Aortic stenosis of the aortic orifice causes and development of symptoms How to treat prognosis

The narrowing of the external tract can form at various levels:

  1. Actually the aortic valve;
  2. Congenital deformed bicuspid AK;
  3. Valvular stenosis;
  4. Fibrous or muscular subaortic stenosis (valve-subvalvular);
  5. Nadklapanny stenosis.

Classification of aortic stenosis according to severity:

  1. I degree – moderate stenosis (full compensation). Signs of AS are detected only upon physical examination;
  2. II degree – severe stenosis (latent heart failure) – there are nonspecific complaints (fatigue, syncope, decreased exercise tolerance); the diagnosis is verified according to echocardiography, ECG;
  3. III degree – severe stenosis (relative coronary insufficiency) – the symptoms are similar to angina pectoris, there are signs of decompensation of blood flow;
  4. IV degree – critical stenosis (pronounced decompensation) – orthopedic, congestive phenomena in both circles of blood circulation;
Severity AK hole area (cm2) The average trans valve pressure gradient (mmHg)
Normal value 2,0 – 4,0
Mild stenosis 1,5 ≥ 0 – 20
Moderate stenosis 1,0 – 1,5 20 – 40
Severe stenosis ≤1 40 – 50
Critical stenosis Less than 0,7 gt; 50

Treatment of aortic stenosis

Treatment of a damaged aortic valve involves conservative and surgical methods. In this case, patients with an asymptomatic course of the disease are under vigilant medical supervision. Every six months to a year, these patients undergo echocardiography, and before visiting the dentist they take antibiotics. Pregnant women with stenosis require monitoring of hemodynamic parameters. Termination of pregnancy may be required only in the most advanced cases.

Conservative treatment pays special attention to neutralizing the effects of arrhythmia and normal blood flow.

Here is a complete list of things to deal with:

  • normalization of blood pressure;
  • elimination of arrhythmias;
  • slowing down the development of heart failure;
  • prevention of coronary heart disease.

The pulmonary circulation is prone to stagnation, so treatment begins with this area. Diuretics are prescribed to the patient (the most common Furosemide), while the collection of subjective, instrumental and clinical data continues. If atrial fibrillation is detected, cardiac glycosides (e.g., Digoxin) are taken. Prescribed by doctors and potassium preparations.

In order for the hypertrophied myocardium to relax a bit, B-blockers are recommended. The second option is calcium blocker antagonists. Groups of nitrates, on the contrary, are contraindicated, since the minute volume of blood and cardiac output are reduced. As the defect develops, conservative treatment begins to be combined with surgical correction, but more on that below.

Drug treatment is relatively effective only in the early stages of pathology. Surgical intervention is the main means of combating the disease. Such treatment directly depends on contraindications and the degree of violations received by the patient. The most common balloon plastic and valve prosthetics. Here are three main indications for surgery:

  1. Satisfactory myocardial function.
  2. Hypertrophy of the left ventricle (development dynamics can be seen on the cardiogram).
  3. Excessive systolic pressure gradient.

With artificial prosthetics of a damaged valve (changes are insignificant) the volume of surgical correction is minimized. Valve flaps in the splicing stage are artificially separated.

In some cases, the tricuspid valve is replaced – then the patient is connected to an artificial blood supply. The aorta is dissected, the affected valve is removed, after which an implant is introduced into the patient’s body.

The prosthetic valve is checked for several indicators.

  • functionality;
  • integrity;
  • matching hole sizes;
  • lack of air bubbles.

After surgical correction, the patient undergoes a long rehabilitation course. There is a risk of infectious endocarditis, so doctors use a wide range of antibiotics. Thromboembolism is also dangerous. This complication must be controlled through antiplatelet agents and anticoagulants (Heparin, Aspirin).

All patients with AK stenosis, even without clinical manifestations, are recommended:

  • Limitation of physical activity;
  • Prevention of infectious endocarditis – deformed valves become an “easy target” for bacterial infection;
  • Constant dispensary observation;
  • Symptomatic Therapy

The role of drug therapy in the treatment of AS is relatively small. Conservative treatment can reduce heart failure, slightly improve hemodynamics.

