Arterial catheterization closure
In 1967, Porstmann performed the first successful closure of a patent ductus arteriosus (PDA) without opening the chest. The technique was first applied in China in 1983, and was successfully used by Rashkind et al. in 1977 to close the PDA by delivering an umbrella patch via the venous route; Cambier used a spring steel ring to close the PDA in 1992, and Masura et al. started to use the Amplatzer blocker to treat the PDA in 1997, and the Amplatzer technique was introduced in China in 1998. At present, the Amplatzer method and the controlled spring bolus method are commonly used at home and abroad.
Indications
I. Amplatzer method
(i) PDA with left-to-right shunt without combined cardiac malformation requiring surgery; narrowest diameter of PDA 3 2.0mm; age: usually 36 months, weight 34kg.
(ii) Post-surgical residual shunts;
PDA with a diameter of 314 mm is often combined with more severe pulmonary hypertension, its operation is difficult, the success rate is low, many complications, should be cautious. At present, the domestic PDA blocker or Amplatzer myocardial septal defect blocker can help to block the larger diameter PDA.
In PDA with severe pulmonary hypertension, right heart catheterization should be performed routinely before blocking. If the pulmonary flow/body circulation flow (QP/QS) is >1.3; femoral oxygen saturation is >90%; and occlusion can be considered. If the pulmonary artery pressure decreases (more than 30 mmHg or 20% of the original pressure), the aortic pressure does not decrease and the oxygen saturation of the femoral artery increases, and the patient has no adverse reaction, and the imaging shows no or only a small amount of residual shunt, the blocker can be released. However, care should be taken to avoid stenosis of the descending aortic arch and left pulmonary artery caused by oversized blocker; in addition, the operation should be gentle, and once it is unsuccessful, the blocker should be retrieved smoothly into the sheath to prevent damage to the PDA and the occurrence of pulmonary artery entrapment. If the pulmonary artery pressure increases instead of decreasing after the trial blocking, or the heart rate slows down, the aortic pressure decreases, and the patient feels chest tightness, shortness of breath, chest pain, dizziness or even syncope and other adverse reactions, the blocking device should be retrieved immediately. Then closely observe the condition and deal with it as appropriate.
Although the pulmonary artery pressure is lower than the aortic pressure before blocking, the oxygen saturation of ascending aorta and femoral artery may be lower than normal (which cannot be explained by the right-to-left shunt caused by PDA with severe pulmonary hypertension). Even if the oxygen saturation of the femoral artery does not return to normal after experimental occlusion, permanent occlusion may be performed if the pulmonary artery pressure decreases satisfactorily and the patient has no adverse effects, although close follow-up is indicated.
In both cases, clinical experience is limited and more cases need to be accumulated to further evaluate the long-term effects.
For PDA combined with other interventional cardiovascular malformations, simultaneous or staged interventions can be performed as appropriate.
For PDA combined with other non-interventional but temporarily not suitable or do not need surgery (such as pediatric mild aortic valve lesions or small coronary artery fistula, etc.), PDA occlusion can be performed first, and the combined malformation should be followed up and observed, and surgical management or interventional treatment at a later stage as appropriate.
Controlled spring embolization method
(a) PDA with left-to-right shunt without combined cardiac malformation requiring surgery; narrowest diameter of PDA (single Cook embolus £ 2.0mm; single pfm embolus £ 3mm). Age: usually 36 months, weight 34 kg.
(ii) Post-surgical residual shunt.
Tiny pda with a diameter <1.5 mm have little hemodynamic impact, except for the potential risk of individual infectious endarteritis. Therefore, the need for intervention in this group of patients is currently debated. If the site and shape of the pda are found to be easier to seal with a spring embolus after aortography, intervention is mostly advocated together. For those small pda that cannot be passed by guidewire or catheter, and whose site and shape are not suitable for occlusion or interventional treatment is difficult, they can be followed up and observed. < span="">
The timing of treatment for arterial catheter failure should be determined by its diameter. Small-diameter PDAs have the possibility of natural closure before 1 year of age. Pneumonia and heart failure often occur before the age of 1 year in large PDAs, and surgical treatment is generally chosen. Children older than 1 year of age with PDA diameter ≥ 2 mm can be treated with intervention, and those < 2 mm can be followed up for observation and intervention at a later date.
Sealing of secondary foramen ovale defects
In 1985, Rashikind et al. reported the successful use of a single disc with hook closure to seal secondary foramen ovale defects (ASD). The Amplatzer occluder was introduced in China in 1995, and was used in 1997 to treat secondary foramen ovale ASDs.
