Role of inflammatory and sympathetic activation in anxiety and depression interaction with myocardial infarction

Authors: N.B. Lebedeva 1, O.L. Barbarash 2

Company: 1- Research Institute for Complex Issues of Cardiovascular Diseases Siberian Branch of the Russian Academy of
Medical Sciences;
2Kemerovo State Medical Academy of Ministry of Health of the Russian Federation


For citation: Lebedeva NB, Barbarash OL. Role of inflammatory and sympathetic activation in anxiety and depression interaction with myocardial infarction. Kreativnaya kardiologiya. 2013; 2: 27-34 (in Russian)

Keywords: depression myocardial infarction autonomic imbalance inflammation

Full text:  

 

Abstract

ИSummary. Ischemic heart disease as well as anxiety and depressive disorders are the diseases that are closely linked by common risk factors and pathogenic mechanisms, such as hyperactivity of the hypothalamic-pituitary-adrenal system, autonomic imbalance, platelet pathology and inflammation.

Objective. To examine the relationships of subclinical inflammation biomarkers, autonomic imbalance and anxiety and depressive syndromes in patients with myocardial infarction (MI).

Material and Methods. 106 patients with ST-segment elevation MI, mean age 61.4±1.6 years, were enrolled. At days 5–7 the heart rate variability was assessed, plasma inflammatory biomarker concentrations (interleukins IL-1β, IL-6, IL-8, IL-10, interferon γ (INFγ), tumor necrosis factor alpha (TNFγ)) were measured by ELISA and psychometric testing using the Zung Self-Rating Depression scales, State-Trait Anxiety Inventory (Spielberger-Hanin) was done. The data were analyzed using the Statistica 6.0 software package (StatSoft).

Results. Patients with depression and increased levels of state and trait anxiety had significantly higher CRP and INFγ plasma concentrations as compared to those without depression or anxiety symptoms. Depression was associated with significantly higher concentrations of inflammatory cytokines IL-1β (72.2±1.3 pg/ml vs 49.5±7.7 in patients without depression, p=0.08), IL-8 (104.5±4.4 pg/ml vs 43.8±1.2, respectively, p=0.009) and reduced anti-inflammatory IL-10 (1.0±0.2 pg/ml vs 2.1±0.4; p=0.01), as well as with the sympathetic nervous system activation, as assessed with the SDNN. In the group of patients with myocardial infarction, who had a marked increase in the sympathetic nervous system activity (SDNN less 70 ms), the levels of IL-1β, IL-8, TNFα and INFγ were significantly higher as compared to those in patients with the normal SDNN values. Indeed, IL-1β levels were 164.5 (152, 174) and 108 (96, 110), respectively, IL-6 levels: 4.48 (2.2, 6.3) and 3.44 (2.4, 4.9) IL-8: 81.3 (76, 92) and 41 (28, 51); TNFFα levels: 37.4 (28.6, 44.4) and 2.63 (1.9, 4.3); INFγ 94.9 (91, 101.2) and 21.6 (18.3, 23), p<0.001 in all cases. The resulting differences did not depend on the severity of myocardial infarction.

Conclusion. The presence of myocardial infarction in patients with sub-acute symptoms of depression and increased anxiety is associated with more severe inflammatory and sympathetic activation, which may explain a well-known adverse prognostic role of anxiety and depression syndrome in MI.

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Chief Editor

Leo A. Bockeria, MD, PhD, DSc, Professor, Academician of Russian Academy of Sciences, President of Bakoulev National Medical Research Center for Cardiovascular Surgery