Acquired Aortic Valve Diseases (Current Status of the Problem)

Abstract

Acquired heart disease – the concept of “acquired heart disease” includes a variety of pathological conditions acquired during the life of the patient. The lion’s share of these diseases are acquired heart defects. The significance of this problem is special for our region, since the incidence of rheumatic diseases and its complications in our Republic is still significant. However, in recent decades, statistical data on acquired defects, especially on aortic heart defects, have changed markedly. Thus, the prevalence of aortic heart disease among the elderly and senile is about 10.7%, significantly increasing for sclerotic lesions of the aortic valve – up to 25–48%. According to Euro Heart Survey on valvular heart disease, damage to the aortic valve was detected in 44.3% of patients with valvular heart disease (33.9% – aortic stenosis, 10.4% – aortic valve insufficiency. At the same time, aortic stenosis in 81.9% and insufficiency – in 50 .3% of patients were of degenerative origin. According to the statistics of our Republic, more than 400 patients with rheumatism per 100 thousand of the population are detected per year, of which, after an appropriate examination, in terms of the population of our Republic, more than 16,000 require surgical correction of acquired heart disease, which confirms the importance of discussing the problem for our healthcare.

1. Introduction

Aim of chapter. In connection with the foregoing, we think that the discussion of modern data on aortic malformation of acquired genesis, namely, the modern idea of changing the etiology, frequency of occurrence, clinical picture, as well as diagnostic issues, including new modern highly informative research methods, determining the tactics of surgical treatment with analysis indications and contraindications to a particular method of treatment, respectively, is of great scientific and practical importance. Therefore, we once again decided to discuss the above issues regarding aortic heart disease of acquired origin.

1.1 Actuality

The trend towards an increase in the general morbidity of the population with diseases of the circulatory system can be clearly seen [1, 2], both according to the results of world statistics, according to the results of the State Report on the state of health of the population of the Russian Federation (2002, 2003), and according to the Ministry of Health of Uzbekistan (2008). The number of open heart surgeries is increasing every year. Reconstructive operations on the aortic valve (AV) are in the center of attention of cardiac surgeons: in economically developed countries, this operation is already in second place in terms of frequency among all cardiac surgical interventions performed in the adult population. The reason for this is the changes that have taken place in the etiology of the formation of aortic valve disease and the change in the demographic structure of society itself. In developed countries, calcified aortic disease is the third most common nosological form after arterial hypertension and coronary heart disease [3].

Knowledge of the etiology of the process that led to aortic malformation can significantly influence both the surgical tactics and the protocol of postoperative treatment of patients and, as a result, the prognosis of the long-term period. Therefore, at all stages of treatment, one should strive to answer the question of the etiology of the primary process that caused valve dysfunction. Sometimes this answer can only be given by a surgeon who visually assesses the nature of the valve lesion already during the operation. In any case, elucidation of the etiology, even with a presumptive conclusion, is extremely important.

2. Etiology

Assessing our own experience, published data of colleagues from other countries and Russian clinics, it should be emphasized that even today aortic malformations of rheumatic etiology dominate in cardiac surgery hospitals, although not as clearly as in the statistics of half a century ago. This figure does not exceed 30–40%. However, if we take into account that only during the period from 1993 to 1998 in Russia the frequency of cardiac rheumatism increased by 7 times [1, 2], then in the future we should again expect an increase in the number of patients with rheumatic valvular defects.

The etiology of pathological changes in AK from the moment of the first operations has changed several times. If at the beginning rheumatic lesions, endocarditis, syphilis and atherosclerosis prevailed; then at present, atherosclerotic (degenerative) and congenital malformations (mainly bicuspid aortic valve) of the aortic valve come to the fore. Such changes in the etiology could not but affect the course of the disease itself, the clinic of the defect and, accordingly, the development of a specific tactic for the introduction of such patients.

