Is atrial defect hereditary?

People will encounter different problems during the process of development. They start to grow from an embryo. At the beginning, it is just a fertilized egg. Finally, the organs are slowly distinguished, four brains are split, and so on. During the embryonic development period, the lungs can breathe autonomously, so it is possible to cause atrial defects, which require examination to know.

Pathogenesis

During the fetal period, the lungs do not need to perform respiratory functions and are in a atelectasis state. The pulmonary circulation resistance is high and the blood flow is very small, so the blood returning to the right atrium must be able to pass through the atrial septum and enter the left atrium to adapt to the special circulatory physiological requirements of the fetal period. For this reason, the atrial septum always has an interatrial foramen during its growth and development, and the interatrial foramen begins to close after birth. Around the end of the first month of the embryonic period, the first septum grows from the midline on the upper back of the primitive atrial wall. At the same time, endocardial cushions also grow inward from the dorsal and ventral sides of the atrioventricular junction. During development, the two endocardial cushions grow larger and fuse together. It is connected to the atrial septum above and grows into the membranous part of the ventricular septum below, which is connected to the muscular part of the ventricular septum. The endocardial cushion tissue on both sides of the atrioventricular septum grows to form the atrioventricular valve tissue, the right side is the septal leaflet of the tricuspid valve, and the left side is the large leaflet of the mitral valve.

No. 1

It grows in a horseshoe shape toward the endocardial cushion. Its front and rear parts are connected to the corresponding endocardial cushions respectively, while a crescent-shaped interatrial foramen remains in the central part of the horseshoe, called the first foramen, through which the blood from the right atrium flows into the left atrium.

Hole 2

When the central part of the first septum is connected to the endocardial cushion and the first hole is about to close, the upper tissue of the first septum is absorbed by itself to form another interatrial hole, called the second hole, to maintain the blood flow channel between the atria on both sides.

No. 2

Then, another septum tissue grows from the atrial wall on the right side of the first septum, which is called the second septum. The second septum is also horseshoe-shaped. Its anterior and inferior end fuses with the ventral endocardial cushion and is divided into two parts. One part grows posteriorly along the bottom of the first septum tissue and connects with the posterior and inferior end of the second septum, forming the lower edge of the foramen ovale. The other part grows between the coronary sinus and the inferior vena cava and participates in the formation of the inferior vena cava valve.

The oval notch in the middle of the second septum is called the foramen ovale. The left side of the foramen ovale is lined by the first septum tissue (oval valve), and the shallow pit formed by this is called the oval fossa. By the 8th embryonic week, the development of the atrial septum is complete. The first and second septum tissues are fused together, and only in the upper part of the oval fossa and the oval valve, blood flow channels are still left on both sides of the atrium. However, since the oval valve acts as a valve, blood can only flow from the right atrium into the left atrium through the oval fossa and the second orifice.

Complete fusion of the foramen ovale and the oval valve occurs after birth. However, according to pathological anatomy data, the foramen ovale persists in about 20% to 30% of people at birth. Because the fetus needs to rely on its own lungs to breathe after birth, the lung tissue expands, pulmonary vascular resistance decreases, pulmonary circulation blood flow increases, left atrial pressure increases and is greater than that of the right atrium, causing the oval valve to tightly cover the oval fossa. Therefore, even though the foramen ovale remains open anatomically, under normal physiological conditions no blood shunting between the atria occurs. However, if there is a pathological condition such as pulmonary artery stenosis or right ventricular outflow tract obstruction, the right atrial pressure will increase, and right-to-left shunt can occur, and the blood from the right atrium enters the left atrium through the patent foramen ovale.

From the growth and development process of the atrial septum, we can see that the second hole type atrial septal defect is caused by the incomplete development of the second septum or oval valve. Type 1 atrial septal defect is caused by incomplete development of the endocardial cushions and failure to completely fuse with the first septum. The formation of atrioventricular common channel is due to the severe hypoplasia of the endocardial cushions. Therefore, in addition to the failure of the first foramen to close, there are also rifts in the septal leaflets of the mitral valve and tricuspid valve. In severe cases, there is also a defect in the membranous part of the ventricular septum. A single-chamber atrium is caused by the lack of development or absence of atrial septal tissue.