RU2844035C1 - METHOD FOR FORMING A PULMONARY-LEFT ATRIAL SHUNT AT PRESSURE IN THE PULMONARY ARTERY OF MORE THAN 65 mm Hg - Google Patents

Abstract

FIELD: medical science.

SUBSTANCE: invention refers to medicine, namely cardiosurgery. Great saphenous vein is separated above the knee up to an anastomosis with the common femoral vein which is cut off and used as an autovenous bypass. Proximal and distal edges of the remained intact vein are underrun and ligatured. That is followed by forming a proximal anastomosis with lateral compression of the pulmonary trunk within the area of the proximal anastomosis formation. Pulmonary trunk wall is excised with forming a round hole of diameter of 6-8 mm. That is followed by creating an end-to-side anastomosis of the autovenous shunt with the pulmonary trunk at angle of 30 degrees. Posterior wall of the anastomosis is formed by suturing without tightening. Suture end is used to bring the autovenous shunt to the pulmonary trunk; an anterior wall of the anastomosis is formed with the same suture. Suture ends are knotted together. Autovenous bypass is arranged along an anterior surface of the heart, enveloping a left ventricle to a left atrial appendage. To form a distal anastomosis, the heart is taken aside laterally to the right. Then, with lateral pressing of the left atrial appendage, a part of the wall of the left atrial appendage is excised, a round hole of 6-8 mm in diameter is formed, and creating a distal end-to-side anastomosis of the autovenous shunt with the left atrial appendage. Posterior wall of the anastomosis is created by means of a tightening suture; a suture end is used to bring the autovenous shunt to a left atrial appendage; the same suture is used to form an anterior wall of the anastomosis; the suture ends are knotted together. Then autovenous shunt is ligatured loop without tightening, with formation of tourniquet, which is brought out through drainage hole outside, where it is fixed.

EFFECT: method enables reducing the right ventricular load and promotes activating the neurohumoral mechanism of reducing the right ventricular outlet resistance by eliminating peripheral angiospasm in the pulmonary circulation, as well as ensuring the prolonged clinical remission.

1 cl, 1 dwg, 3 ex

Description

The invention relates to medicine, namely to cardiac surgery, and can be used as a method for forming a pulmonary-left atrial shunt when the pressure in the pulmonary artery is more than 65 mm Hg.

There is a known method of surgical treatment of pulmonary arterial hypertension (PAH) - atrial septostomy - creation of an opening in the interatrial septum for blood drainage, which leads to a decrease in pressure in the right chambers of the heart, especially in patients with severe forms of PAH (IV FC). The procedure is performed using a special balloon catheter. It is indicated for patients with refractory forms of PAH, when long-term pathogenetic therapy (bosentan or prostaglandins) does not improve their clinical condition. Balloon atrial septostomy in patients with PAH FC IV (WHO) is indicated for frequent syncope and / or refractory right ventricular heart failure (HF), despite drug therapy. Remote results of balloon atrial septostomy are unknown. The procedure is not indicated for patients with terminal stages of right ventricular HF or with significant left ventricular HF. The risk of death during this procedure is 5-6%, it should be performed only in appropriate centers with highly qualified cardiac surgeons. [1. - Jentzer JC, Mathier, MA. Pulmonary Hypertension in the Intensive Care UnitJ. Intensive Care Med. 2016; 31(6):369-385]. This method is accepted as an analogue.

