Ventricular septal defect is the most common congenital heart disease in clinical practice, accounting for approximately 20% of congenital heart diseases. Ventricular septal defect can occur alone or in combination with other cardiac malformations (e.g., ductus arteriosus, aortic constriction, aortic sinus aneurysm, atrial septal defect, etc.) and as a component of certain complex malformations (e.g., tetralogy of Fallot, transposition of the great arteries, permanent arterial trunk, etc.).
The natural course of simple ventricular septal defects varies from spontaneous closure without specific treatment to rapid deterioration after birth, with severe pulmonary hypertension and even Eisenmenger’s syndrome, or life-threatening severe hemodynamic disturbances and heart failure. The impact of ventricular septal defects on the body is mainly related to the degree of abnormal shunting in ventricular septal defects, and in addition, the unique clinical characteristics of different sites of ventricular septal defects may affect the disease outcome and response to treatment. The degree of abnormal shunting, in addition to the size of the defect, depends mainly on the resistance of the pulmonary circulation. Therefore, defect site, defect size, pulmonary circulatory resistance, and cardiac function and hemodynamic status are important disease evaluation indicators for patients with ventricular septal defects, as well as important reference factors to help determine treatment options and prognosis. In this paper, we discuss the interventional treatment strategies for each type of simple ventricular septal defect without other malformations.
I. Staging of ventricular septal defect
1. With reference to the diameter of the aortic valve orifice, the ventricular septal defect can be divided into large ventricular septal defect, moderately large ventricular septal defect and small ventricular septal defect.
Large ventricular septal defect refers to the diameter of ventricular septal defect is equal to or greater than the diameter of its own aortic valve orifice, the resistance of ventricular septal defect to blood flow is small, early pulmonary vascular lesions have not yet occurred, pulmonary vascular resistance is small, the left to right fraction flow is huge, so it is easy to appear respiratory distress, left heart failure and pulmonary infection signs.
Small ventricular septal defect means that the diameter of ventricular septal defect is less than 1/3 of the diameter of the aortic valve orifice. The septal defect has high resistance to blood flow and small left-to-right fractional flow, thus not causing significant hemodynamic abnormalities. The right ventricular pressure and pulmonary vascular resistance are not high, and the pulmonary circulation blood flow/body circulation blood flow (Qp/Qs) is <1.75. Clinically, the defect is usually asymptomatic except for a heart murmur. Multiple small ventricular septal defects can accumulate into one large ventricular septal defect.
A moderate large ventricular septal defect is one that is in between the above two, with a septal defect diameter smaller than the diameter of the aortic valve orifice but larger than 1/3 of it. The fractional flow is sufficient to make the right ventricular pressure rise to 1/2 of the left ventricular pressure, and Qp/Qs reaches 2.0 or more.
2.According to the location of the defect on the ventricular septum and the adjacent relationship, the defect is classified as follows.
(1) Suprascapular septal defect: also called conical septal type, funnel septal type, inferior pulmonary trunk type, inferior arterial trunk type, inferior arterial trunk double outlet type and outflow tract type ventricular septal defect. The defect is garden or oval shaped, its long axis is transverse, located above the supraventricular crest, adjacent to the pulmonary valve and aortic valve, where the septum travels in a spiral pattern, and the shunted blood can enter the pulmonary artery directly because of the high position of the defect. The defect is located in the right ventricular outflow tract when viewed from the right ventricular plane, or in the left ventricular outflow tract if viewed from the left ventricular plane. This type of ventricular septal defect includes the inferior stem defect, which is located adjacent to the pulmonary valve and aortic valve, and the intracrural defect, which is located within the muscle of the supraventricular crest. The infra-dry ventricular septal defect has no muscle tissue at the superior border of the pulmonary or aortic valve. The right coronary valve (and rarely the aortic valve) may prolapse into the superior border of the defect with (or without) aortic valve insufficiency due to loss of annular support. The prolapsed leaflet may occlude the ventricular septal defect in diastole or even close the ventricular septal defect nearly completely, reducing the shunt flow and also causing some degree of right ventricular outflow tract obstruction. The posterior inferior border of this type of defect often has a muscle bundle separating it from the tricuspid annulus, with the bundle of Hitchcock located inferior to the muscle bundle. The subdistal ventricular septal defect varies in size, with large and medium-sized defects being the most common.