The increase in surgical interventions on the aortic valve in the group of patients over 60 years of age has significantly increased the number of atherosclerotic “degenerative” (age-related) aortic valve defects. If the aortic defect is moderately pronounced and is combined with widespread atherosclerosis of the coronary arteries, the aorta and its branches, in combination with distinct specific disorders in lipid metabolism (total cholesterol, low density lipoproteins, triglycerides), then the atherosclerotic origin of the process on the valve is beyond doubt. This is a special and prognostically most severe group of patients. It is to this category of patients that the point of view of some authors extends that aortic stenosis is a special form of manifestation of atherosclerosis with risk factors identical to this systemic disease.

In a real clinical situation, no more than 50% of elderly patients with signs of aortic stenosis have changes in coronary vessels [4, 5]. Such patients have another dystrophic process in the valve with a reduced level of metabolic reactions due to age-related changes: atherosclerosis as such can only play the role of an accelerating factor, especially if accompanied by inflammatory changes in the aortic valve cusps specific for many atheromas due to Chlamydia invasion pneumoniae [6]. Age-related involutional calcium degeneration is, in our opinion, the most appropriate definition for such pathology of the aortic valve. As a special form, it often occurs in elderly patients and, as a rule, falls into the group of atherosclerotic malformations during analysis. The diagnostic line between these two groups of patients (atherosclerosis and age-related dystrophy) is very thin, but it is quite realistic to draw it with known experience. The practical significance of such a diagnosis can be expressed not only in a different prognosis, but also in the amount of drug therapy after surgery (the use of antiplatelet agents, lipid-lowering agents). The group of patients with congenital bicuspid aortic valve configuration adjoins the same type of “degenerative” defects with severe calcification. For us, this was unexpected, but the number of such patients increases as the number of operated elderly patients increases. Actually, the three main causes of aortic heart disease that we have already noted together account for at least 90% of the causes of aortic valve stenosis [4]. All these reasons lead to various pathomorphological, but the same type of functional changes in the aortic valve cusps, limiting their mobility. This process (fibrosis, thickening, formation of adhesions in the area of commissures, calcification) always takes a long time – years, or even decades. Other, rarer causes of aortic stenosis include previous and active infective endocarditis, systemic lupus erythematosus (Libman – Sachs verrucous aseptic endocarditis), hereditary metabolic disorders such as homozygous type II hyperlipoproteinemia and alkaptonuria (ochronosis), metastatic calcification of the aortic valve in patients with chronic renal failure [3].

Changes in the etiology of the disease over a fairly short period of time are associated primarily with the ongoing prevention of rheumatism and rheumatic heart disease. Secondly, such a restructuring in etiology is also associated with a change in the demographic structure of society in economically developed countries, where there is a constant increase in the population of elderly and senile age. Accordingly, this led to an increase in the number of elderly patients with acquired heart defects, where atherosclerotic and degenerative forms of AV malformation already prevail, which affected both the clinical picture of the disease and the age composition of operated patients. At present, either aortic stenosis or combined forms of defect occupy the main place in the structure of the forms of defect.

Statistics of detection of aortic heart disease in Uzbekistan by etiological factors:

1. Rheumatic lesion of aortic valve

2. Atherosclerotic (degenerative) lesion of aortic valve

3. Congenital lesion of aortic valve (bicuspid valve, etc.)

According to the recommendations of the European Society of Cardiology and the European Association of Cardiothoracic Surgeons, aortic valve disease should be surgically corrected in the presence of echocardiographic signs of severe stenosis (blood flow velocity on the valve is more than 400 cm/s, the average gradient on the valve is more than 40 mm.r.st., effective area orifice less than 1 cm², effective orifice area index less than 0.6 cm²/m²) and/or severe regurgitation (grade 3–4 insufficiency, central regurgitation over 65% of the area of the left ventricular cavity, vena contracta more than 0.6 cm, regurgitation volume more than 60 ml/contraction).

