Mechanisms of vibration-induced structural myocardial remodeling

Abstract

The review presents literature data analysis devoted to the study of structural changes in the heart in patients with vibration disease, identified by echocardiographic methods in the form of concentric remodeling of the left ventricle chambers and disturbance of its diastolic function, a decrease in the intensity of the heart structure work compared to healthy ones in 1.2 times (p0.05). The changes in morphometric and bioenergetic parameters of cardiomyocytes against the background of various experimental vibration modes (7 and 56 sessions with a frequency of 8 Hz) confirms the violation of the ideal relationship between the spatial configuration of the heart cavities, the ability to contract and the energy supply potential. The loss of cardiac myofibrils symbolizes the convertion of myocardial hypertrophy to the decompensation stage and the increase in degenerative (dystrophic) signs, in particular the loss of sarcomeres of cardiomyocytes.
 To realize the processes of pathological structural (morphological) and energy restructuring of tissue under the influence of vibration-mediated hemodynamic and ischemic factors, it is necessary to involve in the process numerous mediators that regulate metabolism, proliferation, growth and survival of cells, such as STIM (stromal interaction molecule), SERCA (calcium ATPase of the endo(sarco)plasmic reticulum), IP3R (inositol-1,4,5-triphosphate receptor), Orai (protein that forms CRAC channels), TRPC (transient receptor potential canonical), etc. As one of the most important link of structural cardiac remodeling is performed by the degradation system of the extracellular matrix, including matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs), which regulate the rate of mRNA synthesis on the DNA matrix by binding to specific DNA regions that control cardiac nutrition and plasticity. A lot of analyzed facts make it possible to explain some patterns of the development of cardiac remodeling in patients with vibration disease and to determine the direction of pathogenetically based approaches to therapy, taking into account not only the vibration-protective effect of drugs, but also their ability to inhibit and regress myocardial remodeling.