Preview

Cardiovascular Therapy and Prevention

Advanced search

New perspectives in immunological diagnostics of coronary heart disease

https://doi.org/10.15829/1728-8800-2012-1-49-53

Abstract

Aim. To assess the diagnostic value of immunological markers of endothelial dysfunction (ED) in various clinical variants of coronary heart disease (CHD).
Material and methods. The study included 455 patients with various clinical variants of CHD. The control group (CG) included 70 individuals without clinical CHD symptoms. Solid-phase immunoenzymatic method was used for measuring the serum titres of Chlamydia pneumoniae (Cp), sulphated glycosamineglycanes (s-GAG), collagen (C), and hyaluronic acid (HA) antibodies.
Results. In patients with acute coronary syndrome (ACS), mean titres of Cp, s-GAG, C, and HA antibodies were significantly higher than in patients with chronic CHD or CG participants. Among patients with myocardial infarction (MI), the levels of troponin I (TrI) and MB-creatine phosphokinase (MB-CK) significantly correlated with the titres of s-GAG and C antibodies, while the levels of C-reactive protein (CRP) were linked to the titres of C and HA antibodies. In ACS with ST segment elevation, the measurement of Cp, s-GAG, C, and HA antibodies was comparable to the measurement of CRP, TrI, or MB-CK activity, being significantly more sensitive than echocardiography (EchoCG). In non-ST ACS, immunological parameters were as sensitive as electrocardiography or CRP measurement, more reliable than MB-CK activity measurement or EchoCG, and slightly less reliable than TrI measurement. In unstable angina pectoris (UAP), immunological analysis was significantly more sensitive than the majority of the standard diagnostic methods.
Conclusion. Pathogenetic mechanisms of ACS are closely related to the development of specific autoimmune reactions. The assessed immunological parameters could be used as objective markers of acute CHD variants.

About the Authors

S. I. Davydov
Volgograd State Medical University, Volgograd
Russian Federation


A. A. Tarasov
Volgograd State Medical University, Volgograd
Russian Federation


A. L. Emelyanova
Volgograd State Medical University, Volgograd
Russian Federation


M. A. Kiseleva
Volgograd State Medical University, Volgograd
Russian Federation


A. R. Babaeva
Volgograd State Medical University, Volgograd
Russian Federation


References

1. Всероссийское научное общество кардиологов. Рекомендации по лечению острого коронарного синдрома без стойкого подъёма сегмента ST на ЭКГ. Москва 2008.

2. Довгалевский П. Я. Острый коронарный синдром – патогенез, клиническая картина, аспекты лечения. Что мы знаем и что надо делать? (Обзор). Сердце 2002; 1: 13-5.

3. Кухарчук В.В., Зыков К.А., Масенко В.П. и др. Динамика воспалительного процесса у больных с острым коронарным синдромом и больных со стабильной стенокардией. Биохимические и иммунологические аспекты. Кардиол вест 2007; 02; 2.

4. Нагорнев В.А. Патогенез атеросклероза. СПб 2006.

5. Оганов Р.Г., Калинина А.М., Поздняков Ю.М. Профилактическая кардиология (руководство для врачей). Москва 2007.

6. Руководство по атеросклерозу и ишемической болезни сердца. Под редакцией академика Е.И. Чазова и др. Москва 2007.

7. Шлычкова Т.П, Жданов В.С. Основные типы нестабильных атеросклеротических бляшек и их распространенность в коронарных артериях при остром инфаркте миокарда. Арх пат 2005; 3: 24-8.

8. Albert NM. Inflammation and infection in acute coronary syndrome. J Cardiovasc Nurs 2000; 15: 13-26.

9. Arroyo-Espliguero R, Avanzas P, Cosin-Sales J, et al. C-reactive protein elevation and disease activity in patients with coronary artery disease. Eur Heat J 2004; 25: 401-8.

10. Boersma E, Pieper KS, Steyerberg EW, et al., for the PURSUIT Investigators. Predictors of outocome in patients with acute coronary syndromes without persistent ST-segment elevation. Results from an international trial of 9461 Patients. Circukations 2000; 101: 2557-67.

11. Davies MJ. The pathophysiology of acute coronary syndromes. Heart 2000; 83: 361-6.

12. Zebrack JS, Muhlestein JB, Horne BD, et al. C-reactive protein and angiographic coronary artery disease: independent and additive predictors of risk in subjects with angina. JACC 2002; 39; 632-7.

13. Kuller LH, Tracy RP. The role of inflammation in cardiovascular disease. Arterioscler Thromb Vasc Biol 2000; 20: 901.

14. Madjid M, Vela D,Khalili-Tabrizi H, et al. Systemic infections cause exaggerated local inflammation in atherosclerotic coronary arteries: clues to the triggering effect of acute infections on acute coronary syndromes. Tex Heart Inst J 2007; 34: 11-8.

15. James SK, Armstrong P, Barnathan E, et al and the GUSTO-IV-ACS Investigators., et al: Troponin and C-reactive protein have different relations to subsequent mortality and myocardial infarction after acute coronary syndrome: A GUSTO-IV substudy. JACC 2003; 41: 916.

16. Randriamboavonjy V, Fleming I. Endothelial nitric oxide synthase (eNOS) in platelets: how is it regulated and what is it doing there? Pharmacol Rep 2005; 57 (Suppl): 59-65.

17. Ross R. Atherosclerosis: an inflammatory disease. N Engl J Med 1999; 340: 115-26.

18. Shah PK. Pathophysiology of coronary thrombosis: role of plaque rupture and plaque erosion. Progress in Cardiovascular Diseases 2002; 44: 5.


Review

For citations:


Davydov S.I., Tarasov A.A., Emelyanova A.L., Kiseleva M.A., Babaeva A.R. New perspectives in immunological diagnostics of coronary heart disease. Cardiovascular Therapy and Prevention. 2012;11(1):49-53. (In Russ.) https://doi.org/10.15829/1728-8800-2012-1-49-53

Views: 566


Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.


ISSN 1728-8800 (Print)
ISSN 2619-0125 (Online)