The indications for surgical correction of the defect were a severe degree of aortic valve stenosis (Figure 1), identified during clinical examination and confirmed by echocardiography data with an average transaortic pressure gradient of more than 40 mm Hg, the presence or absence of symptoms of heart failure, manifested at rest or during stress tests (decreased exercise tolerance), as well as in the presence of concomitant left ventricle systolic dysfunction (ejection fraction <50%).

Figure 1.

Indications for surgical correction of aortic heart defects.

Aortic valve insufficiency served as an indication for surgery in case of severe regurgitation in symptomatic patients, regardless of LV systolic function, in the absence of symptoms and the presence of LV systolic dysfunction (ejection fraction <50%). In addition, surgery has been indicated in the absence of symptoms and normal LV ejection fraction, but in the presence of LV dilatation (LV end-systolic dimension >50 mm). Performing neocuspidization according to the formulas is possible only in the absence of aortic root expansion (the diameter at the level of the sinotubular junction is not more than 35 mm and the diameter at the level of the fibrous ring is not more than 25 mm). Otherwise, it is necessary to perform neocuspidization in combination with aortic root replacement in the Moscow (Russian) conduit modification [7, 8].

Symptom complexes characteristic of a particular valvular defect determine modern treatment tactics to a much greater extent than the actual nature of the damage to the aortic cusps. Therefore, any attempt to identify the diagnosis of the condition, substantiate the indications for surgical intervention and surgical tactics only on the data of topical diagnostics (hole diameter, magnitude of leaflet prolapse, magnitude of the pressure drop across the valve, the presence or absence of signs of calcification, etc.) does not testify in favor of comprehensively a clinical analysis of the condition of a particular patient [9].

Cardiologists today reliably diagnose this pathology and promptly send such patients to cardiac surgeons. And yet, when deciding whether to operate on patients older than 70 years, we sometimes encounter some resistance from our fellow cardiologists [10]. Their doubts are based on both an objective factor – a higher risk of surgery, and a subjective one – the uncertainty of the individually “programmed” life expectancy of such elderly patients.

Therefore, in this publication, we specifically present the data of O’Keefe et al., [11], who managed to trace a group of 50 patients awaiting balloon dilatation of a stenotic aortic valve. The average age of patients exceeded 70 years, survival without surgery by the 3rd year of follow-up was only 25%. At the same time, in a randomized group of patients without aortic pathology, the survival rate was 77%. Considering that today the lethality of aortic grafting is minimal, these data should convincingly prove to cardiologists the need for an operative way of treating such patients [12].

In classical situations, the question “when to operate?” does not represent difficulties: digital radiography from the screen of the electro-optical converter, electrocardiography, echocardiography [10], MRI [13] with contrast are sufficient methods for making a topical diagnosis and assessing the state of the left ventricle of the heart. Performing a sounding of the heart cavities in patients with aortic defects in order to determine the pressure drop, regurgitation volume, end-diastolic pressure in the left ventricle or pulmonary capillary wedge pressure today can already be regarded as a diagnostic anachronism.

In practice, of course, we are especially wary of choosing a solution in patients with “minor” symptoms and, even more so, in patients with asymptomatic course. It is known that clinical manifestations and complaints may be absent even in severe severe aortic stenosis with an orifice area of less than 0.8 cm³ and with a decrease in the ejection fraction to 25–30% [14].

An increase in the left ventricle of the heart up to 6 cm or more (in patients with aortic insufficiency), as well as hypertrophy with overload of the left ventricle (in patients with aortic stenosis), are sufficient instrumental criteria for the need for surgery in the presence of a topical diagnosis.

Doppler echocardiography allows you to set the magnitude of the pressure drop with almost the same accuracy as sounding the left ventricle. Understanding the conditionality and multifactorial dependence of this indicator, we consider its value to be 40–50 mm Hg. Art. a sufficient basis for a more detailed examination of the patient and the search for arguments in favor of the operation.

