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Functional phenotyping of cardiac macrophages in patients with myocardial infarction: prospects for implementation to clinical practice

Session Poster Session 1

Speaker Aleksandra Gombozhapova

Event : Heart Failure 2019

  • Topic : heart failure
  • Sub-topic : Acute Heart Failure: Pathophysiology, Other
  • Session type : Poster Session

Authors : A Gombozhapova (Tomsk,RU), Y Rogovskaya (Tomsk,RU), M Rebenkova (Tomsk,RU), J Kzhyshkowska (Tomsk,RU), V Ryabov (Tomsk,RU)

A Gombozhapova1 , Y Rogovskaya1 , M Rebenkova1 , J Kzhyshkowska2 , V Ryabov1 , 1Cardiology Research Institute, Tomsk NRMC - Tomsk - Russian Federation , 2National Research Tomsk State University - Tomsk - Russian Federation ,


Introduction. To the date we have accumulated a large amount of knowledge related to the role of macrophages in development of the cardiovascular pathology. However, there is no significant advancement in clinical studies.

Purpose. The purpose was to assess prospects for implementation of cardiac macrophage phenotyping in patients with MI in clinical practice. 

Methods. The study included 41 patients with fatal MI type 1. Group 1 (n=24) comprised patients who died within 72 hours of MI (the inflammatory phase of MI) and group 2 (n=17) comprised patients who died 4-28 days after MI (the regenerative phase of MI). Macrophage infiltration in the heart was assessed by double immunofluorescence. We used CD163, CD206 and stabilin-1 as markers of M2-like macrophages, while a-smooth muscle actin (a-SMA) was considered as a marker of macrophage transdifferentiation. Cells were counted in the infarct and non-infarct area. Each area was evaluated in 20 random fields.

Results. We identified CD163+/CD206-, CD163-/CD206+, CD163+/CD206+, stabilin-1+/a-SMA-, stabilin-1+/a-SMA+ macrophages. In the infarct area, the number of CD163+/CD206-, CD163+/CD206+, stabilin-1+/a-SMA- macrophage was lower during the inflammatory phase of MI than during the regenerative phase. Group 1 vs group 2 (number of cells in 20 random fields, median): 22 vs 83 (CD163+/CD206-, p=0.03), 12 vs 94 (CD163+/CD206+, p<0.0001), 30 vs 103 (stabilin-1+/a-SMA-, p=0.03). The number of CD163+/CD206+ macrophages in the infarct area (IA) correlated with the incidence of recurrent MI (R=0.46, p=0.006). The number of CD206+/CD163- cells in the IA correlated with in-hospital mortality according to the GRACE risk score: R=-0.43, p=0.01. The number of stabilin-1+/a-SMA+ macrophages in the IA correlated with the incidence of type 2 diabetes (R=-0.4, p=0.04), hypertension (R=-0.6, p=0.003), ventricular aneurysm (R=0.4, p=0.03), and the relative number of peripheral blood monocytes prior to the onset of death (R=-0.6, p=0.04). In the non-infarct area, the quantity of CD163+/206- cells correlated with the history of prior MI (R=0.4, p=0.02) and the incidence of recurrent MI (R=0.4, p=0.02), while the quantity of CD206+/163- macrophages correlated with the absolute number of peripheral blood monocytes at admission (R=0.4, p=0.04).

Conclusions. We revealed subpopulation of stabilin-1+/a-SMA+ macrophages, that indicated the possibility of cellular transdifferentiation and macrophage plasticity. CD206+/CD163- macrophages were proposed as a subpopulation that correlated with adverse scenario of MI. CD206+/CD163- and stabilin-1+/a-SMA- macrophages were proposed as subpopulations that correlated with the development of chronic inflammation in the heart. Our study supports prospects for implementation of macrophage phenotyping in clinical practice that might become a step to precision medicine, a breakthrough in the development of new methods for management of MI and following complications.

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