Morphological changes in structural components of human heart valves associated with chronic haemodynamic trauma

Abstract

The heart valve design is optimally adapted to their physiological function, i.e., the uniform distribution of blood flow in the heart chambers, so even small changes in the structural components of the valves, which are initially functionally compensated, play a significant role in the development of heart disease in the later stages of a patient's life. The study aimed to determine the effect of chronic haemodynamic trauma on the structural reorganisation of human heart valves. A total of 1377 human heart valves were evaluated, which were obtained during valve prosthetics at the Amosov National Institute of Cardiovascular Surgery from 2010 to 2022. The study identified a full range of macro- and microscopic changes in morphological structures that are characteristic of rheumatic heart disease, infective endocarditis, dysplastic and destructive changes in heart valves. The set of all morphological features was combined into the algorithm “Morphological manifestations of acquired heart disease of different genesis”. It has been established that changes in the mitral valve architecture can cause the transformation of its structural components, which causes a violation of the valve's functional capabilities. The study demonstrated that persistent changes associated with chronic haemodynamic injury reduce the mechanical strength of the valve, despite the compensatory mechanism of subendothelial smooth muscle fibre hyperplasia in the heart valve leaflets. Subsequently, these damages can, on the one hand, be complicated by fibrosis, fatty degeneration and calcification, and on the other hand, compensatory mechanisms are involved in the process, namely hyperplasia of subendothelial muscle cells, which often form continuous layers that should strengthen and strengthen the mechanical strength and thus the functional competence of the valves. Mitral valve dysplasia can develop secondary infective endocarditis, rheumatism, and degenerative valve disease. The algorithm for determining the patterns of morphological changes in the valvular apparatus of the heart in various variants of acquired defects of inflammatory and non-inflammatory genesis can be used to improve the etiopathogenetic drug treatment of patients with acquired heart disease, as well as a theoretical basis for the development of new types of valve-preserving operations