(2) Perimembranous ventricular septal defect: also known as subcrural ventricular septal defect. The septal defect is located in the membranous septum below the supraventricular ridge, immediately below the aortic valve. The defect is located between the sinus trabeculae and the conical part of the septum, often between the anterior and posterior branches of the septal bundle, and in the right ventricular view, the defect is located in the membranous part of the septum, below the posterior part of the supraventricular ridge, between the right ventricular outflow tract and the inflow tract, often covered by the tricuspid septal valve or its tendon part, and the defect may extend to the inflow tract, outflow tract or septal trabeculae The defect may extend into the inflow tract, outflow tract, or septal trabeculae, and is further divided into the following subtypes: perimembranous inflow tract, perimembranous outflow tract, and perimembranous myocardial, forming a perimembranous defect. In the left ventricular view, the defect is located in the outflow tract of the left ventricle, below the aortic uncoronary valve and the right coronary valve, and the bundle of Hitchcock travels on the posterior inferior border of the defect, which is often oval in shape, ranging from a few millimeters to more than 3 cm. Sometimes there is an intact fibrous ring around the circumference of the defect, and sometimes the inferior border is muscular. Perimembranous ventricular septal defects are most common due to adhesions of the tricuspid tendon, septal valve, or septal-anterior valve junction to the edges of the septal defect, which can form a membranous tumor, a localized sac that protrudes to the right during systolic left ventricular hyperbaric flow. Membranous tumors can partially or completely occlude the defect. It is clearly visible on two-dimensional ultrasound images. One or more ruptures at the tip of the membranous tumor are caused by the impact of the blood flow.
(3) Myocardial septal defect: Located in different parts of the myocardial septum, the myocardial septal defect can be further subdivided into central, apical, and marginal myocardial types, with the central myocardial type of the septum being the most common. These defects are surrounded by intact muscle tissue and account for approximately 5-20% of all ventricular septal defects. Due to the abundance of trabecular structures on the right ventricular surface, a single ventricular septal defect observed from the left ventricular surface can be seen with several openings on the right ventricular surface. The location of the myocardial ventricular septal defect is not fixed and does not have a constant relationship with the conduction system.
(4) Atrioventricular tubular defect: Atrioventricular septal defect, also known as tubular, endocardial cushion, and inflow tract ventricular septal defect. The defect is located in the right ventricular inflow tract, the deepest part of the ventricular septum, below the tricuspid septal valve, with no muscle tissue between it and the septal valve. It accounts for 8-10% of ventricular septal defects and is often oval or triangular in shape, sometimes surrounded by an intact fibrous ring and sometimes partially by muscle tissue. The bundle of Hitchcock travels along the posterior and inferior edges of the defect, slightly deviating toward the left ventricular surface.
3. When a ventricular septal defect has a moderate to large left-to-right shunt, the workload of the left ventricle increases, followed by left ventricular hypertrophy. The right ventricle receives shunted blood, resulting in a significant increase in pulmonary blood, reflexively causing pulmonary vasospasm and an increase in pulmonary artery pressure, which is power pulmonary hypertension. Due to the increased pulmonary vascular resistance, the workload of the right ventricle is increased. If the lesion is not treated, with time and age, a series of organic lesions gradually occur in the small pulmonary arteries, and then it becomes irreversible resistance pulmonary hypertension. heath and Edwards classified pulmonary vascular lesions in pulmonary hypertension into six grades, and concluded that pulmonary vascular resistance in patients with large ventricular septal defect is positively correlated with the severity of vascular lesions in pulmonary hypertension.
Grade 1: hypertrophy of the middle layer of the vessel with no intimal hyperplasia.
Grade 2: mid-vessel hypertrophy with endothelial cell reaction.
Grade 3: Endothelial fibrous degeneration with mid-layer hypertrophy and possible early extensive vasodilatation.
Grade 4: Extensive vasodilatation with regional vascular obstruction and plexiform lesions due to endothelial fibrous degeneration.
Grade 5: Other dilated lesions of the vessels, such as spongy and angiomatous lesions.
Grade 6: Grade 5 lesions plus the presence of necrotizing arteritis.
Second, the impact of ventricular septal defect typing on its natural course
1. Some ventricular septal defects can close and become smaller on their own, and do not require surgical correction or interventional treatment
About 40% of the ventricular septal defects can be completely closed spontaneously during growth and development, especially the smaller diameter ventricular septal defects have a 75-80% chance of spontaneous closure in infancy and childhood. In addition, approximately 25-30% of ventricular septal defects become spontaneously smaller in diameter to the point where no intervention is required, and although smaller diameter ventricular septal defects are more likely to close spontaneously than larger diameter ventricular septal defects (60% versus 20%), some larger diameter ventricular septal defects, even those that have led to congestive heart failure, have the potential to close spontaneously.
