TY - JOUR

T1 - Numerical Modeling of Myocardial Infarction in Multivessel Coronary Lesion. I. Analysis of Some Model Scenarios

AU - Voropaeva, O. F.

AU - Tsgoev, Ch A.

PY - 2024

Y1 - 2024

N2 - The study of the inflammatory phase of acute myocardial infarction in multivessel coronary lesion was performed using the methodology of mathematical modeling. The minimal reaction-diffusion mathematical model is focused on the description of the functional M1/M2 polarization of macrophages and the influence of factors of aseptic inflammation on the process of cardiomyocyte death. The initial conditions and dynamics of the process in the infarction nucleus are assumed to be consistent with laboratory measurement data. The nature of the spatiotemporal distribution of substances (cell populations and inflammatory mediators) and the features of the formation of nonlinear dynamic structures of demarcation inflammation are studied using model examples. The patterns of functioning of the basic mechanisms of the inflammatory response are analyzed, and the role of the main inflammatory mediators is evaluated. The previously obtained estimates of the effectiveness of anti-inflammatory therapeutic strategies based on cytokine management and macrophage polarization in complex heart attack scenarios with multivessel coronary lesion have been confirmed. The research results allow us to consider the accepted reaction-diffusion model with constant diffusion coefficients as an example of a formal mathematical description of an active environment in which dissipative (diffusion) and local biochemical processes compete with each other, as well as the pro-inflammatory link of innate immunity opposes the anti-inflammatory one. The ability of macrophages to functionally M1/M2 polarization and reprogramming plays a crucial role in this competition.The adequacy of the research results is confirmed by quantitative and qualitative agreement with experimental data.

AB - The study of the inflammatory phase of acute myocardial infarction in multivessel coronary lesion was performed using the methodology of mathematical modeling. The minimal reaction-diffusion mathematical model is focused on the description of the functional M1/M2 polarization of macrophages and the influence of factors of aseptic inflammation on the process of cardiomyocyte death. The initial conditions and dynamics of the process in the infarction nucleus are assumed to be consistent with laboratory measurement data. The nature of the spatiotemporal distribution of substances (cell populations and inflammatory mediators) and the features of the formation of nonlinear dynamic structures of demarcation inflammation are studied using model examples. The patterns of functioning of the basic mechanisms of the inflammatory response are analyzed, and the role of the main inflammatory mediators is evaluated. The previously obtained estimates of the effectiveness of anti-inflammatory therapeutic strategies based on cytokine management and macrophage polarization in complex heart attack scenarios with multivessel coronary lesion have been confirmed. The research results allow us to consider the accepted reaction-diffusion model with constant diffusion coefficients as an example of a formal mathematical description of an active environment in which dissipative (diffusion) and local biochemical processes compete with each other, as well as the pro-inflammatory link of innate immunity opposes the anti-inflammatory one. The ability of macrophages to functionally M1/M2 polarization and reprogramming plays a crucial role in this competition.The adequacy of the research results is confirmed by quantitative and qualitative agreement with experimental data.

KW - cardiomyocytes

KW - cytokines

KW - demarcation inflammation

KW - fractional step method

KW - interaction of population waves

KW - macrophage polarization

KW - mathematical model

KW - multivessel lesion

KW - myocardial infarction

KW - quasistationary structure

KW - reaction– diffusion equations

UR - https://www.scopus.com/record/display.uri?eid=2-s2.0-85200318193&origin=inward&txGid=f8768191fbe0fa573163048f9f25f01b

UR - https://www.mendeley.com/catalogue/ccede4b5-d501-3300-b4b7-61e84d910ac1/

U2 - 10.17537/2024.19.183

DO - 10.17537/2024.19.183

M3 - Article

VL - 19

SP - 183

EP - 211

JO - Mathematical Biology and Bioinformatics

JF - Mathematical Biology and Bioinformatics

SN - 1994-6538

IS - 1

ER -