The calculation of the effective orifice is less dependent on the characteristics of blood flow through the area “left ventricle-aortic valve-ascending aorta”, but this indicator is also quite arbitrary and “semi-quantitative”. And yet, we always take into account the instructions of ultrasound diagnostics specialists to limit the opening of the valve leaflets to less than 1.5 cm, and with a hole size of less than 1 cm, the indications for surgery are almost absolute. An even more accurate expression of the degree of stenosis is the ratio of the size of the stenosis to the total body surface area – a value of less than 0.6 cm/m² is critical [3]. If at the same time there is information about valve calcification, then it is not worth postponing the operation, since the progression of the process is inevitable.

If the arguments in favor of the operation are not absolute, then with aortic stenosis we calculate the pressure loss on the valve (mm Hg/ml stroke volume) – the value is 1 mm Hg. Art./ml and more significant and weighty. If necessary, repeat these calculations under load. In aortic insufficiency, a decrease in the ejection fraction of less than 55% and its further decrease (or invariance) under stress test conditions also indicate the limit of compensatory reserves of the left ventricular myocardium and serve as a more than convincing criterion in favor of surgery.

In the presence of concomitant coronary pathology requiring surgical correction, or concomitant mitral valve defects, the criteria for revision and intervention on the aortic valve can be much more liberal and are often determined by the individual decision of the operating surgeon.

It should be remembered that aortic stenosis progresses regardless of any patterns. However, with degenerative defects, this process is faster than with rheumatic or in the presence of a bicuspid valve. With slow progression, the opening of the aortic valve narrows by 0.02 cm² per year, and with rapid progression, more than 0.3 cm² per year. When the peak velocity of blood flow through the valve reaches about 4 m/s, the two-year survival rate without surgery is only 21%. Thus, calcification, the rate of progression of stenosis during the year, and positive exercise tests (slight rise or even decrease in blood pressure during exercise) are real factors for deciding on surgery for asymptomatic aortic stenosis.

In asymptomatic aortic insufficiency, the prognosis is based on an assessment of left ventricular function and the degree of dilatation of the ascending aorta. Threatening signs are an increase in end-diastolic pressure of the left ventricle more than 70 mm, end-systolic pressure more than 50 mm (index more than 25 mm/m² of the patient’s body surface), a decrease in the ejection fraction to 50%. If the ascending aorta is dilated more than 55 mm, surgery should be offered regardless of the degree of aortic regurgitation and left ventricular function. In patients with a bicuspid valve or with Marfan syndrome, the indications for surgery are even more stringent – the threshold for making a decision is the diameter of the ascending aorta is 50 mm.

Regular routine monitoring of the condition is necessary for all patients with symptoms of aortic valve disease and is mandatory every 12 months in order not to miss the time for possible surgical interventions.

3. Diagnostics of aortic heart defects

1. Clinical symptoms

2. Laboratory research

3. Electrocardiography’s

4. X-ray examination

5. Doppler echocardiography

6. angiography, Aortography

7. MRI with contrast

8. Radioisotope research

3.1 X-ray examination and ECG in aortic disease

X-ray of the chest organs – evaluates the size and location of the heart, changes in the configuration of the heart (protrusion of the shadow of the heart in the projection of the aorta and left ventricle in aortic disease) (Figures 2 and 3).

Figure 2.

ECG – Signs of left ventricular hypertrophy with overload.

Figure 3.

Echocardiographic features of aortic stenosis.

Aortic stenosis thickening of the aortic valve cusps, decreased mobility.

Concentric LV hypertorphia.

Pressure gradient between aorta and LV

Assessment of the degree of calcification of the aortic valve and aortic root.

Assessment of the degree of left ventricular myocardial hypertrophy.

Assessment of the degree of dilatation of the cavities of the heart.

Doppler echocardiography.

Increased flow rate through the aortic valve into systole.