A method of surgical treatment of PAH in extreme pulmonary hypertension is known - transplantation of the heart-lung complex to patients in the intermediate or high risk zone, but noting clinical deterioration despite maximum drug therapy with antihypertensive drugs for the treatment of patients with PAH. The operation is indicated for progressive PAH, when, despite adequate drug therapy, the patient's condition corresponds to III-IV FC. All patients, according to the results of the 6-minute walk test less than 400 m, can be considered as candidates for heart-lung transplantation. Over the past decade, the median survival of patients with PAH after heart-lung transplantation has increased significantly: from 1.9 (1982-1991) to 5.6 years (2002-2012). Heart-lung transplantation is recommended for patients with PAH if combination therapy is ineffective. It is recommended to include patients with PAH and patients with inoperable chronic pulmonary embolism with a high risk of a fatal outcome in the waiting list for heart-lung transplantation when prescribing triple combination specific therapy. Survival after heart-lung transplantation in patients with idiopathic PAH in the best cardiac surgery centers is: after 1 year - 64% (in recent years - up to 74%), after 3 years - 54%, and after 5 years - 44% [2. - Baumgartner H, De Backer J, Babu-Narayan SV, et al. 2020 ESC Guidelines for the management of adult congenital heart disease. Eur Heart J. 2021; 42(6):563-645]. This method is taken as a prototype. However, this method is labor-intensive, requires careful donor selection and lifelong immunosuppressive therapy.

The goal is to increase efficiency while reducing labor intensity.

The technical result is achieved in that in the method of forming a pulmonary-left atrial shunt at a pressure in the pulmonary artery of more than 65 mm Hg, which includes the isolation of the great saphenous vein above the knee to the junction with the common femoral vein, which is cut off and used as an autovenous shunt, while the proximal and distal edges of the remaining intact vein are sutured and ligated; then, a proximal anastomosis is formed, while lateral pressing of the pulmonary trunk is performed in the area of formation of the proximal anastomosis, the wall of the pulmonary trunk is excised, thereby forming a round opening with a diameter of 6-8 mm, then an anastomosis of the autovenous shunt with the pulmonary trunk is created according to the "end to side" type at an angle of 30 degrees, the posterior wall of the anastomosis is formed by applying a suture without tightening, then the end of the thread is used to bring the autovenous shunt closer to the pulmonary trunk, the anterior wall of the anastomosis is formed with the same thread, the ends of the thread are secured together with knots, the autovenous shunt is placed along the anterior surface of the heart, the left ventricle is encircled to the left atrial appendage, to form a distal anastomosis, the heart is diverted laterally to the right, then, with lateral pressing of the left atrial appendage, part of the wall of the left atrial appendage is excised, forming a round opening with a diameter of 6-8 mm, and create a distal anastomosis of the autovenous shunt with the left atrial appendage according to the "end to side" type, while forming the posterior wall of the anastomosis by means of a suture without tightening, with the end of the thread bring the autovenous shunt closer to the left atrial appendage, then by means of a suture with the same thread form the anterior wall of the anastomosis, the ends of the thread are secured together with knots, then a ligature loop is applied to the autovenous shunt without tightening, forming a tourniquet, which is brought out through the drainage hole to the outside, where it is fixed.

Fig. 1 shows a diagram of the formation of a pulmonary-left atrial shunt.

The method is carried out as follows.

Clinically, patients report complaints of shortness of breath during high and moderate physical exertion, increased fatigue, weakness, and dizziness. At later stages, syncopal states and/or a symptom complex caused by right ventricular heart failure appear: lower limb edema, hepatomegaly, ascites, and pulsation of the jugular veins. Patients with long-standing PAH may experience chest pain of the angina type. Myocardial ischemia may be based on relative coronary insufficiency due to low cardiac output and increased right ventricular wall tension, hypoxemia, and compression of the left coronary artery by an aneurysmally dilated pulmonary artery. Another symptom associated with high long-standing PAH is hemoptysis, which occurs in no more than 6% of cases in patients without congenital heart disease (CHD).

In patients with Eisenmenger syndrome, one of the manifestations of PAH, pulmonary hemorrhages are recorded in 43% of cases and in 8% of cases are the cause of death. The source of bleeding in 90% of cases are altered bronchial arteries, which are especially often detected in patients with PAH against the background of congenital heart defects (CHD). Significant expansion of the pulmonary artery can cause its dissection or rupture, which is clinically accompanied by cardiac tamponade. The symptomatology of PAH can vary significantly depending on the underlying disease in which it develops and the concomitant pathology. It should be noted that the clinical picture can change depending on both the pathology that caused PAH or the associated condition, and the presence of another concomitant disease.

