Influence of Complex Treatment Including Antiplatelet Agents on the Humoral Indicators of Endothelial Dysfunction in Patients with Atrial Fibrillation

M. A. Orynchak, M. V. Vasylechko

Abstract


Objective of the research was to compare the effect of complex treatment including omega-3 polyunsaturated fatty acids (omega-3 PUFA), antiplatelet monotherapy with acetylsalicylic acid (ASA) and its combination with L-arginine on the activity of systemic inflammation according to the C-reactive protein (C-RP) parameter and the renin-angiotensin-aldosterone system (RAAS) according to aldosterone levels in the blood at patients with atrial fibrillation (AF) depending on the presence or absence of insulin resistance. Material and methods. The study involved 137 patients with AF and with metabolic syndrome (MS). Paroxysmal AF was detected in 35 patients, persistent – in 12 and permanent – in 90 cases. Depending on the treatment patients were divided into 3 groups: group 1 consisted of 44 patients receiving standard therapy and ASA; group 2 included 46 patients receiving standard therapy and omega-3 fatty acids; group 3 – 47 patients treated with standard therapy, ASA and L-arginine. Oral glucose-tolerance test (OGTT) was conducted along with a parallel determination of glucose (oxidase method) and endogenous insulin (EI) (immunoassay) in the blood plasma.  In each group patients with normal levels of EI, reactive and spontaneous hyperinsulinemia (HI) were detected. C-RP and circulating aldosterone levels were determined using ELISA methods. The survey was performed before and after 2 months of complex treatment. Control group comprised 20 healthy individuals of appropriate age. Results and discussion. After treatment the level of HI did not significantly change in all patients (p1<0.1). The significant decrease of aldosterone levels by more than 60% was observed in patients with reactive and spontaneous HI (p1<0.05) and only by a tendency to decrease in patients with normal levels of EI (p1<0.1). Aldosterone levels reduced in patients with reactive and spontaneous HI in paroxysmal and persistent AF, and did not change in the remaining patients. Levels of C-RP in patients with reactive and spontaneous HI under paroxysmal and persistent AF reduced to a greater extent in patients of groups 2. In all patients of group 3 with paroxysmal and persistent AF C-RP levels reached the control. In 43.47% of patients with permanent AF the normalization of the C-RP was noted compared to the levels before treatment. Conclusions. Chronic inflammation parameter C-RP and secondary hyperaldosteronemia levels are humoral markers of endothelial dysfunction under insulin resistance in patients with AF and MS. Inclusion of medications (omega-3 polyunsaturated fatty acids, or aspirin with L-arginine) into basic therapy promotes more intensive reduction of EI, C-RP and aldosterone levels in the blood compared to aspirin alone.


Keywords


aldosterone; C-reactive protein; insulin resistance; atrial fibrillation; treatment

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References


Mitchenko O. I., Korpachov V.V., Bagriy A.E. [et al.]. Diagnosis and treatment of metabolic syndrome, diabetes, and prediabet CVD. 2009; 9 – 17.

Sychev O.S., Kovalenko V.N., Dzyak G. [et al.] Diagnosis and treatment of atrial fibrillation. Recommendations of the Working Group on Disturbances of Heart Rhythm of the Association of Cardiologists of Ukraine. 2011; 27 – 30.

Zhigunova A. Antyarythmic effects of the blockers of the renin-angiotensin system and their role in the treatment and prevention of atrial fibrillation. Ukrainian Medical Journal. 2012; 5 (91): 13 – 15.

Slobodskiy V.A. Experience of using Tivortin aspartate in patients with stable angina pectoris. Ukrainian Medical Journal. 2009; 5 (73):40 – 43.

Orynchak M.A., Vakalyuk I.I. Postinfarction heart and metabolic syndrome: features of the course, diagnosis and treatment: Monograph. Ivano-Frankivsk. 2013; 106.

Protasova E.A., Furman N.V., Reshetko A. Modern capabilities of prevention of atrial fibrillation. Rational Pharmacotherapy in Cardiology. 2012; 4: 561 – 568.

Fushtey I.M., Holdovskuy B.M., Sid E.V. Inflammatory activation in patients with atrial fibrillation. Medicine of Emergency Conditions. 2012; 2 (41):34 – 38.

Acevedo M., Corbalan R., Braun S. et al. C-reactive protein and atrial fibrillation: Evidence for the presence of inflammation in the perpetuation of the arrhythmia. American Journal of Cardiology. 2005; 26 (20): 2083 – 2092.

Chung M.K., Martin D.O., Sprecher D. et al.C-reactive protein elevation in patients with atrial arrhythmias: inflammatory mechanisms and persistence of atrial fibrillation. Circulation. 2001; 104: 2886 – 2891.

Ingellson E. Hulthe J., Lind L. Inflammatory markers in relation to insulin resistance and the metabolic syndrome. European Journal of Clinical Investigation. 2008; 38 (7):502 - 509.

Shinozaki K., Ayajiki K., Nishio Y.. Evidence for a causal role of the renin-angiotensin system in vascular dysfunction associated with insulin resistance. Journal of Hypertension. 2004; 43: 255 – 262.




Copyright (c) 2017 M. A. Orynchak, M. V. Vasylechko

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