V., Hegedüs, K., Hegedüs, C., Schmid, M., Módis, L., Ringelstein, E. B., Csiba, L. 2001. Accuracy of In Vivo Carotid B-Mode Ultrasound Compared with Pathological Analysis. Stroke, 32(7):1520–1524.
Singh, H., Goyal, M., Sen, J., Kumar, H., Handa, R., Garg, S. 2011. Correlation of intima-media thickness (as a marker of atherosclerosis) with activity and duration of rheumatoid arthritis using carotid ultrasound. J Indian Acad Clin Med, 12(1):15–20.
Superko, H.R., Haskell, W.L., Wood, P.D. 1985. Modification of plasma cholesterol through exercise. Postgraduate Medicine, 78(5):64–75.
Turesson, C. 2004. Increased incidence of cardiovascular disease in patients with rheumatoid arthritis: results from a community-based study. Annals of the Rheumatic Diseases, 63(8):952–955.
Wållberg-Jonsson, S., Cederfelt, M., Dahlqvist, S. 2000. Hemostatic factors and cardiovascular disease in active rheumatoid arthritis: an 8-year follow up study. The Journal of Rheumatology, 27(1):71–75.
Wållberg-Jonsson, S., Dahlén, G. H., Nilsson, T. K., Rånby, M., Rantapää-Dahlqvist, S. 1993. Tissue plasminogen activator, plasminogen activator inhibitor-1 and von willebrand factor in rheumatoid arthritis. Clinical Rheumatology, 12(3):318– 324.
Authors
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.