All patients admitted to the hospital undergo physical examination. Heart auscultation reveals an accentuated second tone on the pulmonary artery and a systolic murmur of tricuspid regurgitation.

Chest X-ray reveals dilation of the pulmonary artery trunk (the second arc along the left contour of the heart) and depletion of the pulmonary vascular pattern, and less commonly, dilation of the right chambers of the heart.

When examining the function of external respiration, a mild or moderate decrease in lung volumes is revealed, associated with the severity of the disease. When analyzing the gas composition of the blood, the partial pressure of oxygen in arterial blood (PaO2) at rest remains within the normal range of 96-98 mm Hg, and the partial pressure of carbon dioxide (PaCO2) is reduced due to alveolar hyperventilation.

Echocardiographic signs characterize the size of the right ventricle (RV) and its pressure overload, the nature of the blood flow velocity from the RV, the diameter of the pulmonary artery and the cross-sectional area. Dopplerography shows an increase in blood pressure in the PA.

Transvenous right heart catheterization and invasive pulmonary artery pressure measurement are recommended in patients suspected of having PAH to confirm the diagnosis and determine treatment strategy.

Chest computed tomography with intravenous bolus contrast in all patients with PAH helps to identify the underlying cause of the disease: chronic thromboembolic pulmonary hypertension (CTEPH) or lung disease, to detect signs of PAH-associated conditions (esophageal dilation or presence of congenital heart disease), and to obtain information on the prognosis of the disease. Signs such as an increase in the pulmonary artery diameter (≥29 mm), a pulmonary artery to ascending aorta ratio ≥1.0, and a segmental artery to bronchial diameter ratio of more than 1:1 in three or four lung lobes have been shown to have high specificity for the diagnosis of PAH. Ground-glass opacity is typical for patients with CTEPH, resulting from ventilation-perfusion mismatches. Ground-glass opacity is seen in patients with advanced PAH.

Coronary angiography is recommended for patients with PAH in the presence of angina symptoms or risk factors for coronary heart disease, as well as in the planned surgical treatment of patients with CTEPH.

The group of patients with increased PA BP over 65 mm Hg included 35 patients who underwent surgical correction of PAH by applying a shunt between the pulmonary artery and the left atrial appendage. It is based on the principle of hemodynamic correction of intracardiac blood flow by reducing the work of the right ventricle on the resistance of the pumped blood, which is achieved by dumping part of the blood volume from the pulmonary artery to the left atrium by forming a special anastomosis between them (pulmonary-left atrial shunt). This principle, in addition to ensuring a decrease in the load on the right ventricle, helps to include (activate) the neurohumoral mechanism of reducing resistance at the exit from the right ventricle due to the elimination of peripheral vasospasm in the pulmonary circulation.