Calculation of the maximum and average systolic pressure gradient across the aortic valve.

Classification of the degree of aortic stenosis depending on the maximum and average transvalvular pressure gradient.

Calculate the area of the aortic orifice using the continuity equation:

positions and measurements, calculated parameters.

Calculation of the aortic orifice area index.

3.2 Echocardiographic signs of aortic insufficiency

The study of the size of the chambers of the heart, the mass of the myocardium of the left ventricle (Figure 4) [14].

Figure 4.

Aortic insufficiency.

The study of contractility of the left ventricle. The study of the volume, shape of the myocardium of the left ventricle.

Doppler echocardiography.

Pulse wave doppler.

Assessment of the degree of aortic regurgitation by the depth of the jet in the outflow tract of the left ventricle.

Continuous wave doppler also allows assessing the degree and significance of aortic regurgitation.

Ways to reliably assess the severity of aortic regurgitation:

1. Calculation of the half-decay time of the aortic pressure gradient regurgitation.

2. Calculation of the fraction of the regurgitant volume.

3.3 Invasive research methods for aortic stenosis

In order to measure the pressure gradient between the left ventricle and the aorta, probing of the heart cavities is performed. to which allows you to indirectly judge the degree of aortic stenosis. Ventriculography needed to detect concomitant mitral regurgitation. Aortography and coronary angiography are used for the differential diagnosis of aortic stenosis with an aneurysm of the ascending aorta and ischemic heart disease (Figure 5).

Figure 5.

Magnetic resonance imaging (MRI) of the heart.

Magnetic resonance imaging (MRI) of the heart is a method of tomographic diagnostics, based on scanning the heart tissue with radio waves when the patient is in a powerful magnetic field. In the process of MRI, images of slices of the heart are obtained in different planes. High resolution characteristics of MRI make it possible to obtain detailed information about the structure of the cavities and valves of the heart, to conduct a study of the functional parameters of cardiac activity [8, 9, 13].

3.4 Invasive diagnostic methods for aortic insufficiency

Catheterization of the heart cavities with angiography in patients with aortic insufficiency is necessary to determine the magnitude of cardiac output, LV end-diastolic volume and regurgitation volume, as well as other necessary parameters.

3.5 Radionuclide studies of the myocardium in aortic disease

Radionuclide myocardial scintigraphy is used in evaluating the results of surgical correction of aortic heart defects.

With AS, LV wall tension occurs, which leads to coronary microcirculatory dysfunction. Scintigraphically after surgery, most patients show an improvement in myocardial perfusion.

The above research methods (Figure 6) are performed in almost all specialized cardiology and cardiac surgery institutions, where they thoroughly deal with the problems of modern diagnostics and the solution of surgical tactics for the treatment of acquired aortic heart defects. We only considered it necessary to briefly dwell on the problems of diagnosing and determining the surgical tactics of acquired aortic valve defects, knowing that dynamically these issues are resolved individually, depending on the capabilities of clinics and specialists involved in “adult cardiac surgery” at the present stage.

Figure 6.

Radionuclide myocardial scintigraphy of myocardium.

3.6 Surgical methods for the treatment of aortic heart disease

The requirement of modern cardiac surgery is the widest possible use of valve-saving technologies in heart valve surgery, namely in the surgical treatment of aortic heart defects. However, as is known from the specialized literature, according to the leading authors of the post-Soviet period of development, the opinion remained that valve replacement operations were preferable in surgery for aortic heart defects, in view of the peculiarities of hemodynamics, the relationship of the left heart and the aortic valve. Therefore, the preferential performance of prosthetic aortic valves rather than plastic reconstructive interventions during these periods is explained. But, the trend towards the implementation of valve-saving technologies is especially noticeable in recent decades, when the development of a number of plastic interventions on aortic valves began [15, 16, 17, 18]. It is appropriate to bring plastic surgeries, such as “Open valvuloplasty of the aortic valves” with stenosis, or preferential preservation of the structure of the valve, without gross morphological changes (calcification, gross fibrosis, etc.). Performing parietal resection of thickened leaflets with the addition of commissural sutures in case of fibrous change, stenosis or predominant stenosis of the aortic valves. It should be noted that they were performed with a normal tricuspid aortic valve structure. There are many attempts to perform plastic operations on the aortic valves. However, many of them did not have sufficiently stable good long-term results and required repeated valve replacement operations in a short period of postoperative follow-up. I think that among the many methods of plastic surgery on aortic valves, the following deserve attention:

