**5. Clinical picture**

Symptoms attributed to mitral valve prolapsus (MVP) cannot clearly be explained by the degree of prolapse or mitral regurgitation. However, autonomic or neuroendocrine dysfunction has been suggested as a possible cause of the nonspecific symptoms in many patients with MVP. Patients with MVP tend to exhibit the following findings when compared to controls [3, 4]:


The specificity of these findings for MVP is uncertain. One study found a series of abnormalities in patients with symptoms of autonomic dysfunction, which did not correlate with the presence or absence of MVP [5].

An association between panic disorder and MVP has also been suggested by several studies, including a meta-analysis [6]. However, these studies have been criticized because of inconsistencies in the diagnostic criteria used for both panic disorder and MVP and the use of imperfectly matched controls. In addition, panic disorder and MVP are both common illnesses with similar age and gender distributions, suggesting that their association may only be a coincidence.

development and progression of mitral valve prolapse [28]. However, modern protocols for

At the basis of the development of secondary MVP lies the violation of myocardial contractility of the left ventricle and dysfunction of the papillary muscles. It develops under the following pathological conditions: inflammatory processes (myocarditis), cardiomyopathy, myocardial dystrophy [10, 16], ischemic heart disease, a decrease in tissue elasticity as a result of left ventricular contraction asymmetry and papillary muscle ischemia and tendon chords, violation of autonomic innervation and impulse conduction in myocarditis, extrasystole, WPW syndrome, with neuroses and hysteria. Also, the cause of secondary MVP can serve as a blunt trauma to the heart [22]. Most researchers are supporters of the "valve" theory. This theory presupposes the presence of a genetically determined collagen defect, which leads to the "weakness" of the connective tissue of the mitral valve flaps and their prolapse into the atrial cavity. Three gene loci are described on 16, 11, and 13 chromosomes, but the genetic defects underlying them are not known to date. The recessive form of MVP associated with the X chromosome is known as myxomatous dystrophy of the heart valves, and mutations of the gene for the pathogen have

There are several possible pathogenetic mechanisms that can explain the onset of MVP. According to some data, the role of magnesium deficiency in the development of MVP is great. The lack of magnesium reduces the activity of magnesium-dependent adenylate cyclase, which ensures the removal of defective collagen [29] and affects the ability of fibroblasts to produce collagen [16]. In addition to the direct participation of magnesium ions in the processes of collagen formation, the role of magnesium in the functioning of the vegetative nervous system is undoubtedly important, since a deficiency of magnesium ions promotes an increase in the level of catecholamines of the blood plasma, that is, the development of hypercatecholaminemia, changes in the tone of the papillary muscles, and the formation of MVP.

Symptoms attributed to mitral valve prolapsus (MVP) cannot clearly be explained by the degree of prolapse or mitral regurgitation. However, autonomic or neuroendocrine dysfunction has been suggested as a possible cause of the nonspecific symptoms in many patients with MVP. Patients with MVP tend to exhibit the following findings when compared to controls [3, 4]:

The specificity of these findings for MVP is uncertain. One study found a series of abnormalities in patients with symptoms of autonomic dysfunction, which did not correlate with the

management of patients with MVP do not provide for antibiotic prophylaxis [3].

recently been identified [6].

84 Structural Insufficiency Anomalies in Cardiac Valves

**5. Clinical picture**

presence or absence of MVP [5].

• elevated urine and plasma catecholamine levels;

• an exaggerated heart rate response to phenylephrine;

• a less than expected bradycardiac response to the dive reflex; • the reproduction of symptoms with isoproterenol infusion.

