Foramen ovale insufficiency

Introduction In the human fetal period, a small hole in the left and right atrial septum, that is, the blood in the left and right atrium of the fetal period is connected. Later, after the lung cycle was completed, the hole was closed. This is a trace of the legacy of human history. Congenital heart disease such as tricuspid atresia, tricuspid valvular deformity can occur in the foramen ovale regurgitation. The hemodynamic changes of the tricuspid valvular movement are determined by the severity of tricuspid regurgitation, whether there is an atrial septal defect and the size of the defect and the extent to which right ventricular function is affected. Different degrees of tricuspid regurgitation due to enlargement of the atrioventricular and right ventricles and deformation of the leaflets are common. When the right atrium contracts, the right ventricle relaxes, and the part of the ventricular chamber also dilates, causing the right atrial blood to fail to enter the right ventricle. When the right atrium is diastolic, the right ventricle contracts, and the right ventricle of the room is also contracted. The right atrium receives blood from the vena cava, the atrialized right ventricle, and the tricuspid regurgitation, resulting in increased right atrial blood volume and enlarged lumen. The right atrial pressure rises and finally leads to heart failure. There were cases of patent foramen ovale or atrial septal defect. When the right atrial pressure was higher than that of the left atrium, a right-to-left shunt was generated. The blood oxygen content of the systemic circulation decreased with purpura and clubbing (toe). When the room is intact and the right ventricle contracts, the amount of blood exchanged into the lungs is reduced, and the difference in arteriovenous blood oxygen is small, which can cause flushing of the cheeks and mild purpura at the fingertips.

Cause

(1) Causes of the disease

It is generally believed that in the normal development of the embryo, the endocardial pad is fused, and the atrioventricular tube is equally divided into two left and right nozzles and participates in the formation of the membrane ventricular septum and the closed atrial septum. The tricuspid valve is differentiated from the endocardial pad and the right ventricular myocardium. In this process, the tricuspid dysplasia is abnormal, the leaflet is degenerated, degenerated, the leaflet tissue is lacking, the valve hole is surrounded by fibrous tissue, and the valve is finally closed. The valve is locked. (It is generally considered that the fusion site of the endocardial pad is biased to the right side before and after the embryonic period, and the right ventricular septum is displaced to cause uneven separation of the atrioventricular septum. The right atrioventricular canal occlusion will form a tricuspid atresia in the future.)

(two) pathogenesis

1. Pathological changes: About 90% of cases of tricuspid atresia, the tricuspid valve fuses into a decidual membrane, and the pulmonary trunk is poorly developed. Occlusion can also involve the right ventricular outflow tract and the total trunk of the pulmonary artery, while the pulmonary valve is severely stunted. The right ventricle can range from severe stunting to normal size and even expansion. Tricuspid valves have varying degrees of insufficiency.

In the autopsy of the tricuspid atresia, the left ventricle tends to enlarge and hypertrophy, but the mitral valve is normal or enlarged. There have also been reports of mitral valve mitral malformation, mitral valve mitral and mitral valve straddle of the hypoplasia of the right ventricle. Tricuspid atresia usually includes the following malformations:

1 tricuspid occlusion, no right atrium between the right ventricle;

2 atrial septal defect or patent foramen ovale;

3 ventricular septal defect or patent ductus arteriosus.

Tricuspid atresia is congenital closure, there is no valve hole, only a small depression is seen at the bottom of the right atrium, surrounded by muscle fibers, a few fibrous or membranous structures. 80% of the traffic in the heart chamber is a patent foramen ovale, which may also be atrial septal defect, or even a single atrium.

There are five types of right atrium and right ventricle connections for tricuspid atresia:

1 muscle type accounts for 76% ~ 84%, the muscle at the bottom of the right atrium, a small dimple near the side wall, directly across the left ventricle and no connection with the right ventricle;

2 diaphragm type accounts for about 8% to 12%, a closed diaphragm between the right atrium and the right ventricle;

3 valve type accounts for about 6%, there is an open valve at the junction of the right atrium and the right ventricle, but there are diaphragms and muscles underneath that completely separate the right atrium from the right ventricle to form a lock;

4Ebstein malformation accounted for about 6%, forming a locked tricuspid valve between the right atrium and the right ventricle;

5 endocardial pad defect type accounted for about 2%, the common atrioventricular valve atresia from right atrium to right ventricle.

Edward and Burchell first classified the tricuspid atresia into three types based on the relationship between the aorta. Secondly, according to the presence or absence of pulmonary atresia or stenosis, it is further divided into 8 types: Ia type, Ib type, Ic type, IIa type, IIb type, IIc type, IIIa type and IIIb type. Among the cases of tricuspid atresia, type Ib, Ic, IIb, IIc, and IIIa are most common.

Type I tricuspid atresia (69%): This type is characterized by normal vascular relationships. Type Ia, pulmonary atresia; type Ib, pulmonary stenosis with small ventricular septal defect; type Ic, pulmonary stenosis with large ventricular septal defect.

Type II tricuspid atresia (27%): This type is characterized by complete type of large vessel translocation. Type IIa, pulmonary atresia; type IIb, pulmonary stenosis with small ventricular septal defect; type IIc, normal pulmonary artery with large ventricular septal defect.