1. There are several modifications of Operation Ozaki. The author’s methods, the meaning of which is in the complete reconstruction of the aortic valve from the autopericardium or from the xenopericardium, differ in the types of meters and templates. So, for example, the Benaki operation uses gauges made from the flexible material nitinol, as opposed to the rigid Ozaki gauges. Due to the special properties of this material, gauges can be modeled, giving them the desired shape and allowing more convenient measurement of the distance between the commissures, then they are also used as templates for cutting the leaf. In addition to improved meters, Benaki’s operation uses special “three-armed” forceps for the comfort of creating aortic valve neocusps [7]. Known special holding device for the formation and simultaneous plastics of the aortic valve leaflets (MAAZOUZI APS AORTIC PLASTY-SIZER). In the work of A.S. Nesmachny describes in detail the technique of using the device in clinical practice [7, 16, 19].

The positioning of future leaflets in the holding device before implantation allows quickly and accurately, in accordance with the diameter of the aortic annulus, to form a neovalve.

4. Stages of operation Ozaki

1. A known method of forming the leaflets of the aortic valve, cut after intraoperative measurement of intercommissural distances (Figure 7). The length of the free edge of each nonvalve should be 20% greater than the intercommissural distance, the valve height is 0.866 of the intercommissural distance. The leaflets are fixed to the aortic ring with a continuous suture (Figure 8). The disadvantage of this method is the absence of the results of the application of this technique in clinical practice described in the literature.

2. It should be noted that in this case we are discussing the simplest, most effective methods of surgical correction of aortic defects, which are the fundamental methods of surgical treatment of this pathology.

3. Considering that in more complex variants of aortic malformations complicated by other changes in the aorta itself, its part, valvular or tubular apparatus, more complex, modified methods of surgical correction of aortic valve malformations are invariably performed [3, 17, 20]. An example is the performance of plastic surgeries on the aortic root, valvular apparatus, ascending (sometimes the arch, descending part) of the aorta, such as David-Jakub operations, Bental-DeBono’s basic operation in various modifications, and others. We decided to note only the main points of plastic surgery on the aortic valve, using the Ozaki operation as an example.

4. The classic operation – replacement of the aortic valve with artificial prostheses (Figure 9), is the most common method of surgical correction of aortic heart defects to date [21].

Figure 7.

Forming cusps from pericardium.

Figure 8.

Final view of the operation.

Figure 9.

Classic surgery: Aortic valve replacement and aortic valve leaflet plasty.

4.1 Endovascular aortic valve replacement

Here it is necessary to indicate the importance of choosing an aortic valve prosthesis, since the last decades have been marked by the rapid development of the production of biological valves, frameless, framed biological aortic valves, homografts, the use of biological valves for endovascular methods of aortic valve implantation, and many others [22, 23, 24].

But, I think our task is to determine the basics of the correct surgical tactics for the treatment of aortic heart defects, indicating the main methods for diagnosing these heart defects. To this end, we briefly want to acquaint the reader with the basics of the pathogenesis of the development of pathology, the anatomical and hemodynamic foundations of aortic heart defects [12, 25].

In recent decades, the technology of endovascular implantation of an artificial aortic valve has been developed (Figure 10).

Figure 10.

Transcatheter aortic valve implantation.