The operation is performed from a median sternotomy or from a left-sided thoracotomy (IV-V intercostal space). In case of a left-sided thoracotomy, unilateral pulmonary ventilation is performed. Layer-by-layer tissue dissection is performed, access to the pericardium is achieved, which is dissected with a T-shaped incision and taken on holders. To form a shunt, a large saphenous vein is used, isolated above the knee to the junction with the common femoral vein (the largest diameter). When isolating the vein, the lateral tributaries are untied, and the proximal and distal edges of the remaining intact vein are sutured and ligated when cutting off the mobilized conduit. In this case, the distal edge of the isolated vein is then used to form a proximal anastomosis. During lateral retraction of the pulmonary trunk in the area of proximal anastomosis formation, a portion of the wall is excised, forming a round opening with a diameter of 6-8 mm. A proximal end-to-side anastomosis of the autovein with the pulmonary trunk is created at an angle of 30 degrees: the posterior wall of the anastomosis is formed using a continuous wraparound or U-shaped suture without tightening (5/0 non-absorbable thread). By pulling the ends of the thread under minimal tension, the autovein is brought closer to the pulmonary trunk, then, using a continuous wraparound or U-shaped suture, the anterior wall of the anastomosis is formed with the same thread, the ends of the thread are secured together with several knots. The lateral retraction is removed and after preventing air embolism and filling the autovenous shunt with blood, a clamp is applied to its distal end. The shunt is placed along the anterior surface of the heart, enveloping the left ventricle to the left atrial appendage - the required length of the conduit is selected so that there is no tension or kinking, the excess part is cut off. To create a distal anastomosis, the heart is retracted laterally to the right. With lateral pressing of the left atrial appendage, part of the wall of the left atrial appendage (apex) is excised, thereby forming a round opening with a diameter of 6-8 mm. A distal anastomosis of the autovein with the left atrial appendage is created according to the "end to side" type: the posterior wall of the anastomosis is formed using a continuous wrapping or U-shaped suture without tightening (5/0 thread made of non-absorbable material). By pulling the ends of the thread under minimal tension, the autovein is brought closer to the left atrial appendage, then, using a continuous twisting or U-shaped suture, the anterior wall of the anastomosis is formed with the same thread, the ends of the thread are secured together with several knots. After preventing air embolism, the lateral squeeze is removed. After creating the anastomoses, the blood flow through the shunt is controlled by transverse compression and assessment of filling, the pressure in the pulmonary trunk and left atrium is invasively measured for several minutes. A ligature loop is applied to the autovenous shunt without tightening, and a tourniquet is formed, which is brought out through the drainage hole to the outside, where it is fixed (to be able to regulate the volumetric blood flow rate through the shunt and possible occlusion of the shunt in the postoperative period without a repeat operation). The pericardial and pleural cavities are drained, layer-by-layer suturing of the wound with osteosynthesis of the sternum is performed (when performing a median sternotomy).

In the postoperative period, anticoagulant therapy is recommended for antithrombotic prophylaxis (warfarin with target INR values of 2.5-3.0; in the early postoperative period, heparin is administered in a prophylactic dose until target INR values are achieved). Shunt occlusion by tightening the ligature is performed 2-3 weeks after surgery; if necessary, the shunt may not be ligated (Fig. 1).

The method is confirmed by the following examples:

Example 1. Patient T., 76 years old, was hospitalized on a planned basis for surgical treatment of an atrial septal defect (ASD).

If a patient complains of shortness of breath when walking, climbing stairs two floors, or with minor physical exertion.

Medical history: acute myocardial infarction, acute cerebrovascular accident and diabetes mellitus are denied. Syncope and anginal pain were noted. According to echocardiography, congenital heart disease: ASD was diagnosed. The patient was under outpatient observation by a cardiologist, no surgical treatment was performed. Over the past 5 years, she has noted a decrease in exercise tolerance (ET) in the form of shortness of breath with minor exertion. Over time, the symptoms progressed. Recently, she noted the appearance of a feeling of irregular and rapid heartbeat. She was hospitalized at her place of residence, a paroxysm of atrial flutter was detected. Drug treatment was carried out. Subsequently, she noted rare paroxysms 2-3 times a year.

