Email this article Brachial artery responsiveness in patients with systemic lupus erythematosus and scleroderma systematica
- Authors: Vinogradov A.A.1, Shilkina N.P.1, Kostyreva N.A.1, Vinogradov AA2, Shilkina NP2, Kostyreva NA2
-
Affiliations:
- Yaroslavl State Medical Academy
- Issue: Vol 82, No 1 (2010)
- Pages: 43-46
- Section: Editorial
- URL: https://ter-arkhiv.ru/0040-3660/article/view/33394
- ID: 33394
Cite item
Full Text
Abstract
Aim. to evaluate brachial artery (BA) endothelial vasomotor function in patients with systemic lupus erythematosus (SLE) and scleroderma systematica (SDS), by using noninvasive studies.
Subjects and methods. Sixty-five patients, including 25 with SLE, 20 with SDS, and 20 with atherosclerosis (AS) obliterans of lower extremity peripheral arteries, were examined. A control group consisted of 30 apparently healthy individuals matched with the study groups for gender and age. The ultrasound technique described by D. Celermajer, et al. was employed to evaluate endothelium-dependent vasodilation (EIVD). Endothelium-independent vasodilation (EIVD) was assessed by the nitroglycerin test. The coefficient of BA susceptibility (CS) to reactive hyperemia was calculated.
Results. In all study patient groups EDVD values were significantly lower (7.3 ± 1.35% in SLE, 6.91 ± 0.9% in SDS, and 7.64 ± 1.9% in AS; p < 0.05) than in the controls (11.23 ± 1.1%). An adequate vascular bed response was found in 5 (20%) patients with SLE and in 2 (10%) patients with SDS. A paradoxical vasoconstrictor response to reactive hyperemia was encountered in 9 (36%) patients with SLE, 11 (55%) with SDS. In all the study groups, the patients had normal EIVD with lower CS. In SLE and SDS, CS was decreased than that in the controls. The impaired BA responsiveness in SLE and SDS significantly correlated with the duration and activity of the disease, Raynaud's syndrome, capillaritides, mean blood pressure, renal lesions, as well as with the laboratory values of the activity of inflammation and blood lipid composition.
Conclusion. In SLE and SDS, there was a reduction in EDVD and EIVD, as well as paradoxical vasoconstriction. CS is an independent indicator of endothelial dysfunction with the normal values of EIVD. Impaired BA responsiveness was associated with the course of systemic inflammation and severe lesion of organs.
Subjects and methods. Sixty-five patients, including 25 with SLE, 20 with SDS, and 20 with atherosclerosis (AS) obliterans of lower extremity peripheral arteries, were examined. A control group consisted of 30 apparently healthy individuals matched with the study groups for gender and age. The ultrasound technique described by D. Celermajer, et al. was employed to evaluate endothelium-dependent vasodilation (EIVD). Endothelium-independent vasodilation (EIVD) was assessed by the nitroglycerin test. The coefficient of BA susceptibility (CS) to reactive hyperemia was calculated.
Results. In all study patient groups EDVD values were significantly lower (7.3 ± 1.35% in SLE, 6.91 ± 0.9% in SDS, and 7.64 ± 1.9% in AS; p < 0.05) than in the controls (11.23 ± 1.1%). An adequate vascular bed response was found in 5 (20%) patients with SLE and in 2 (10%) patients with SDS. A paradoxical vasoconstrictor response to reactive hyperemia was encountered in 9 (36%) patients with SLE, 11 (55%) with SDS. In all the study groups, the patients had normal EIVD with lower CS. In SLE and SDS, CS was decreased than that in the controls. The impaired BA responsiveness in SLE and SDS significantly correlated with the duration and activity of the disease, Raynaud's syndrome, capillaritides, mean blood pressure, renal lesions, as well as with the laboratory values of the activity of inflammation and blood lipid composition.
Conclusion. In SLE and SDS, there was a reduction in EDVD and EIVD, as well as paradoxical vasoconstriction. CS is an independent indicator of endothelial dysfunction with the normal values of EIVD. Impaired BA responsiveness was associated with the course of systemic inflammation and severe lesion of organs.