The next high-tech operation is endovascular implantation of aortic valve prosthesis [22, 23, 26]:

5. Pathological anatomy (by the example of aortic stenosis)

The basis of pathological changes in aortic disease, in this case, aortic stenosis is rheumatic inflammation – valve valvulitis. Rheumatic valvulitis gradually leads to thickening and compaction of the aortic cusps. This is facilitated by the organization of fibrous overlays on the ventricular surface of the valve, as well as the growth of valve tissue due to mechanical irritation by blood flow. These factors underlie the soldering of the free edges of the leaflets, as a result of which the valve opening gradually decreases. In the area of commissures, fibrin plates form bridges that connect the valves between themselves and the aortic wall. Subsequently, the plates are organized into fibrous tissue. The narrowed valve opening has a triangular or slit-like shape and is usually located eccentrically. When the valves are wrinkled, one or another degree of aortic insufficiency is formed. In the altered valve, degenerative processes develop, followed by calcification. Calcification can move to structures adjacent to the aortic valve: the interventricular septum, the anterior leaflet of the mitral valve, the wall of the left ventricle. Bicuspid AV is often associated with a subvalvular membrane, sometimes with abnormal origin and course of the coronary arteries, the presence of three or even four coronary orifices, and in adulthood is complicated by calcification and/or endocarditis of the AV. Under the valvular membrane (Williams’ disease) in the left ventricular outflow tract (LVOT) may or may not fuse with the AV leaflets, be circular or semilunar in shape in a limited area. Such patients have a characteristic “elf face” and lag behind in mental development. LVOT obstruction in hypertrophic cardiomyopathy (HCM) is often associated with anterior leaflet prolapse of the mitral valve (AMVP). Aortic stenosis causes significant morphological changes in the myocardium of the left ventricle (LV). Prolonged illness leads to progressive hypertrophy and the development of relative coronary insufficiency. Dystrophic changes develop in the heart muscle: protein and fatty degeneration of muscle fibers, and later diffuse and focal sclerosis [14].

6. Pathological physiology (by the example of aortic stenosis)

Hemodynamic manifestations of aortic stenosis develop with a decrease in the area of the aortic ostium less than 1 cm², which is usually combined with a pressure gradient between the LV and aorta of 50 mm Hg. Art. The “critical” area of the Aorta opening, corresponding to the picture of a sharp aortic stenosis, is 0.5–0.7 cm² with an aortic systolic gradient of 100–150 mm Hg. Art. To ensure adequate cardiac output, the LV during systole must develop a pressure of 200–250 mm Hg. Art. Possessing powerful compensatory capabilities, hypertrophied LV intensifies contractions and copes with the defect for a long time. Gradually, the amount of “residual” blood in the cavity of the left ventricle increases and diastolic filling increases. The cavity of the left ventricle expands, and tonogenic dilatation occurs. Additional mobilization of the myocardium occurs due to the activation of the Frank- Starling mechanism. When a further increase in the length of muscle fibers ceases to be accompanied by an increase in contraction, the so-called myogenic dilation occurs; LV decompensation gives rise to a phase of general heart failure. Long-term existence of AV stenosis and compensatory hyperfunction leads to the development of LV myocardial hypertrophy, the mass of which can reach 1200 g or more (at a rate of 250–300 g). The consequence of this is relative coronary insufficiency. In addition, in patients with aortic stenosis, there may be an absolute deterioration in coronary blood flow due to a sharp increase in intraventricular and intramyocardial pressure, as well as a drop in pressure at the base of the aorta (blood is ejected into the aorta in a thin and strong jet), making it difficult to fill the coronary arteries during diastole. For these reasons, in patients with aortic stenosis, angina pectoris occurs in 70% of cases, although only half of the patients have coronary atherosclerosis. Due to developing myocardial ischemia in this category of patients, the risk of sudden death is high [3, 27, 28]. When stenosis is combined with aortic valve insufficiency (more often with a bicuspid aortic valve), an increase in “preload” is added to the increased “afterload” of the LV, which leads to greater stress in the LV wall and a decrease in effective stroke volume.

