**3. Classification**

For the first time, mitral valve prolapse was described by J.B. Barlow et al. in 1963.

There are multiple ways of classifying MVP, underscoring the heterogeneity of this disorder:


The 2014 American Heart Association/American College of Cardiology guidelines for the management of patients with valvular heart disease separate mitral regurgitation by a mechanism into primary (disease of one or more valve components including leaflets, chordae tendineae, papillary muscles, or annulus) and secondary (disease of the left ventricle) [22]. In this classification, primary disease includes all forms of MVP along with other causes of MR involving the components of the valve (e.g., calcific degeneration, cleft mitral valve, leaflet perforations, etc.). Isolate primary (congenital, idiopathic) and secondary prolapse develops against the background of the already existing diseases of the cardiovascular system. Primary prolapse of the mitral valve is a hereditary violation of the formation of the connective tissue [6, 7, 10, 11]. It should be noted that in the MVP structure, the primary occurs much more often. The share of the secondary accounts for only 5% of the total number of observations. Clinically anatomically, MVP is a syndrome that accompanies many nosological forms [10, 15, 16].

Currently, there are several MVP variants [23]:

**1.** pleiotropic manifestation of some classified hereditary disorders of the connective tissue (syndromes Marfan, Ehlers-Danlo, etc.). Thus, the combination of MVP with aortic dilatation and signs of connective tissue dysplasia of seven or more points gives reason to consider it as associated with the Marfan syndrome. However, it should be emphasized that only 1–2% of patients with MVP have one of the monogenic undifferentiated disorders of the connective tissue [6];


With the exclusion of MVP syndrome, prolapse of the valves without their thickening and significant mitral regurgitation can be regarded as one of the variants of a small heart anomaly, the number of which, as is well known, closely correlates with the number of external signs of dysembryogenesis detected [24].