Indications (Amplatzer method)
I. Age: usually ≥3 years.
II. diameter ≥ 5 mm, with increased right heart volume load, ≤ 36 mm secondary foramen ovale type left-to-right shunt ASD;
III. Distance from the edge of the defect to the coronary sinus, superior and inferior vena cava and pulmonary veins ≥ 5 mm; to the atrioventricular valve ≥ 7 mm.
The diameter of the interatrial septum > the diameter of the left atrial lateral disc of the selected blocker;
V. No other cardiac malformations that must be combined with surgical procedures.
VI. Post-surgical residual shunt.
For patients with ASD whose diameter is not proportional to the degree of cardiac enlargement or pulmonary hypertension (i.e., the diameter of the defect is not large but the cardiac enlargement is more obvious or the pulmonary hypertension is more severe), other cardiovascular malformations that depend on the presence of ASD (including ASD with unexplained pulmonary hypertension, combined with partial or complete pulmonary venous malformation drainage, etc.) or ASD combined with myocardial or valvular disorders should be excluded. Although these patients are sometimes not technically difficult to treat, ASD occlusion is not recommended.
In patients with short and thin edges of ASD defects and large areas, especially near the inferior vena cava side, the success rate of occlusion is low and the incidence of postoperative blocker dislodgement is high, so intervention is generally not recommended. Some patients with short or even absent defect margins only near the aorta can be treated with intervention, but the blocker margins on the left and right atrial side should be wrapped around the aortic root in a “V” shape. After surgery, close follow-up should be performed to be alert for potential complications in the near to middle and late stages, such as aortic-right atrial fistula, aortic-left atrial fistula and pericardial tamponade due to mechanical abrasion of the blocker edge.
The timing of atrial septal defect treatment should be determined by the size of the defect diameter. Small ASDs (<5 mm in diameter) without clinical symptoms echocardiography and without increased right heart volume load generally do not require interventional therapy, but if the asd is found to be gradually increasing in size and with increased right heart volume load during follow-up, or if cerebral embolism due to lower extremity venous thrombosis occurs, interventional therapy to seal the asd may be considered.< span="">
There was a case of an 85-year-old female patient with an atrial septal defect of 16.7 mm in diameter with pulmonary hypertension and atrial fibrillation for 10 years, who has not yet undergone surgery or intervention and is still being followed up.
Ventricular septal defect occlusion
In 1988, Lock et al. firstly applied the double-sided umbrella to seal the ventricular septal defect (VSD) successfully, and the subsequent clinical use of sealing devices include Rashikind, CardioSEAL, Clamshell and Sideris umbrella, etc., all of which have not been popularized due to narrow indications, high residual shunt rate and many complications. Currently, the Amplatzer blocker is mainly used to close VSDs (including perimembranous and myocardial VSDs).
Indications
I. Age usually ≥3 years;
II. Simple VSD with hemodynamic significance;
Perimembranous VSD diameter >3 mm; myocardial VSD diameter >5 mm;
IV. The upper edge of the VSD is ≥2 mm from the right coronary valve of the aorta;
V. No aortic right coronary valve prolapse and aortic valve closure insufficiency;
Sixth, the choice of the timing of treatment of post-surgical residual ventricular septal defect should also be determined by the diameter of the defect; children with a defect diameter < 5mm generally do not have active surgery, and can be followed up and observed, and some of them can be closed naturally. children with large diameter VSD between 6 months and 1 year need surgery; children with huge VSD of 6 months should have surgery for a limited period of time.
Small VSDs (<3mm in diameter) have very little left-to-right shunt flow and generally do not cause increased left heart volume load and pulmonary hypertension, and most clinical patients are asymptomatic and can be followed up regularly. In addition, the time of natural closure of VSD is usually between 2 and 5 years of age, and even if there is no natural closure, if the diameter of the defect does not change, the patient can continue to be followed up until adulthood. In a 45-year-old patient with VSD (4 mm in diameter), there were no symptoms except for a heart murmur on auscultation, and the echocardiogram, electrocardiogram, and chest X-ray were normal. The other patient with a 56-year-old VSD (5 mm in diameter) had only a mildly enlarged left ventricle on echocardiography and no clinical symptoms. Gabriel et al. reported 229 cases of small VSD with a maximum follow-up of 30 years, with a natural closure rate of 6% (14/229) and no cases of pulmonary hypertension or death; the incidence of infective endocarditis was 1.8%, and only one case of echocardiographic enlargement of the left ventricle.