The clinical manifestations of prolapsus of the mitral valve differ in variety [5, 6]. At the same time, most researchers note the polymorphism of the clinical picture [3, 17]. Data on the frequency of clinical symptoms and the pathogenetic mechanisms of their formation are contradictory [3, 10, 11, 13]. However, the recognition of prolapsus is accompanied by a fairly clear and definite clinical picture. It is proposed to isolate clinically and morphologically significant MVP syndromes:


**6.** the vegetative crises (sympathetic-adrenal, vago-insular, mixed). These are the most striking manifestations of MVP;

pulmonary ejection clicks (occurring early in systole, at the foot of the carotid upstroke) and from other cardiac sounds (split first or second heart sounds, pericardial sounds, atrial septal

Mitral Valve Prolapse in Pregnancy: Modern Concept http://dx.doi.org/10.5772/intechopen.76692 87

With a routine clinical examination and auscultation of cardiac tones, a systolic click is heard between the I and II heart tones, together or without middle diastolic or late systolic murmur, which is a characteristic symptom. The presence of these auscultative data may vary depending on the position of the body of the pregnant woman or the degree of her hydration. Similar auscultative changes can occur in healthy women during pregnancy, varying in the time of click occurrence and in mitigating or shortening the time of noise, and when series of echocardiographic studies in the presence of MPV in some women EchoCG signs of

In most pregnant women who do not show any other clinical signs, so in the absence of significant regurgitation in *echocardiography*, women should talk about the safety of pregnancy and childbirth, as well as the absence of a negative effect on the fetus of this condition [3]. MVP is diagnosed at the maximum systolic displacement of the mitral valve flaps beyond the ring line in the parasternal longitudinal position by more than 2 mm. The use of the parasternal longitudinal section for the diagnosis of MVP is due to the peculiarities of the shape of the mitral valve ring, while the isolated displacement of the anterior valve beyond the ring line seen in the four-chamber apex position is the main cause of its overdiagnosis. In echocardiographic conclusion, it is necessary to indicate the depth of prolapse, the length and thickness

The normal length of the front leaf is 21–24 mm, the rear is 12–14 mm. Depending on the thickness of the leaf, the classic MPV is distinguished, with a valve thickness of more than 5 mm in diastole (reflects the presence of myxomatous degeneration of the valves) and non-

The determination of the degree of mitral regurgitation is currently conducted according to the recommendations of the ANA/ACC [6]. For this purpose, the following qualitative indices are used: the diameter of the vein of the regurgitation jet (vena contracta), the volume of regurgitation, and the area of the regurgitation opening calculated according to the area of the proximal equal-velocity surface (PISA). Specific for MPV is the mitral regurgitation that

The evaluation of LV systolic function is also an important component of EchoCG study. It is an important prognostic factor in patients with MVP and severe MH [6, 12]. There is evidence of worsening of LV systolic function in young patients with MVP and without significant

The development of 3D technology, especially real-time 3D-TEE, provides excellent rendering of the mitral valve complex. Live 3D-TEE has become routine in pre/intraoperative imaging of the mitral valve and in percutaneous mitral valve interventions. 3D-TEE efficiently identifies

of each of the valves, and the degree of mitral regurgitation [6, 12] (**Figure 2**).

occurs at the end of the systole; it is usually high speed and eccentric.

classical MPV—with a thickness of less than 5 mm.

mitral regurgitation [35].

aneurysm clicks).

it disappear [6].

**6.2. Diagnostic imaging techniques**

**7.** the mental disorders: neurasthenia, anxiety disorders, anxiety-phobic disorders, mood disorders. When assessing the results of a comprehensive psychological examination, it was found that in persons with mitral valve prolapse, there are a number of distinguishing features from healthy people: inadequate self-esteem (32.1%), low level and inadequacy of attitudes (50.9%), high situational anxiety (32.7%), low emotional stability (39.0%), and a decrease in the dynamic indicators of mental activity [6].

Along with the widespread point of view about the propensity of patients with mitral valve prolapse to hypotension, recently there have been isolated reports of the presence of arterial hypertension in patients with prolapse of the mitral valve [5]. The possibility of hereditary predisposition to arterial hypertension, mixed with hereditary pathology of connective tissue, is not excluded.

However, not all authors agree with the presence of MPV syndrome with the above-described clinical symptoms [3], believing that PMC is only an anatomical feature of the valve structure, if it is not a manifestation of the Martha syndrome. Clinical manifestations of approximately equal frequency are observed in women with and without EchoCG signs of MPV.