The incidence of spontaneous closure of ventricular septal defects decreases with age. Kirklin’s data suggest that the incidence of spontaneous closure of ventricular septal defects found in newborns is 80% at one month, 60% at three months, 50% at six months, 25% at 12 months, and very low after 12-18 months of age. Spontaneous closure of ventricular septal defects occurs before the age of 2 years and is less common above the age of 5 years, but spontaneous closure may occur in adolescence and adulthood.
The incidence of spontaneous closure of ventricular septal defects is very closely related to the type of ventricular septal defect pathology, with the highest incidence of spontaneous closure in myocardial ventricular septal defects (approximately 80%). Spontaneous closure of outflow tract ventricular septal defects is extremely low, while spontaneous closure of inflow tract ventricular septal defects has not been reported.
The mechanism by which spontaneous closure occurs is closely related to the anatomic relationship between the site of the ventricular septal defect and the local pathologic process. The myocardial defect closes as the peripheral myocardium shrinks due to development of fibrous tissue proliferation, adhesions, and thickening. Infective endocarditis may cause edema, exudation, redundancy formation, fibrous tissue proliferation, adhesions, and closure of the margins of the ventricular septal defect. Displacement of the tricuspid valve leaflets and formation of septal membrane tumors are the main mechanisms for spontaneous closure of septal defects in the membrane and perimembranous regions.
2. Pulmonary vascular lesions
The risk of pulmonary hypertension vasculopathy in patients with large septal defects increases with age, and the severity of increased pulmonary vascular resistance is positively correlated with the age of the patient. Thereafter, if the septal defect remains small, more severe pulmonary vasculopathy may or may not occur with age. In infants and children with small septal defects, pulmonary vasculopathy does not occur.
3. Infective endocarditis
Infective endocarditis is rare in patients with ventricular septal defect, about 0.15-0.3% of patients? years. Prevalent in small ventricular septal defects, more men than women, more incidence above 20 years of age, infected redundant emboli can sometimes cause embolism of the body circulation arteries or pulmonary arteries.
4.Death
In infants and children with large ventricular septal defects, if untreated, about 9% die of heart failure within 1 year of age, mostly occurring in the first 2 to 3 months of life. It may be that the hypertrophy and degeneration of the middle layer of the small fetal-type pulmonary artery at this time reduces pulmonary vascular resistance and increases the left-to-right shunt flow through the ventricular septal defect, gradually leading to the formation of resistance pulmonary hypertension and eventually Eisenmenger syndrome. Repeated episodes of pulmonary infection are also a cause of death.
5. Aortic valve prolapse and insufficiency of closure
A small number of patients with ventricular septal defects are prone to complications of aortic valve prolapse and insufficiency of closure, commonly in the sub-stem and membranous type of large ventricular septal defects. Aortic valve insufficiency is rarely present at birth, but occurs and progressively worsens within the age of 10 years, and is often severe by the age of 20 years. When aortic valve closure insufficiency worsens, the left-to-right shunt flow is reduced due to blockage of the ventricular septal defect by the prolapsed valve leaflets.
III. Impact of septal defect staging on indications for interventional treatment
Interventional treatment of ventricular septal defect has undergone nearly 20 years of development, firstly, the Rashkind double-sided umbrella blocker was adopted by Lock in 1988 to treat ventricular septal defect, then Clamshell, Cardioseal blocker and Sederis button patch appeared, but the above blockers have limited the clinical use due to complicated operation and many complications. However, the complexity and complications of the above-mentioned occluders have limited their wide use in clinical practice. The number of cases that can be successfully blocked is very small, and only a few cases have been reported. With the continuous development of interventional materials, the operation method has been improved and perfected. In particular, the invention of Amplatzer nickel-titanium alloy sealer in 1997 has strongly promoted the promotion and popularity of interventional treatment for ventricular septal defects. At present, some types of ventricular septal defects can be cured by interventional treatment. Interventional treatment has become an alternative to surgical correction. In China, the Amplatzer blocker was first used in 2002 to treat ventricular septal defects, and it has achieved good recent results and satisfactory medium- and long-term results.