Examination on admission: the patient is in a moderate condition, conscious, cooperative, and adequate. The skin is of physiological color, normal moisture, and clean. Swollen shins are noted. The chest is cylindrical, painless on palpation, and symmetrically participates in the act of breathing. Percussion reveals clear pulmonary sounds over symmetrical areas of the lungs. Auscultation reveals breathing in all parts of the lungs, is harsh, and no wheezing is heard. Respiratory rate is 20 per minute. The cardiac area is visually unchanged. Percussion boundaries of relative cardiac dullness are widened to the right and upward. Heart sounds are muffled and rhythmic. Heart auscultation reveals an accentuated and split second tone, systolic murmur in the second or third intercostal space to the left of the sternum, and diastolic murmur in the projection of the pulmonary artery valve. Heart rate is 72 per minute. Blood pressure is 120/90 mm Hg. Pulsation on the dorsum of the feet is preserved. The abdomen is soft, painless on palpation. The liver does not protrude from under the edge of the costal arch, the spleen is not palpated. The kidney area and ureter points are painless. The percussion symptom is negative on both sides. Urination is not frequent, painless.

Results of the completed survey:

According to X-ray data, the lungs are without visible pathological changes. An increase in the pulmonary pattern is noted. The waist of the heart is smoothed out, an increase in the right chambers of the heart is noted.

According to ECG data, sinus rhythm, heart rate - 75 bpm, deviation of the electrical axis of the heart to the right, signs of enlargement of the right atrium, incomplete block of the right bundle branch of His. AV block of the 1st degree.

According to echocardiography data, a central defect measuring up to 1.5 cm was detected in the projection of the interatrial septum; the diameter and location of the defect was assessed based on a sequential analysis of three echocardiographic projections (4-chamber projection, parasternal short-axis projection, and subcostal projection).

Enlargement of the right chambers of the heart is noted:

1. 4-chamber projection - basal size 4.5 cm (RVD1), average size 3.8 cm (RVD2), vertical size - 7.7 cm (RVD3);

2. Parasternal short-axis projection at the level of the aortic valve - proximal diameter of the RV outflow tract (RVOT1) - 3.6 cm, distal diameter of the RV outflow tract (RVOT2) - 3.3 cm.

3. The average size of the right atrium (RA minor axis) is 5.0 cm. The volume of the right atrium is 73 ml.

Color Doppler mapping in the defect area revealed an intensely colored left-to-right flow and tricuspid valve insufficiency with grade 2 regurgitation. A quantitative assessment of the shunt size was performed: Qp/Qs>1.0.

The patient had an increase in mean pulmonary artery pressure to 67 mm Hg and an increase in pulmonary vascular resistance to 7 Wood units. Global contractility of the left ventricle was not impaired, EF was 67%.

Based on the clinical picture, physical examination data, laboratory and instrumental examination results, the patient has a clinical diagnosis: Congenital heart defect: primary atrial septal defect. Pulmonary arterial hypertension stage 3. Heart rhythm disturbance: paroxysmal atrial flutter. CHF PB FC III according to NYHA

Intraoperatively, before connecting the CPB apparatus, the pressure in the pulmonary trunk was invasively assessed (69 mm Hg). The patient underwent atrial septal defect suturing under CPB conditions and, given the increase in PA blood pressure, surgical correction of PAH by applying a shunt between the pulmonary artery and the left atrial appendage of the heart (according to the above-described technique). After disconnecting the CPB apparatus, a control invasive assessment of the pressure in the pulmonary trunk was performed (55 mm Hg).

The shunt occlusion by tightening the ligature was performed 14 days after the operation. During the postoperative control observation (after 12 months), the pressure in the PA was 37 mm Hg.

Example 2. Patient K., 65 years old, was hospitalized in the thoracic surgery department with a diagnosis of central cancer of the left lung, severe pulmonary hypertension.

Upon receipt of complaints of paroxysmal cough, constant fatigue, weakness, loss of appetite, shortness of breath that significantly increases with minimal physical exertion, difficulty breathing in a horizontal position.

History of the disease: has been coughing for 10 years, suffered from severe pneumonia six months ago, was treated with antibiotics, after discharge began to notice episodes of shortness of breath against the background of usual physical activity. Over the past 6 months, the condition has significantly worsened, a cough with the separation of blood clots has appeared.

