**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

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

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:


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%).

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.)

**Figure 1.** *Indications for surgical correction of aortic heart defects.*

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/m<sup>2</sup> 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.