The morphology of the ventricular septal defect, the diameter of the defect, and the distance of the defect from the aortic and tricuspid valves determine the choice of the indication for occlusion therapy. Generally speaking, all types of ventricular septal defects, such as the edge of the defect is more than 2 mm from the aortic valve and tricuspid valve and other important structures, and the diameter of the defect is 10-15 mm or less can be tried for interventional treatment.
1.Supra-crestal ventricular septal defect.
Supra-crural ventricular septal defect includes sub-stem type defect located adjacent to the pulmonary valve and aortic valve and intra-crural type defect located in the muscle of supra-crural crest.
The sub-stem type ventricular septal defect is characterized by no distance from the pulmonary valve, and the short-axis view of the cardiac ultrasound aorta is usually located at the 1:00 to 2:00 position. Currently, it is believed that the upper edge of the infra-dry ventricular septal defect has no muscle tissue but pulmonary valve or aortic valve, which lacks annular tissue support, making it difficult to fix the blocking parachute and easily affecting the function of the valve, and can cause right ventricular outflow tract obstruction, so interventional treatment is generally not chosen.
Intra-crestal ventricular septal defects are located within the supraventricular crest and the defect is far from the bundle of Hirschsprung. The short-axis view of the aorta on ultrasound is mostly between 11:30 and 1:30. The intramural septal defect is surrounded by myocardial tissue, and the superior border of the intramural septal defect is closer to or even adjacent to the right coronary valve of the aortic valve. If the defect is within 5 mm and does not combine with aortic valve insufficiency and aortic valve prolapse, trial occlusion can be performed and an eccentric type occluder can be used to ensure that the short side of the left ventricular side of the occluder faces the aortic valve. In most cases, it is difficult to accurately display the defect and estimate the diameter of the defect under X-ray, and the delivery catheter is easily twisted during intervention, which increases the difficulty of interventional treatment of this type of ventricular septal defect. The left anterior oblique to left side position (65° to 90°) imaging is generally chosen during the procedure, and the right anterior oblique position imaging is also desirable, combined with ultrasonography to determine the size of the defect orifice in order to select the appropriate size of the blocking device.
Since the rim of the intracrural defect is all muscle tissue, the blocker is usually easy to fix. The intracrural ventricular septal defect is farther away from the Hirschsprung bundle, and the blocker implantation usually does not cause atrioventricular conduction block.
2.Perimembranous ventricular septal defect
If the upper edge of the ventricular septal defect is more than 2 mm from the aortic valve and tricuspid valve, and the diameter of the defect is less than 10-15 mm, interventional treatment can be tried.
The presence of perimembranous ventricular septal defects is often accompanied by membranous aneurysm formation, which increases the complexity of interventional treatment, but also provides a new and safer option for interventional treatment of certain ventricular septal defects that are closer to the aortic valve.
The key issue in the interventional treatment of membranous ventricular septal defects within 2 mm of the right coronary valve of the aortic valve is to avoid the occurrence of aortic valve insufficiency. In the early days of the Amplatzer blocker for ventricular septal defects, membrane ventricular septal defects within 2 mm of the right coronary valve of the aorta were contraindicated for interventional blocking, namely to avoid postoperative aortic valve insufficiency. The introduction of eccentric blockers has been a boon for these patients with ventricular septal defects.
3. Post-septal ventricular septal defect
The defect is located in the right ventricular inflow tract, in the deepest part of the ventricular septum, below the tricuspid septal valve, with no muscular tissue between the septal valve. It is often oval or triangular in shape, sometimes surrounded by a complete fibrous ring and sometimes partially by muscle tissue. The course of the bundle of Hitchcock is beneath it and should be noted during intervention.
4.Muscular ventricular septal defect
Myocardial ventricular septal defects can be located anywhere in the myocardium of the ventricular septum, including the inflow tract, outflow tract, or right ventricular trabeculae. The incidence of serious complications is low because the myocardial ventricular septal defect is located away from structures such as valves and conduction bundles. Prior to the Amplatzer occluder, there were several reports of successful occlusion of various muscular ventricular septal defects using the Rashkind double-sided umbrella, Sideris button patch device, and Cardioseal device. The edges of the defect are muscular and vary in size with myocardial diastole. Some ventricular septal defects are porous, and the University of Chicago Children’s Medical Center has reported a case of a sieve-shaped myocardial ventricular septal defect that was successfully treated with the use of seven blocking umbrellas. Interventional treatment is not recommended for scattered multiple ventricular septal defects in general.