The list of drugs used:

  • Cardiac glycosides – preferably Korglikon, Strofantin, Celanide;
  • Diuretics – Veroshpiron, Hypothiazide (reduce cardiac output)
  • Peripheral vasodilators – hydralazine, ACE inhibitors (controlled by blood pressure);
  • β-blockers, antagonists of Ca 2 (with angina pectoris, compensated stenosis);
  • Anticoagulants – in the presence of thromboembolic complications;
  • Class III antiarrhythmic drugs – Amiodarone (with atrial and ventricular arrhythmias).

The choice of invasive correction method depends on the clinical condition of the patient, his age and form of the defect. Contraindications to surgery are I and IV stages of AK stenosis.

Types of surgical interventions:

  1. Percutaneous aortic balloon valvuloplasty is an endovascular method performed in infants with critical stenosis or in pregnant women;
  2. Aortic valvulotomy – used in children, performed on an open heart;
  3. Prosthetics AK – performed with congenital anomalies in the structure of AK (single-leaf, displazed bicuspid) or in patients after valvotomy with progressive stenosis.
  4. Use a mechanical prosthesis, pork bioprosthesis, aortic alograft, pulmonary valve autograph;
  5. Autologous transplantation of a pulmonary trunk with a valve into the aortic position and reconstruction of the ventricular outflow tract with a homograft (Ross operation) – indicated for children of the 1st year of life;
  6. Dilatation of the aortic root with valve replacement (Konno operation) – indicated for severe stenosis or obstruction in the form of a tunnel.

In severe aortic stenosis, medication is usually ineffective. The only radical treatment is aortic valve replacement. Already after the onset of symptoms of the disease, the chances of surviving without surgery are sharply reduced. On average, patients after the onset of symptoms such as heart pain, signs of left ventricular failure, fainting, live no more than five years.

After the diagnosis of “stenosis of the aortic valve” is established, the patient is necessarily recommended preventative measures against infectious endocarditis.

With asymptomatic aortic stenosis, drug treatment is aimed at maintaining sinus rhythm, preventing coronary heart disease and normalizing blood pressure.

After the appearance of complaints when it is impossible to carry out the operation, medication is prescribed. So, in the presence of heart failure with the help of medicines, they try to eliminate stagnation in the pulmonary circulation by taking diuretics. However, their too active use may contribute to the development of excessive diuresis, hypovolemia and arterial hypotension. With systolic dysfunction of the left ventricle, Digoxin is prescribed as a symptomatic agent, especially with atrial fibrillation.

With aortic stenosis, vasodilators are contraindicated for the patient, since their use can lead to fainting. However, in severe heart failure, careful administration of sodium nitroprusside is allowed.

With congenital aortic stenosis in children, aortic balloon valvuloplasty can be used. This method allows you to reduce the maximum transvalvular gradient by 65%, however, mainly this technique requires reoperation for 10 years. After valvuloplasty, patients may develop aortic insufficiency.

The most effective treatment for aortic stenosis is the surgical method of aortic valve replacement. Aortic valve replacement is indicated for severe aortic stenosis in the following cases:

  • the presence of fainting, angina pectoris, or heart failure;
  • in combination with coronary artery bypass grafting;
  • in combination with operations on other valves.

Surgical treatment of aortic stenosis significantly improves the patient’s well-being and prognosis of survival. It can be successfully carried out even in elderly patients without the risk of developing serious pathologies. For prosthetics, autografts, allogeneic prostheses, allografts, mechanical prostheses or pork bioprostheses and bovine pericardium prostheses are used.

Special types of aortic stenosis

In addition to the actual valve stenosis, there are narrowing of the external tract of congenital etiology or without primary damage to the AK fold.

Subaortic stenosis is a narrowing in the external tract of the LV distal to the valve ring in the form of an intermittent membranous diaphragm or fibrous membrane. Congenital structural features of the LV excretory tract contribute to the development of this type of AS, but the clinical manifestations of the disease do not occur at an early age.

There are three main anatomical types of subaortic stenosis:

  1. Membrano-diaphragmatic – discrete subaortic membrane;
  2. Fibrous-muscular collar (roller) – with asymmetric hypertrophy of the breast;
  3. The fibro-muscular tunnel is a diffuse subvalvular stenosis.

Turbulent blood flow causes secondary damage to the AK, which exacerbates the effects of stenosis and leads to the development of aortic insufficiency. Due to relative coronary insufficiency in patients, areas of subendocardial ischemia are formed with subsequent myocardiofibrosis. The main causes of death are fatal arrhythmias and myocardial infarction.