About the authors
Aleksey Alekseevich Vinogradov
Email: vinograd@fromru.com
Nataliya Petrovna Shilkina
Email: shilkin39@mail.ru
Natal'ya Aleksandrovna Kostyreva
Email: kostyrevanatalya@yandex.ru
A A Vinogradov
Yaroslavl State Medical AcademyYaroslavl State Medical Academy
N P Shilkina
Yaroslavl State Medical AcademyYaroslavl State Medical Academy
N A Kostyreva
Yaroslavl State Medical AcademyYaroslavl State Medical Academy
References
- Лелюк В. Г., Лелюк С. Э. Ультразвуковая ангиология. М.: Реальное время; 1999.
- Мач Э. С. Особенности поражения сосудов при РА: влияние возраста, течения. Клинич. ревматол. 1994; 2: 19-21.
- Петрищев Н. Н., Власов Т. Д. Физиология и патофизиология эндотелия. Дисфункция эндотелия. Причины, механизм, фармакологическая коррекция / Под ред. Н. Н. Петрищева. СПб.: СПбГМУ; 2003.
- Bulkley B. H., Roberts W. C. The heart in systemic lupus erythematosus and the changes induced in it by corticosteroid therapy. A study of 36 necropsy patients. Am. J. Med. 1975; 58: 243-264.
- Shin C. M. Increased lung uptake of technetium-99m hexamethylpropylene amine oxime in SLE. Respiration 2002; 3: 69- 76.
- Clancy R., Marder G., Martin V. et al. Circulating activated endothelial cells in systemic lupus erythematosus: further evidence for diffuse vasculopathy. Arthr. and Rheum. 2001; 44(5): 1203-l208.
- Clancy R. M. Circulating endothelial cells and vascular injury in systemic lupus erythematosus. Curr. Rheumatol. Rep. 2000; 2(1): 39-43.
- Celermajer D. S., Sorensen K. E., Gooch V. M. et al. Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis. Lancet 1992; 340: 1111-1115.
- Rajagopalan S., Somers E. G., Brook R. D. et al. Endothelial cell apoptosis in systemic lupus erythematosus: a common pathway for abnormal vascular function and thrombosis propensity. Blood 2004; 103(10): 3677-3683.
- Tam L. S., Fan B., Li E. K. et al. Patients with systemic lupus erythematosus show increased platelet activation and endothelial dysfunction induced by acute hyperhomocysteinemia. J. Rheumatol. 2003; 30(7): 1479-1484.
- El-Magadmi M., Bodill H., Ahmad Y. et al. Systemic lupus erythematosus: an independent risk factor for endothelial dysfunction in women. Circulation 2004; 110(4): 399-404.
- Lima D. S., Sato E. I., Lima V. C. et al. Brachial endothelial function is impaired in patients with systemic lupus erythematosus. J. Rheumatol. 2002; 29(2): 292-297.
- Soer J. B., Mictus-Snyder M., Malloy M. J. et al. Assessment of atherosclerotic risk factors and endothelial function in children and young adults with pediatric-onset systemic lupus erythematosus. Arthr. and Rheum. 2004; 51(3): 451-457.
- Кароли Н. А., Ребров А. П., Орлова Е. Е. Эндотелиальная дисфункция у больных системной склеродермией. Науч.-практ. ревматол. 2005; 3: 57.
- Инамова О. В., Ребров А. П. Повреждение и дисфункция эндотелия при ревматоидном артрите на фоне различной терапии. Науч.-практ. ревматол. 2005; 3: 52.
- Скрябина Е. Н., Попова М. А., Юдакова Ю. Н. Эндотелиальная дисфункция у больных неспецифическим аортоартериитом. Науч.-практ. ревматол. 2003; 2: 91.
- Fischer D., Rossa S., Landmesser U. et al. Endothelial dysfunction in patients with chronic heart failure is independently associated with increased incidence of hospitalization, cardiac transplantation, or death. Eur. Heart J. 2005; 26: 65-69.
Supplementary files