5. Management of small ventricular septal defects
There are different views on whether to choose surgical treatment for asymptomatic patients over 5 years of age with a defect diameter of less than 0.5 cm. One view is that no treatment is needed because these patients can be asymptomatic for life, and corrective surgery is not absolutely safe. Another view is selective intervention, for some special parts of the septal defect (such as intracrural and perimembranous defects, etc.), it may cause serious consequences such as aortic valve lesions due to long-term blood flow impact; in addition, without surgery, the chance of complicating bacterial endocarditis is 1 times greater than those who have surgery, and the morbidity and mortality rate after endocarditis is high; on the contrary, surgical correction is relatively mature and safe. Considering the possible psychological burden and social factors faced by these patients such as higher education and employment, interventional treatment can also be performed if the patient has treatment intention and the lesion is suitable for interventional treatment.
Fourth, the impact of ventricular septal defect staging on the complications of interventional treatment
1.Bundle branch block and atrioventricular conduction block
In patients with perimembranous ventricular septal defect, the atrioventricular node is located at the apex of Koch’s triangle, and in general the apex of the triangle is always at the inflow side of the defect. The atrioventricular node sends out the bundle of Hirsch’s bundle and then crosses the central fiber body at the base of the aortic valve without coronary valve and sends out bundle branches, which cross and walk on the posterior inferior edge of the defect and turn to the left ventricular side of the defect, and the left bundle branches are rapidly distributed in a waterfall-like manner in the myocardium and trabeculae, and the right bundle branches travel through the top of the defect The right bundle branch penetrates into the myocardium at the top of the defect up to the internal papillary muscle. In inflow tract ventricular septal defects, the top of Koch’s triangle is displaced crosswise toward the heart, and the degree of displacement depends on the degree of septal hypoplasia. The area of vulnerable conduction tissue is where the atrioventricular bundle enters the ventricle from the right atrium, in addition to the bundle branches being encased in the white tissue of the central fibrous body, near the perimembranous septal defect and the inflow tract septal defect. Surgical procedures are highly prone to produce III° AV block, and the incidence of AV block caused by blocker implantation is approximately 2%, similar to the incidence of surgical procedures. In addition to the defect site, mechanical injury to the edge of the ventricular septal defect during surgery, as well as the size of the blocker selected, the contact area between the blocker and the ventricular septal defect, and the tension of the blocker may also have a relationship with the occurrence of AV block. Intraoperative bundle branch block and atrioventricular block are important signs of conduction system damage and should be taken seriously, and the procedure should be terminated or the blocking parachute surgically removed as soon as possible. AV block usually occurs during surgery, and most of them can recover on their own without complete AV block, but a few of them can appear within 7-10 days after surgery and show complete AV block, and complete AV block has been reported in China more than one and a half years after surgery. According to incomplete statistics, since the interventional treatment of ventricular septal defect was carried out in China in 2002, nearly 20 cases of permanent complete atrioventricular block occurred, and most of them received permanent pacemaker implantation.
2. Residual leak
The incidence of residual shunts after closure of ventricular septal defects with the previously applied Rashkind and Cardioseal blockers was high, with an incidence of 30% within 24 hours, which was reduced to 4% in long-term follow-up. The incidence of postoperative residual shunts is lower with the newer nickel-titanium alloy sealer for ventricular septal defects, such as single-port ventricular septal defects, which generally leave no residual leak. The residual leak can occur after surgery for multiport ventricular septal defect, which may be related to the fact that the blocker only partially closes the defect opening.
3.Tricuspid valve insufficiency
The relationship between inflow ventricular septal defect and tricuspid valve is close, such as the blocker implantation clamping the tricuspid valve, affecting the tricuspid valve closure can cause obvious tricuspid regurgitation, in addition to the tricuspid regurgitation caused by the tricuspid tendon or papillary muscle injury caused by the operation of interventional treatment is also increasingly important. The effect of the blocker on the tricuspid valve should be observed before releasing the blocker, especially in large ventricular septal defects, and if tricuspid valve dysfunction and regurgitation occur, blocking therapy should be abandoned. In addition, the interventional procedure should be performed gently, and the pushing and pulling of the orbital guidewire should be performed under the protection of the catheter as much as possible, and the travel of the catheter and guidewire should be kept in mind to avoid possible injury to the tricuspid tendon cords or papillary muscles. When retrieving an open blocking block, it is important to keep the blocking block away from the tendon cord or papillary muscle to avoid possible injury to the tricuspid tendon cord or papillary muscle caused by the relative motion of the blocking block to the head end of the delivery catheter. If necessary, trial occlusion of the ventricular septal defect can be considered during interventional treatment, and tricuspid regurgitation can be observed by bedside echocardiography; if tricuspid regurgitation disappears or is reduced to a permissible level, release of the occluding umbrella can be considered.