7. Pathogenesis of development of aortic stenosis

Pathogenesis and changes in hemodynamics. The narrowing of the aortic orifice by more than 50% creates a significant obstruction to the flow of blood from the left ventricle to the systemic circulation. With its narrowing, the minute volume decreases by 75%, although the area of the hole, which is even 10–20% of the norm, is compatible with life [29]. To ensure more or less sufficient systolic ejection in aortic stenosis, a number of compensatory mechanisms are activated. One of them is the lengthening of the systole of the left ventricle and the increase in pressure in the cavity of the left ventricle. As a result, a large pressure gradient is created between the aorta and the left ventricle, the latter is sharply hypertrophied without a significant increase in the cavity. The narrowing of the mouth of the aorta, like no other defect, is characterized by severe hypertrophy of the left ventricle. The minute volume remains normal for a long time or slightly decreases, the defect remains compensated. With a pronounced degree of defect or a decrease in the contractility of the left ventricle, the minute volume decreases significantly. In the latter case, the left ventricle dilates, it increases the end-diastolic pressure. This further leads to a rise in pressure in the left atrium, and then retrograde in the pulmonary veins. There is passive (venous) pulmonary hypertension, which does not reach large values and usually does not lead to severe hypertrophy of the right ventricle. Over time, congestion may occur in the systemic circulation. Coronary blood flow in aortic stenosis is reduced, especially during systole, which is explained by the influence of high intraventricular pressure and increased resistance in the thickness of the myocardium to coronary inflow. The main cause of coronary insufficiency is considered to be a disproportion between the increased need for nutrition of a hypertrophied muscle and its relatively low blood supply [30]. Additional factors are slow filling of the aorta, a decrease in systolic and mean pressure in the aorta (especially in the circumference of the valves) (Figure 11).

Figure 11.

Hemodynamic disturbances in aortic stenosis.

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 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.

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.

9. Conclusion

Thus, when discussing the above problem of cardiology and cardiac surgery, it should be noted that the statistics of detection of aortic malformations have indeed changed over the past decades, in terms of frequency, which come out on the third place after coronary heart disease and hypertension. A particularly large percentage refers to aortic stenosis. Another feature is the change in the etiological factors in the development of aortic heart defects. So, if earlier the rheumatic genesis of the development of aortic malformations prevailed all over the world, now the degenerative nature of the development of aortic malformations is clearly increasing.

The third feature is the change in the social structure of aortic heart disease, i.e. with a noticeable increase in the age of the population, the number of patients over 60 years of age who undergo open correction sharply prevails. It follows from the above that open corrections are also changed. It follows from the above that the principles of diagnosing aortic heart defects have also changed, non-invasive highly informative computer technologies are increasingly being used that help to accurately determine the surgical tactics of treatment and evaluate the results of corrections of aortic heart defects.

The combination of valvular pathology and atherosclerotic lesions of the coronary vessels and the aortic wall sharply increases. Accordingly, the number of simultaneous large reconstructive operations on the valves of the aorta and root, and coronary vessels and others is increasing. It follows from the above that the principles of diagnosing aortic heart defects have also changed, non-invasive highly informative computer technologies are increasingly being used that help to accurately determine the surgical tactics of treatment and evaluate the results of corrections of aortic heart defects. The combination of valvular pathology and atherosclerotic lesions of the coronary vessels and the aortic wall sharply increases.

Accordingly, the number of simultaneous large reconstructive operations on the valves of the aorta and root, and coronary vessels and others is increasing. Open corrections are made. Accordingly, there is a need to revise the approaches to studying the issues of etiology, clinic and diagnostics, determining the tactics of treatment, performing the stages of surgical correction and evaluating the results of the latter in patients with acquired aortic heart disease at the present stage of development of cardiology and cardiac surgery.