[The role of connective tissue dysplasia in the forming of mitral valve prolapse].

Connective tissue (CT) is a multifunctional universal structure of great importance to the human organism. Constituting about 50% of the body mass, CT forms a frame (skeleton) and outer cover (skin), as well as the inner medium, through which all structural elements receive nutrients and extract metabolic products. The great number of links, constituting the CT system, each of which is controlled genetically and is liable to genetic lesions, creates conditions for heterogeneity of malformations and diseases involving CT. Non-differentiated CT dysplasia (NDCTD) is a genetically heterogenous group, presenting a basis for various chronic diseases. NDCTD may present the cause of dysplastic changes in the CT of different organs and systems. Thanks to modern diagnostic techniques, NDCTD is revealed frequently. NDCTD is underlied by molecular-, onto-, and pathogenetic mechanisms, leading to structural and functional changes in CT. This CT "weakness" is manifested by the peculiarities of the structure of various organs and systems. Mesenchimal heart dysplasias are the most widespread visceral markers of the given CT pathology. CT dysplasias of the heart are often combined with varied manifestations of system CT anomaly. Mitral valve prolapse (MVP) is the most wide-spread and well-studied minor heart anomalies. Primary MVP is a hereditary or congenital pathology and is not connected with a particular disease. It is a genetic pathology--CT dysplasia with autosomal dominant inheritance. Patients with MVP have an increased expression of Bw35 antigen of HLA system, which causes dysmetabolism of collagen in the mitral cusps. It has been revealed that tissue deficiency of magnesium is associated with antigen expression and correlates with clinical symptoms in MVP. Exogenic factors influencing MVP have been described.