4.Aortic valve insufficiency
If the implanted blocker is close to the aortic valve, it may affect the closure of the aortic valve and cause aortic valve insufficiency. In order to avoid the impact of the blocking umbrella on the aortic valve function, the early intervention indication requires the defect to be at least 5 mm away from the aortic valve, and it is recommended to use an asymmetric blocking umbrella. Practice has shown that for perimembranous ventricular septal defects, if the defect is 2 mm from the aortic valve or even completely absent, trial intervention can also be considered. The key is that aortography should be routinely performed to determine the effect of the blocker on valve closure before releasing the blocking umbrella, and any new aortic regurgitation found intraoperatively should not be released. In individual patients with pre-interventional aortic valve prolapse, the left ventricular flap can partially or completely lift the prolapsed valve after blocking umbrella implantation, improving aortic valve prolapse.
5.Vascular injury
The selection of the delivery catheter for interventional therapy is based on the diameter of the blocker, which depends on the diameter of the ventricular septal defect, and a larger diameter blocker is more likely to damage the peripheral vasculature than a smaller diameter blocker. V. Ventricular septal defect staging
The influence of ventricular septal defect staging on the interventional treatment strategy
1. Rational use of echocardiography and radiography to comprehensively evaluate the morphology of ventricular septal defect and its relationship with surrounding structures
Preoperative ultrasound examination can determine the site, number, size, fraction flow of ventricular septal defect and the relationship with aortic valve, atrioventricular valve, tendon cords and other structures. Ultrasound examination can basically determine whether interventional treatment can be performed. Transthoracic two-dimensional ultrasound can directly show defects of 2 mm or more, with a detection rate of more than 95%, and can determine the site and size of the defect. For small defects with suspected echogenic loss, the sensitivity of concurrent pulsed Doppler is 96% and the specificity is 100%. The detection rate of septal defects can be 98% to 100% if color Doppler is also used for 2D ultrasound. Transthoracic ultrasonography must examine the long-axis view of the right ventricular outflow tract, the short-axis view of the aortic root, the parasternal, apical and subxiphoid four-chamber and five-chamber heart views, and the long-axis view of the left ventricle. The size of the ventricular septal defect, the morphology of the defect, and the relationship of the defect to the aortic and tricuspid valves can be clearly demonstrated in these views.
In the interventional management of ventricular septal defects, X-ray and ultrasound have their own different applications. Echocardiography allows the size of the ventricular septal defect and the width of the color Doppler shunt beam to be observed in different angles and views, and its apical five-chamber view is similar to that of conventional x-ray left ventriculography. For membranous ventricular septal defects, radiography can accurately determine the location of the septal defect and its actual size, and is superior to echocardiography. In the case of intracrural ventricular septal defect, due to the high location of the defect, the conventional X-ray angles often cannot clearly show the defect opening, and it is difficult to distinguish it from the subdural ventricular septal defect because it is adjacent to the aortic valve, thus affecting the accurate judgment of the size and type of intracrural ventricular septal defect. In this case, ultrasound can accurately determine the location, morphology, relationship with the right coronary valve of the aorta and its size, as well as the presence or absence of prolapse of the right coronary valve and its degree, and the width and direction of the colored shunt bundle. Ultrasound multi-angle and multi-sectional views of crestal intraventricular septal defects are significantly better than the single angle of X-ray left ventriculography.
In addition to the size of the defect, the distance between the stump of the perimembranous or intracranial ventricular septal defect and the aortic valve or pulmonary valve is very important for the interventional treatment of ventricular septal defects. Ultrasound is significantly better than X-ray left ventriculography in determining the distance between the stump of intracrural ventricular defect and pulmonary valve. The distance between the stump of the defect and the tricuspid valve is also very important for the possibility of interventional treatment, and ultrasound is significantly better than X-ray left ventriculography in determining the distance between the membrane ventricular septal defect, the tricuspid valve leaflets, and the tendon cords because it can clearly show the subtle anatomy and the adjacent relationship in real time.
