Aortic Valvopathy

Anatomy

The aortic valve is the initial part of the aortic root, forming an aortic valve complex composed of:

  • Valsalva Sinuses
  • Interim fibrous triangles (between leaflets)
  • Three valve leaflets

 

The insertion plane of the leaflets marks the beginning of the aortic root and the sinotubular junction separates this root from the ascending aorta. The posterior portion of the aortic annulus is in close contact with the mitral annulus and orifice and the interventricular septum. Thus, about 2/3 of the posterior portion is in contact with the interventricular septum and 1/3 is in contact with the mitral-aortic intervalvular fibrosa (MAIVF).

As described, the aortic valve is composed of 3 leaflets with semilunar implantation, along the annulus. The free edge of each one curves slightly from the commissures and presents a slight thickening at the tips, a point called “Arantius”. Each of the leaflets is identified by the relationship with the coronary ostia in: right coronary, left coronary and noncoronary.

Valsalva’s sinuses are areas of expansion of the aortic root wall, being separated from each other by the fibrous triangles. When the leaflets are opened during systole, there is no obliteration of the coronary ostia because of these expansions. Flow vortices are formed in this region ensuring coronary perfusion. In the absence of these triangles, the sinus loses its crown shape and this change is correlated with aortic stenosis.

Virtually, the point that connects the lowest site of implantation of each leaflet, forms the aortic valve annulus, which has a slightly elliptical conformation, with a three-dimensional measurement around 4.0 ± 0.8 cm2. Given this spatial conformation, the three-dimensional measurement, whether by echocardiography or tomography, is much more reliable and reproducible than the two-dimensional measurement obtained by ordinary transthoracic echocardiography.

Ventricular Adaptation

 

In all valvular disorders with hemodynamic repercussions, the left ventricle starts to deal with certain overloads. Thus, the ventricle uses three basic mechanisms to deal with this:

  • Frank-Starling mechanism
  • Adrenergic Neurohumoral Systems
  • Remodeling of chamber

 

It is worth mentioning at this point in the discussion that hypertrophy and remodeling are not synonymous. Hypertrophy means an increase in mass, while remodeling means a change in geometry and/or volume. Therefore, we must understand that the terms can coexist, but not necessarily.

During aortic stenosis, a systolic gradient appears that the left ventricle must generate more than necessary to overcome the anatomical barrier for blood ejection. This leads to a biological response of concentric hypertrophy and/or remodeling of the left ventricle with the formation of sarcomeres in parallel, thickening of the wall and increased mass. As it is an adaptive process, it is expected that hypertrophy will go to the level where the wall stress returns to normal. However, in some patients, this process fails to maintain proper balance and failure.

Patients with left ventricular dysfunction have a hemodynamic balance with high afterload for the degree of hypertrophy, which did not occur in the proportion that it should. The opposite can also occur, with high hypertrophy in the face of a certain increase in afterload. This is the case of patients with congenital bivalvar aortic valve and elderly women. In this group of patients, even with a preserved ejection fraction, we can experience different degrees of diastolic dysfunction and a drop in the ventricular strain pattern, indicating the presence of disease.

Patients with aortic regurgitation experience not only volume overload, but mixed overload. These patients also have a high afterload due to a high stroke volume in the face of peripheral vascular resistance increased by chronic adrenergic stress. Thus, of all valve lesions, aortic regurgitation is the one with the greatest left ventricular mass. There is an activation of the myofilament production process with a reduction in its degradation, which was supposed to be physiological.

In some animal models, the study of the myocardium showed that the increase in the extracellular matrix seemed to hinder the contractile dynamics, which may be one of the explanations for the drop in the ejection fraction in these cases. However, the surgical procedure for correcting valvular heart disease caused the contractile function to return, which can be explained by the regression of this extracellular matrix in the face of a significant reduction in the postoperative afterload.

From that moment on, we will separate the discussion into two large groups according to the specific valve dysfunction, between stenosis and aortic valve regurgitation.

Suggested literature:

1 – Otto CM, Bonow RO. A Valvular Heart Disease – A companion to Braunwald’s Heart Disease. Fourth Edition, 2014.