**8. Pathogenesis of the development of aortic valve insufficiency**

As a result of incomplete closure of the aortic valve leaflets during diastole, there is a reverse flow of blood from the aorta to the left ventricle [31, 32]. From 6 to 50% or more of the systolic volume of blood can return to the left ventricle. As a result of

## *Acquired Aortic Valve Diseases (Current Status of the Problem) DOI: http://dx.doi.org/10.5772/intechopen.113014*

increased blood supply (as well as normally from the atrium, and also additionally from the aorta), the left ventricle dilates, its function increases, since it must eject more blood during systole (ventricular systolic volume can reach 200–220 ml). As a result, the left ventricle is moderately hypertrophied due to the lack of resistance to the ejection of blood [32]. Dilatation of the same ventricle is compensatory, combined with the preservation of the contractile function of the left ventricle; it is called adaptive (tonogenic, primary), in contrast to the secondary (myogenic), which develops with a decrease in the contractile function of the myocardium. The defect is also compensated for by shortening the isometric contraction phase and lengthening the ejection phase, i.e., facilitating the expulsion of an increased amount of blood from the left ventricle. This is due to a more rapid increase (under the influence of additional blood volume coming from the aorta) pressure in the left ventricle to the level required to open the aortic valve, as well as a decrease in overall vascular resistance. With a large valvular defect and as decompensation develops, the diastolic pressure in the left ventricle increases, which results in isometric hyperfunction of the left atrium. The overload of the left atrium increases when, due to significant dilatation of the left atrium and left ventricle, the expansion of the left atrioventricular orifice, relative mitral valve insufficiency is formed. In the future, as decompensation progresses, congestion in the pulmonary circulation (passive pulmonary hypertension) may occur, pressure in the pulmonary artery rises, isometric hyperfunction and hypertrophy of the right ventricle develop, followed by right ventricular failure (**Figures 12–20**).

**Figure 12.** *Hemodinamic disorders in aortic insufficiency.*

**Figure 13.** *Rheumatic lesions of the aortic valve.*

**Figure 14.** *Atherosclerotic degenerative changes of the aortic valve.*

*Acquired Aortic Valve Diseases (Current Status of the Problem) DOI: http://dx.doi.org/10.5772/intechopen.113014*

**Figure 15.** *Congenital aortic valve (bicuspid aortic valve) lesions.*

**Figure 16.** *Congenital aortic valve (bicuspid aortic valve) lesions.*

#### **Figure 17.**

*Difference in calcinosis in rheumatic (a) and degenerative (b) lesions of the aortic valve.*

#### **Figure 18.**

*Morphological picture of removed aortic valve (rheumatic lesions).*

#### **Figure 19.** *Morphological picture of removed aortic valves (in degenerative lesion).*

**Figure 20.**

*Morphology of the valve in congenital defects of the aortic valve.*