Intra-cardiac ultrasound can more clearly display the ventricular septal defect and its surrounding structures, and effectively guide the interventional treatment of ventricular septal defect, showing a better application prospect.
2. Timing of interventional treatment: Patients with simple ventricular septal defect should be considered for correction of ventricular septal defect if the following conditions occur: severe hemodynamic disorders (e.g., heart failure, pulmonary hypertension) and growth disorders occur in patients with ventricular septal defect; infective endocarditis, obvious aortic valve prolapse or incomplete closure in patients with ventricular septal defect. Considering the slow progression of most simple ventricular septal defects and the tendency of some patients to close spontaneously, some patients diagnosed with ventricular septal defects (especially solitary myocardial and perimembranous ventricular septal defects with a high chance of spontaneous closure) can be given a chance to close spontaneously with close monitoring of hemodynamic and structural changes in the heart. Larger diameter ventricular septal defects, as well as outflow tract and inflow tract ventricular septal defects, have a lower chance of spontaneous closure. Considering the complications of vascular injury with intervention, it is generally recommended that the age of treatment be defined as 3 years or older for patients who are interested in receiving intervention.
3. Choice of access vessels: The establishment of an arteriovenous track across the ventricular septal defect is a basic prerequisite for interventional treatment of ventricular septal defects. Customarily, the majority of ventricular septal defects near the base of the heart can be treated by means of femoral artery and femoral vein puncture to establish an arteriovenous track, which facilitates surgical operation. However, in the defects close to the apical part of the heart (such as myocardial ventricular septal defects in the eccentric apical part), if the way of establishing the track from the femoral artery and femoral vein is also adopted, it is often difficult to deliver the long sheath to the left ventricle because the bending angle of the track wire in the horizontal alignment of the ventricular septal defect is too large, so the operation way of establishing the arteriovenous track from the internal jugular or subclavian vein and the femoral artery on one side is generally adopted.
4, the choice of blocking umbrella type and specifications: in the inflow channel, outflow channel and perimembranous septum is thin, but the muscle septum is thicker, therefore, for the former, the blocking umbrella with short waist is generally used, while for the muscle septal defect and part of the perimembranous septal defect with membrane tumor, the blocking umbrella with long waist can be used with large spacing between the left and right ventricular septa. In addition, considering the possible impact of the blocking umbrella on the structure and function of the heart around the ventricular septal defect, it is recommended to use an asymmetric blocking umbrella for perimembranous or intracrural ventricular septal defects where the edge of the defect is less than 2-5 mm from the aortic valve or pulmonary valve. For porous ventricular septal defects in close proximity, a special umbrella with a large waist and a thin waist may be considered for simultaneous closure of multiple defects when the umbrella is not expected to affect important structures around the defect. Unlike ventricular septal defect, the aperture of ventricular septal defect is small and the structural support around the defect is more ideal, so the blocking umbrella is generally easier to fix, and the blocking umbrella with 0-2mm larger than the aperture of the defect can be used.
5. Determination of the placement of blocking umbrella: Most of the septal blocking umbrellas can be placed directly at the opening of the defect, so that the left and right ventricular lateral umbrella pieces are opened and the waist rides across the defect. But for the periventricular septal defect with membrane aneurysm, there are different blocking strategies with reference to the imaging data. For patients with small defect aperture, the defect edge is at a certain distance from the aortic valve, and the opening of the membrane aneurysm is larger or more scattered, the blocking umbrella can be considered to be placed directly at the defect site; on the contrary, for patients with larger defect aperture, the defect edge is closer to the aortic valve, and the opening of the membrane aneurysm is single and On the contrary, for patients with a large defect aperture, the edge of the defect is close to the aortic valve, and the opening of the membranous aneurysm is single and small, the blocking umbrella can be considered to be placed directly at the opening of the membranous aneurysm, but attention should be paid to the outflow tract obstruction after the blocking umbrella is in place.
6.Postoperative treatment: If the immediate effect of interventional treatment is satisfactory, the recovery is generally smooth and the echocardiogram can be reviewed 1-2 days after the operation. It is generally recommended that steroids be used routinely for 3-5 days after surgery to prevent or reduce edema and inflammation around the defect, and that patients be hospitalized for a week or so for early identification and management of possible atrioventricular block.