Neuroimmune and endocrine mechanisms of unfavorable geriatric status in patients with acute coronary syndrome

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Background: Acute coronary syndrome (ACS) is the cause of above 70% of deaths in patients of older age. Frailty that develops in elderly patients provokes pro-inflammatory and neuroimmune inflammatory responses in the body that promote deterioration of the ACS course.

Aim: To study neuroimmunoendocrine alterations in elderly patients with ACS depending on the presence or absence of the frailty syndrome.

Materials and methods: The study was performed by retrospective, cross-sectional and prospective evaluation of the ACS patient registries within an international project GIRAFFE (Gerontological Research International Against Frailty: Fit Experience) in 2011–2015. We analyzed the results of measurement of serum tumor necrosis factor alfa (TNF-α) and the interleukin family (IL-1β, IL-4, IL-6, IL-10) in 633 patients with non-ST ACS (n = 270) and with ST-ACS (n = 363) at days 5, 12, and 26 from the beginning of the pain syndrome. From those, 265 patients were non-frail, 97 were pre-frail, and 271 patients had the frailty syndrome. The control group included 116 patients without significant somatic disease.

Results: In all study groups of patients with non-ST ACS, there was an increase in IL-4, IL-6 and IL-10 levels, compared to their reference ranges, at day 5 from the beginning of the pain syndrome. Subsequently, these parameters were changing with therapy, similarly in all groups: IL-4 level gradually decreased by the end of the follow-up, IL-10 level increased by day 12 from the beginning of the pain syndrome and decreased by day 26. The lowest IL-10 levels compared to the reference range (1.5 ± 0.2 pg/mL) were seen in the elderly frail patients: 2.9 ± 0.6 pg/mL at day 5 from the beginning of the pain syndrome, 7.2 ± 1.2 pg/mL at day 12, and 1.9 ± 0.3 pg/mL at day 26, compared to 8 ± 1.2, 15.5 ± 1.6 and 6.2 ± 1.1 pg/mL in the isolated ACS group, respectively (all p < 0.05). In the group with non-ST ACS, higher TNF-α and IL-1β levels, compared to the control, were registered only in the elderly frail patients. Under treatment, these parameters did not reached the reference ranges, being 187.7 ± 6.5 and 310.2 ± 29.5 pg/mL at day 5 from the beginning of the pain syndrome, 165 ± 6 and 299.5 ± 29.4 pg/mL at day 12 and 154 ± 5.9 and 265.9 ± 27.9 at day 26, respectively, compared to 68.7 ± 3 pg/mL (p < 0.05 for all comparisons to the control group). In the ST-ACS patients, TNF-α, IL-1β, IL-4, IL-6, and IL-10 levels exceeded the reference ranges in all groups studied for the whole study duration. In the patients with the elderly frailty syndrome the serum concentrations of TNF-α, IL-1β, IL-6 and IL-10 were higher than in the non-frail and pre-frail patients with ST-ACS. The IL-4 levels were not informative for the assessment of the contribution of the elderly frailty to the ST-ACS course.

Conclusion: The frailty syndrome of the elderly provokes the activation of the pro-inflammatory system that is confirmed by the consistent increase of serum pro-inflammatory mediators associated to the degree of the frailty syndrome in ACS patients.

About the authors

E. V. Sedova

Saint Petersburg Institute of Bioregulation and

Author for correspondence.

MD, PhD, Senior Research Fellow

25 Kuznetsovskaya ul., Saint Petersburg, 196105, Russian Federation. Tel.: +7 (921) 937 92 44

Russian Federation

F. N. Paleev

Moscow Regional Research and Clinical Institute (MONIKI)


MD, PhD, Professor, Member-Correspondent of Russian Academy of Sciences, Director

61/2 Shchepkina ul., Moscow, 129110, Russian Federation

Russian Federation

K. I. Prashchayeu

Research Medical Center “Gerontology”


MD, PhD, Professor, Director

6–VI–1–4 1-ya Aeroportovskaya ul., Moscow, 125319, Russian Federation

Russian Federation

E. I. Korshun

Research Medical Center “Gerontology”


MD, Researcher, Department of Clinical Gerontology

6–VI–1–4 1-ya Aeroportovskaya ul., Moscow, 125319, Russian Federation

Russian Federation


  1. Манюкова ЭТ, Шаленкова МА, Михайлова ЗД. Модель «CVCACS» для прогнозирования развития кардиоваскулярных осложнений в госпитальном периоде острого коронарного синдрома. Медицинская иммунология. 2015;17(1): 81–6.
  2. Ильницкий АН, Прощаев КИ, Варавина ЛЮ, Кривецкий ВВ. Старческая астения (frailty): оксидативные и нейроиммуноэндокринные изменения. Медицина и здравоохранение. 2013;(3): 37–9.
  3. Хавинсон ВХ, Линькова НС, Трофимов АВ, Полякова ВО, Севостьянова НН, Кветной ИМ. Морфофункциональные основы пептидной регуляции старения. Успехи современной биологии. 2011;131(2): 115–21.
  4. Крулевский ВА, Губарев ЮД, Горелик СГ, Кветной ИМ. Роль современной диагностики в гериатрии с позиций таргетности. Геронтология. 2015;(2). Доступно на:
  5. Пальцев МА, Кветной ИМ. Руководство по нейроиммуноэндокринологии. М.: Медицина; 2006. 384 с.
  6. Berrut G, Andrieu S, Araujo de Carvalho I, Baeyens JP, Bergman H, Cassim B, Cerreta F, Cesari M, Cha HB, Chen LK, Cherubini A, Chou MY, Cruz-Jentoft AJ, De Decker L, Du P, Forette B, Forette F, Franco A, Guimaraes R, Guttierrez-Robledo LM, Jauregui J, Khavinson V, Lee WJ, Peng LN, Perret-Guillaume C, Petrovic M, Retornaz F, Rockwood K, Rodriguez- Manas L, Sieber C, Spatharakis G, Theou O, Topinkova E, Vellas B, Benetos A. Promoting access to innovation for frail old persons. IAGG (International Association of Gerontology and Geriatrics), WHO (World Health Organization) and SFGG (Société Française de Gériatrie et de Gérontologie) Workshop – Athens January 20-21, 2012. J Nutr Health Aging. 2013;17(8): 688–93. doi: 10.1007/s12603-013-0039-2.
  7. Палеев ФН, Белокопытова ИС, Минченко БИ, Москалец ОВ. Роль цитокинов в патогенезе ишемической болезни сердца. Креативная кардиология. 2011;(1): 75–80.
  8. Сайгитов РТ, Глезер МГ, Семенцов ДП, Малыгина НА. Особенности прогнозирования при остром коронарном синдроме у мужчин и женщин. Кардиоваскулярная терапия и профилактика. 2006;5(1): 63–70.
  9. “GIRAFFE” – “Gerontological International Research Against Frailty: Fit Experience” [Internet]. Available from:

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Copyright (c) 2017 Sedova E.V., Paleev F.N., Prashchayeu K.I., Korshun E.I.

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