Clinical features of this type of defect are: earlier onset of symptoms, frequent fainting, with auscultation there is no click opening AK during systole at the apex of the heart, soft diastolic murmur.

Nadklapanny stenosis is a narrowing of the lumen of the ascending aorta (local or diffuse) in the region of the sinotubular region. Aorta, brachiocephalic, abdominal, and pulmonary vessels are involved in the stenotic process.

By etiology, the forms are divided:

  • Sporadic (consequences of intrauterine infection with rubella);
  • Hereditary (autosomal dominant type);
  • Williams syndrome (combined with mental retardation).

In this type of AS, the coronary vessels are located proximal to stenosis and are exposed to high pressure, so they are dilated, convoluted, and prone to the development of early arteriosclerosis.

Clinical manifestations of AS are combined with multiple organ abnormalities, impaired vitamin D metabolism, hypercalcemia, anginal attacks are more common, there is a difference in blood pressure on the hands.

The term “critical aortic stenosis” is used in the context of:

  • Severe stenosis, manifested during the first months of life;
  • LV dysfunction or a critical decrease in SV (cardiac output);
  • Possibilities of systemic blood flow exclusively with the open Botallic duct.

The presence of a critical narrowing of the LV extension tract is a direct indication for emergency surgical intervention.

This definition is used in pediatrics in relation to newborns with extremely low SV and decompensated circulatory failure. Symptoms of critical stenosis are similar to those with hypoplasia of the left heart. The life of such children is determined by the functioning of the Botallal duct, the early use of prostaglandins E1 and emergency surgery.

In children, AS is combined with other vices:

  • Double-wing or single-wing configuration of AK;
  • Coarctation of the aorta;
  • Open Botallus duct;
  • DMZhP;
  • Mitral insufficiency;
  • Left ventricular endocardial fibroelastosis;
  • WPW Syndrome;

AS is 2-4 times more often found in boys and is often combined with connective tissue diseases.

As the child grows older, stenosis is aggravated due to the growth of the heart muscle and the progression of fibro-sclerotic changes on the valve.

There are three types of aortic stenosis:

  • valvular (congenital or acquired);
  • supravalvular (only congenital);
  • subvalvular (congenital or acquired).

The main causes of acquired aortic stenosis are:

  • atherosclerosis of the aorta;
  • degenerative changes of valves with their subsequent calcification;
  • rheumatic valve disease (the most common cause of the disease);
  • infectious endocarditis.

Rheumatic damage to the valve cusps (rheumatoid endocarditis) provokes a reduction in the valve cusps, as a result they become rigid and dense, which is the reason for narrowing the valve opening. Often there is calcification of the aortic valve, which contributes to an even greater decrease in leaflet mobility.

In infectious endocarditis, similar changes are observed leading to the development of aortic stenosis. Often the causes of the formation of the disease are systemic lupus erythematosus and rheumatoid arthritis.

Atherosclerosis of the aorta is accompanied by severe degenerative processes, sclerosis, stiffness and calcification of the valves of the fibrous valve ring, which also complicate the outflow of blood from the left ventricle.

Sometimes in elderly people, the cause of aortic stenosis is primary degenerative valve changes. This phenomenon is called “idiopathic calcified stenosis of the aortic orifice.”

Congenital aortic stenosis occurs as a result of defects and abnormalities in valve development. In the late stages of the development of the disease, pronounced calcification joins the symptoms of aortic stenosis, which exacerbates the course of the disease.

Thus, in all patients, to a certain degree of aortic stenosis, regardless of the cause, aortic valve deformity and severe calcification are observed.

Svetlana Borszavich

General practitioner, cardiologist, with active work in therapy, gastroenterology, cardiology, rheumatology, immunology with allergology.
Fluent in general clinical methods for the diagnosis and treatment of heart disease, as well as electrocardiography, echocardiography, monitoring of cholera on an ECG and daily monitoring of blood pressure.
The treatment complex developed by the author significantly helps with cerebrovascular injuries and metabolic disorders in the brain and vascular diseases: hypertension and complications caused by diabetes.
The author is a member of the European Society of Therapists, a regular participant in scientific conferences and congresses in the field of cardiology and general medicine. She has repeatedly participated in a research program at a private university in Japan in the field of reconstructive medicine.

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