Examination on admission: The patient's condition is moderate, the patient is conscious. Normostenic constitution. Bed rest, with the head of the bed elevated. The skin is flesh-colored, of normal moisture, without pathological rashes. Symmetrical edema of the shins up to the upper third. The chest is painless on palpation, symmetrically participates in breathing. Auscultation reveals harsh breathing, weakened in the lower sections, wheezing is noted. Respiratory rate is 23 per 1 min. Percussion boundaries of relative cardiac dullness are widened. Heart sounds are muffled, the rhythm is regular, the second sound is accentuated over the pulmonary artery, systolic murmur in the area of the tricuspid valve. Heart rate is 85 per minute. Pulsation of the arteries of the extremities is preserved. Blood pressure is 100/80 mm Hg. The abdomen is painless on palpation. The liver protrudes from under the costal arch edge +0.5 cm. Dimensions according to Kurlov are 13×11×8 cm. Stool is regular. The percussion symptom is negative on both sides. Urination is independent, free, painless.

Results of the completed survey:

Electrocardiography: signs of hypertrophy and overload of the right ventricle, dilation and hypertrophy of the right atrium (P-pulmonale), deviation of the electrical axis of the heart to the right, sinus rhythm with a heart rate of 84 beats per 1 min.

Echocardiography: Left ventricle: end-diastolic volume 140 ml, end-systolic volume 47 ml, stroke volume 93 ml; EF 66%, global systolic function of the left ventricle is normal. Right ventricle: basal dimension 4.3 cm (RVD1), mean dimension 3.9 cm (RVD2), vertical dimension - 7.0 cm (RVD3), proximal diameter of the right ventricular outflow tract (RVOT1) - 3.7 cm, distal diameter of the right ventricular outflow tract (RVOT2) - 3.5 cm; right atrium: 66 ml; paradoxical motion of the interventricular septum due to increased pressure in the right ventricle; when assessing the free wall of the RV, thickening up to 8 mm is noted. Tricuspid valve insufficiency with regurgitation of grade 2-3; calculated pulmonary artery pressure - SPPA 70 mm Hg. Dilation of the IVC to 1.8 cm, does not collapse on inhalation.

X-ray of the lungs: a non-uniform spherical shadow with fuzzy edges is visualized at the root of the left lung, the root of the lung is dilated, signs of pulmonary hypertension are noted (enlargement of the pulmonary artery arch; expansion of the shadow of the roots of the lungs, increased pulmonary pattern).

Bronchoscopy revealed that the tumor originated from the initial sections of the main bronchus with its 70% stenosis, with endobronchial growth to the upper lobe bronchus; a biopsy was performed. Histological examination revealed moderately differentiated squamous cell carcinoma of the left main bronchus. No metastases were detected.

Intraoperatively, the pressure in the pulmonary trunk was invasively assessed (73 mm Hg). Before pulmonectomy, surgical correction of PAH was performed by applying a shunt between the pulmonary artery and the left atrial appendage (using the above-described technique). Control invasive assessment of pressure in the pulmonary trunk (58 mm Hg).

The pulmonary-left atrial shunt was not ligated in the postoperative period.

During follow-up observation upon rehospitalization after 6 months, pulmonary artery blood pressure was 45 mm Hg. The patient was brought into clinical remission.

Example 3. Patient B., 57 years old, was hospitalized on a planned basis for surgical treatment of peripheral cancer of the right lung.

Upon receipt of a complaint about paroxysmal painful cough with the release of blood and shortness of breath with minimal physical exertion.

History of the disease: oncological disease was first diagnosed more than 7 years ago, refused surgical treatment, was under outpatient observation. Over time, the symptoms progressed. Recently, I began to notice a decrease in tolerance to physical activity in the form of shortness of breath with minor exertion, paroxysms of irregular and rapid heartbeat, chest pain.

An X-ray tomographic examination revealed a tumor-like formation (peripheral cancer) in the upper and middle lobes of the right lung with tumor infiltration of the vessels of the root of the right lung.