Type III tricuspid atresia (4%): Type III is characterized by corrective large vessel translocation. Type IIIa, pulmonary stenosis; type IIIb, subaortic stenosis. Patients with pulmonary atresia (ie, type Ia, IIa) die in infancy. Those with pulmonary stenosis (types Ib, IIb, and IIIa) accounted for 70% of childhood cases and 100% of adult cases.

Tricuspid atresia may combine multiple heart and large vessel malformations. The traffic in the heart room always exists, in which the patent foramen ovale accounts for 80%, and the rest is atrial septal defect. Twenty-two percent of patients had a left superior vena cava that was usually drained to the coronary sinus and occasionally drained directly to the left atrium. Pulmonary venous drainage and coronary artery malformation are less common. Patients with congenital pulmonary artery dysplasia often have membranous tricuspid atresia. 20% of patients with tricuspid atresia combined with juxtaposition of the auricle. It is also possible to have aortic coarctation, dysplasia or atresia, aortic arch disconnection, and aortic valve atresia.

2. Pathophysiology: patients with tricuspid atresia, systemic venous return blood can not directly into the right ventricle, the right atrium blood can only reach the left atrium through the heart room traffic, the left atrium becomes a mixed heart cavity of the body and pulmonary circulation venous blood . The mixed blood enters the left ventricle through a relatively normal mitral valve orifice and then exits the left ventricle through the normally connected aortic valve orifice and aorta. Therefore, all patients have varying degrees of arterial oxygen saturation reduction, the degree of reduction depends on the severity of pulmonary blood flow obstruction. If the blood flow in the lungs is normal or increased, and the blood flow to the pulmonary veins is normal or increased, the arterial oxygen saturation is only slightly lower than normal, and there is no clinical or mild bun in the clinic. If the blood flow in the lungs is reduced and the blood flow to the pulmonary veins is reduced, the arterial oxygen saturation is significantly reduced, 70% of hypoxemia occurs, and clinical manifestations are obvious. If the atrial septal defect is small, the right to left shunt is limited, and severe autovenous hypertension and right heart failure occur after birth.

Due to dysplasia of the right ventricle, the left ventricle alone bears the pumping work of the body and the pulmonary circulation. The left ventricle needs extra work to promote blood flow in a large number of pulmonary circulation, and continuous overload operation can lead to left heart hypertrophy and left heart failure. In cases of reduced pulmonary blood flow, the left ventricle only adds a small amount of volumetric load and often does not produce heart failure. However, in cases of increased pulmonary blood flow, the left ventricle is often increased due to chronic volume load, left ventricular end-diastolic volume and myocardial contractile function, and then left ventricular enlargement, heart failure. If there is aortic coarctation or aortic disconnection, it promotes the development of left ventricular hypertrophy and heart failure.

The development of the right ventricle of the heart varies with the size of the ventricular septal defect and the degree of pulmonary stenosis. There are usually pulmonary stenosis and small ventricular septal defect. A small part of blood enters the dysplastic right ventricle from the left ventricle through the ventricular septal defect, and then enters the lung through the narrow pulmonary artery, reducing pulmonary blood flow. A small number of patients have only mild or no pulmonary stenosis, accompanied by large ventricular septal defect, and more blood enters the well-developed right ventricle and pulmonary artery from the left ventricle, increasing blood flow to the lungs. A rare condition is no ventricular septal defect, pulmonary valve atresia, and the only passage of blood to the lungs is the patent ductus or bronchial artery that is not closed.

an examination

Related inspection

Cardiovascular angiography M-mode echocardiography (ME) Dynamic electrocardiogram (Holter monitoring) Electrocardiogram ultrasound diagnosis of cardiovascular disease

(A) Symptoms : A small number of patients can present with difficulty breathing, purpura and congestive heart failure within 1 week of birth. However, most patients gradually develop fatigue, palpitations, cyanosis and heart failure after they have entered their childhood. Patients in all age groups can present supraventricular tachycardia, and some patients have pre-excitation syndrome.

(B) Signs : Most patients have poor growth and development, and their body size is small. About 1/3 of patients have cheek flushes similar to the mitral valve face, often with varying degrees of purpura. In the case of enlarged heart, the left front chest is raised, the heart sounds are enlarged, and the left sternal border can swell to the systolic tremor caused by tricuspid regurgitation. The apex of the apical area and the apical area are normal or weak. Due to the enlarged height of the right atrium and the right ventricle, the jugular vein beat is not obvious. Cardiac auscultation, light heart sound, systolic murmur caused by tricuspid regurgitation can be heard on the left sternal border, and diastolic murmur caused by tricuspid stenosis can sometimes be heard. As the enlarged anterior tricuspid lobes are delayed in closure, the first tone splits and the delayed appearance increases. The second heart sound is also often split and the pulmonary valve closing sound is lighter, and some cases can be galloped. Abdominal examination may cause swollen liver but rarely liver pulsation. Childhood patients with severe purpura may have clubbing (toes).