On the other hand, patients with small VSDs with increased or no change in diameter during follow-up, or their relatives, urgently requested interventions to avoid infective endocarditis, surgical pain, scars, and psychological barriers caused by heart murmurs, in view of future schooling, employment, and insurance coverage. Interventional physicians need to comprehensively synthesize clinical and imaging data, estimate the success rate of interventional treatment and the benefits and possible complications after the procedure, weigh the advantages and disadvantages, and obtain the consent of the patient and his relatives for the interventional treatment.
For VSD with preoperative arrhythmias, especially those with complete right bundle branch block and left anterior branch block or complete left bundle branch block, the advantages and disadvantages of postoperative blockade should be weighed to prevent serious complications such as cardiac arrest.
In a few cases of VSD, the feasibility and necessity of intervention can be determined only after completion of left ventricular and ascending aortic angiography. Sometimes, angiography can more accurately observe the location of VSD, the distance from the right coronary valve of the aorta, the diameter and number of defects on the left and right ventricular surfaces of VSD, and the presence of combined membranous aneurysms, aortic valve prolapse and regurgitation.
For VSDs with two defects on the left ventricular surface that are close to each other, if the Amplatzer asymmetric VSD blocker is used, the defect on the aortic valve side is blocked as close as possible, and some scholars block the defect far from the aortic valve side by rotating the long disk of the left ventricular surface originally pointing to the apical part clockwise to the aortic valve side, but the operation technique is demanding, and improper operation is prone to the risk of blocker dislodgement or The risk of aortic regurgitation or dislodgment of the blocker is high; a domestic symmetric VSD blocker can also be used to block the defect away from the aortic valve side. In the case of perimembranous VSD with two defects on the left ventricular surface that are far apart, it is often difficult to completely close both defects with one blocker, leaving a residual shunt; and the use of two blockers may cause aortic regurgitation and significantly increase the cost, which is generally not suitable for interventional treatment.
For VSD with combined membranous aneurysms and multiple “breaches” on the right ventricular surface, intervention should be performed through the large “breaches” and seal the defect on the left ventricular surface as much as possible to achieve complete closure.
For VSD with mild tricuspid regurgitation, the blocker can be released if there is no increase in tricuspid regurgitation flow after blocking.
For VSD combined with mild aortic valve prolapse without aortic regurgitation, VSD occlusion can be performed on a trial basis. If the sharp edge of the blocker does not contact the prolapsed aortic valve after blocking and there is no aortic regurgitation or residual shunt, the blocker can be released. Strict postoperative follow-up should be performed.
Percutaneous pulmonary balloon valvuloplasty
Percutaneous balloon pulmonary valvuloplasty (PBPV) was first reported by Kan et al. in 1982 for the treatment of simple pulmonary stenosis (PS), and since 1986, this technique has been performed in China and is now the preferred method for the treatment of simple PS.
Indications
I. Clear indications
(a) The best age is 2-4 years, but the rest of the age can be performed;
(b) Typical simple pulmonary stenosis;
(C) right heart catheterization collapse pulmonary valve systolic pressure difference ≥ 50 mmHg.
II. Relative indications
(a) Typical pulmonary stenosis with a systolic pressure difference across the pulmonary valve <50mmHg, ≥35mmHg by cardiac catheterization.
(B) Severe neonatal pulmonary stenosis.
(C) Severe pulmonary stenosis with right-to-left shunt at the atrial level.
(iv) Mild or severe dysplastic pulmonary valve stenosis.
(v) Typical pulmonary stenosis with other preexisting heart disease that can be treated with simultaneous intervention.
Pulmonary stenosis can be combined with varying degrees of secondary hypertrophic right ventricular outflow tract stenosis, mainly manifested as right ventricular outflow tract stenosis in ventricular systole on right ventriculography, but not in ventricular diastole, i.e., not fixed stenosis, for which pulmonary balloon valvuloplasty can be performed. After dilatation, the right ventricular outflow tract stenosis is gradually relieved as the resistance of the pulmonary valve orifice decreases.
Whether balloon valvuloplasty should be performed in children with mild pulmonary stenosis is controversial, but a group of 32 children with mild pulmonary stenosis underwent balloon valvuloplasty in China and obtained satisfactory clinical results. Several foreign scholars have shown that some patients with pulmonary valve stenosis progress during childhood, especially in infancy, which is mainly related to the incompatibility between the development of the pulmonary valve annulus and the rapid growth of pulmonary blood flow during the rapid growth of children. Therefore, timely pulmonary balloon valvuloplasty is beneficial to the growth and prognosis of the child.