Echocardiography: left ventricle: end-diastolic volume 130 ml, end-systolic volume 55 ml, stroke volume 75 ml; EF 57%, global systolic function of the left ventricle is not impaired. Right ventricle: basal dimension 4.7 cm (RVD1), mean dimension 4.1 cm (RVD2), vertical dimension - 7.2 cm (RVD3), proximal diameter of the right ventricular outflow tract (RVOT1) - 3.8 cm, distal diameter of the right ventricular outflow tract (RVOT2) - 3.6 cm; right atrium: 69 ml; paradoxical motion of the interventricular septum, due to increased pressure in the right ventricle. Tricuspid valve insufficiency with regurgitation of grade 2-3; estimated pulmonary artery pressure - SPPA 75 mmHg. Dilation of the IVC up to 1.9 cm, does not collapse on inhalation.

Intraoperatively, the pressure in the pulmonary trunk was invasively assessed (77 mm Hg). The patient underwent pulmonectomy and surgical correction of PAH with the imposition of a shunt between the PA and the left atrial appendage (according to the above-described technique). Control invasive assessment of the pressure in the pulmonary trunk (62 mm Hg).

The postoperative period was uneventful, antibacterial therapy was administered. Positive dynamics in the form of increased tolerance to physical activity, expansion of the motor regime, reduction of pain syndrome, increase in motor activity, and improvement of well-being were noted against the background of the treatment. The pulmonary-left atrial shunt was not ligated in the postoperative period. A control echocardiographic study confirmed the positive dynamics of clinical symptoms - a decrease in pressure in the pulmonary artery trunk (46 mm Hg).

35 patients were treated, who had an increase in PAH of more than 65 mm Hg. The surgical treatment allowed the patients to enter into long-term clinical remission.

Sources of information

1. Jentzer JC, Mathier, MA. Pulmonary Hypertension in the Intensive Care Unit. J. Intensive Care Med. 2016; 31(6):369-385].

2. Baumgartner H, De Backer J, Babu-Narayan SV, et al. 2020 ESC Guidelines for the management of adult congenital heart disease. Eur Heart J. 2021; 42(6):563-645].

Claims (1)

A method for forming a pulmonary-left atrial shunt when the pressure in the pulmonary artery is more than 65 mm Hg, including the isolation of the great saphenous vein above the knee to the junction with the common femoral vein, which is cut off and used as an autovenous shunt, while the proximal and distal edges of the remaining intact vein are sutured and ligated; then, a proximal anastomosis is formed, while lateral pressing of the pulmonary trunk is performed in the area of formation of the proximal anastomosis, the wall of the pulmonary trunk is excised, thereby forming a round opening with a diameter of 6-8 mm, then an anastomosis of the autovenous shunt with the pulmonary trunk is created according to the "end to side" type at an angle of 30 degrees, the posterior wall of the anastomosis is formed by applying a suture without tightening, then the end of the thread is used to bring the autovenous shunt closer to the pulmonary trunk, the anterior wall of the anastomosis is formed with the same thread, the ends of the thread are secured together with knots, the autovenous shunt is placed along the anterior surface of the heart, the left ventricle is encircled to the left atrial appendage, to form a distal anastomosis, the heart is diverted laterally to the right, then, with lateral pressing of the left atrial appendage, part of the wall of the left atrial appendage is excised, forming a round opening with a diameter of 6-8 mm, and create a distal anastomosis of the autovenous shunt with the left atrial appendage according to the "end to side" type, while forming the posterior wall of the anastomosis by means of a suture without tightening, with the end of the thread bring the autovenous shunt closer to the left atrial appendage, then by means of a suture with the same thread form the anterior wall of the anastomosis, the ends of the thread are secured together with knots, then a ligature loop is applied to the autovenous shunt without tightening, forming a tourniquet, which is brought out through the drainage hole to the outside, where it is fixed.