(3) Auxiliary inspection

(1) X-ray examination performance: in typical cases, the right atrium is enlarged and the right ventricular outflow tract is moved to the outside, the upper mediastinum is narrowed, and the pulmonary vascular texture is normal or reduced. In a few cases, the heart shadow can be free of abnormal signs.

(2) ECG examination: typical manifestations of right atrial hypertrophy, P wave high tip, incomplete or complete right bundle branch block. The right axis of the electric axis is biased, the R-wave voltage of the chest lead is lowered, the PR interval is prolonged, and there is often a supraventricular rhythm disorder. About 5% of the patients show type B pre-excitation syndrome.

(3) Segmental echocardiography and Doppler examination: the anterior leaflet of the tricuspid valve is enlarged and the range of motion is large. The leaflets and posterior leaflets are obviously moved down, dysplasia, and poor mobility. The tricuspid valve is closed, the valve position is shifted to the left, and the interventricular septum is abnormal. The right atrium and the right atrium of the room show a large right atrium cavity, and the functional right ventricular cavity is shortened. Doppler examination can show atrial horizontal right to left shunt and tricuspid regurgitation.

(4) Right heart catheter and selective angiography: the right atrium cavity is huge, the pressure is increased, and the pressure curve a wave and V wave are both high. The right ventricle of the room is atrial pressure curve, the intracardiac electrocardiogram is right ventricular type, and the atrial septal defect can enter the left atrium from the right atrium. Atrial level can present right to left shunt, right ventricular systolic pressure increases normal diastolic pressure, and in some cases tricuspid valve transvalvular pressure difference can be measured. Right heart angiography showed that the right atrium was significantly enlarged to occupy the left ventricle position, and the right ventricle was located in the right ventricular outflow tract. The valve port is moved to the left edge of the spine, and the lower edge of the right ventricle shows a tricuspid annulus and another notch between the ventricular and functional ventricles. The total trunk and branches of the pulmonary artery are small, and the left atrium is developed in advance with a right to left shunt at the atrial level.

The pathological changes of Ebstein malformation are quite different. The basic lesions are tricuspid valve leaflet and right ventricular dysplasia with the valvular and posterior lobes moving down to the right ventricle, attached to the tricuspid annulus by the chordae papillary muscle. Below the right ventricular wall. The tricuspid valve leaflets enlarge or shrink, and the thickening deformation is often shortened. The lesions most often involve the lobes, followed by the posterior leaflets, and the lobes and posterior lobes may be partially absent. Lesions involving the anterior leaflet are rare. The anterior leaflet originates from the normal tricuspid annulus, which can be enlarged, such as a sail, and sometimes has many small holes that are attached to the ventricular wall by shortening and underdeveloped chordae and papillary muscles. The downwardly moving leaflet divides the right ventricle into two parts. The enlarged ventricle above the leaflet is called the ventricular ventricle, and its function is similar to that of the right atrium; the lower part of the leaflet is the functional right ventricle. The right atrium is enlarged and the fibrosis of the wall is thickened. The right atrium and the highly enlarged thin-walled right ventricle connect into a large heart chamber, which acts to store blood, while the functional right ventricle below the leaflets functions to discharge blood. Cases of tricuspid valvular dislocation often show a dysfunction due to the enlargement of the tricuspid annulus and the right ventricle and the abnormality of the leaflet. If the free edge of the leaflet is partially adhered, the enlarged anterior leaflet may cause different degrees of tricuspid stenosis due to blood flow obstruction between the atrial ventricle and the functional right ventricle. The anatomy of the atrioventricular node and the atrioventricular bundle is normal, but the right bundle branch may be thickened by endocardial compression to produce a right bundle branch block. In about 5% of cases, the abnormal Kent conduction bundle presents a pre-excitation syndrome. About 50-60% of patients with tricuspid valvular disease have a patent foramen ovale or atrial septal defect. The atrial level shows a right-to-left shunt, arterial oxygen saturation decreases, and purpura appears clinically. Other malformations include pulmonary stenosis, ventricular septal defect, patent ductus arteriosus, tetralogy of Fallot, aortic dislocation, aortic coarctation, and congenital mitral stenosis.

Differential diagnosis

Diagnosis of incomplete ovate hole closure:

Fossa ovalis: The foramen ovale is a life channel necessary for fetal development. The umbilical vein blood from the mother enters the left heart chamber of the fetus through this channel and is then distributed throughout the body to provide fetal development. Oxygen and nutrients. When the child is born, with the first cry, the left atrial pressure rises, the oval fossa is pressed against the edge of the fossa ovalis to form a functional closure, and the anatomical complete closure is generally 5-7 months after birth. . Therefore, it is possible to remain open within one year of age, there may be a small amount of shunt, and even 5% to 10% of the human foramen ovale remain open and not closed for a lifetime, but has no effect on the hemodynamics of the heart. Therefore, the patent foramen ovale in infancy is a normal physiological phenomenon, not a congenital heart disease, and generally does not require surgery. However, if the central defect of the interatrial septum is larger than 8-10 mm and the flow rate is large, it is called a central atrial septal defect and requires surgical repair. The timing of surgery should be completed when the child is 2 to 4 years old.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.