Ventricular septal defect in children

Introduction to ventricular septal defect Ventricular septal defect (VSD) is one of the most common types of congenital heart disease in children. Large VSD causes severe symptoms in infants and even in neonatal period. basic knowledge The proportion of illness: 0.013% Susceptible people: children Mode of infection: non-infectious Complications: subacute infective endocarditis heart failure

Pediatric ventricular septal defect

(1) Causes of the disease

The key period of cardiac embryo development is that in the second to eighth weeks of pregnancy, congenital cardiovascular malformations also occur mainly at this stage. There are many reasons for the occurrence of congenital heart disease, which are roughly divided into internal and external types. Among them, the latter are more common, and the internal factors are mainly related to heredity, especially chromosomal translocations and aberrations, such as 21-trisomy syndrome, 13-trisomy syndrome, 14-trisomy syndrome, 15-trisomy syndrome. And 18-trisomy syndrome, etc., often associated with congenital cardiovascular malformations; in addition, the incidence of cardiovascular malformations in children with congenital heart disease is significantly higher than the expected incidence, the most important external factors are intrauterine infection Especially viral infections such as rubella, mumps, influenza and Coxsackie virus; others such as exposure to large doses of radiation during pregnancy, use of certain drugs, metabolic diseases or chronic diseases, hypoxia, maternal age (close to Menopause), etc., all pose a risk of congenital heart disease.

(two) pathogenesis

1. Defect and diversion

According to the development of the embryo, the pathological types of ventricular septal defect can be divided into three types: membrane defect, funnel defect and muscle defect. Among them, membrane defect is the most common, muscle defect is the least, and membrane defect is divided into simple membrane. Partial defect, infraorbital defect and subvalvular defect; funnel defect is divided into dry type and intraorbital type defect. When there is a defect in the interventricular septum, part of the blood flow passes through the defect from the left ventricle into the right ventricle, resulting in Left to right shunt, the size and direction of the sub-flow depends on the size of the defect and the pressure difference between the two ventricles. The small ventricular septal defect has a small left-to-right flow, and is not prone to pulmonary hypertension. It can be clinically long-term asymptomatic; Larger ventricular septal defect produces a large number of left-to-right shunts, pulmonary vascular resistance is slightly increased, right heart load is increased, and clinical symptoms can be moderate; large ventricular septal defect has a large left-to-right flow, which forms faster Severe pulmonary hypertension, right ventricular pressure rises close to or exceeds left ventricular pressure, bidirectional shunt occurs, and even right to left shunt forms Eisenmenger syndrome.

2. Pathological anatomy

The ventricular septum consists of four parts: the septum interval, the ventricular entrance interval, the trabecular space and the ventricular exit or the funnel interval, and the fibrosis interval is defective due to developmental defects, poor growth or poor fusion. Defects are the most common. This type of defect is called the perimembranous defect because the defect is larger than the membrane and accompanied by peripheral muscle defects. The second type is the muscle septal defect. This type of defect can affect the entrance. Department, trabecular part and apical muscle interval, type 3 is the outlet part of the defect, also known as supra-type, pulmonary valve or funnel septal defect, type 4 defect occurs in the atrioventricular septum called atrioventricular septum Defects or atrioventricular pathways and portal septal defects, Kirklin further classified ventricular septal defects into the following 5 types based on the location of the defect:

(1) Type I: is the defect above the supraorbital sac, the defect is located in the right ventricular outflow tract, above the upper iliac crest and the main, directly below the pulmonary valve, the main, pulmonary fiber is the part of the defect, a few merged master, Pulmonary valve regurgitation, according to domestic analysis, this type accounts for about 15%.

(2) Type II: is the defect under the supraorbital sac, the defect is located in the lower aortic annulus or the posterior lower part of the supraventricular iliac crest. The tricuspid valve leaflet is only close to the defect posterior margin, but can not completely cover the defect. This type is most common. , about 60%.

(3) Type III: the defect after the septum, the defect is located in the right ventricular inflow tract, the deepest part of the interventricular septum, the tricuspid valve leaf cover defect, easy to be ignored during surgery, this type accounts for about 21%.

(4) Type IV: is a muscle defect, mostly a defect between the trabeculae near the apex, sometimes multiple, due to contraction of the ventricular septal myocardial contraction, so that the defect is reduced, so the left to right shunt is smaller, the heart The impact of the function is small, this type is less, only 3%.

(5) V-type: for the complete absence of ventricular septum, also known as single ventricle, the blood flowing into the common ventricle by the mitral and tricuspid valve or the common atrioventricular valve, and then injected into the main pulmonary artery .

The diameter of the ventricular septal defect is more than 0.1 ~ 3.0cm, usually the membrane defect is larger, and the muscle defect is smaller, called Roger disease, such as the diameter of the defect <0.5cm, the left-to-right sub-flow is very small, no clinical symptoms The defect is round or elliptical. The endocardium of the defect edge and the right ventricle facing the defect can be thickened by blood flow impact, which is easy to cause infective endocarditis. The heart enlargement is not significant, and the defect is small to the right ventricle. The increase was dominant, and the left ventricle was significantly more pronounced than the right ventricle.

3. Pathophysiology

Since the left ventricular pressure is higher than the right ventricle, the left-to-right shunt occurs in the ventricular septal defect. According to the size of the ventricular septal defect and the number of shunts, it can be generally divided into four categories:

(1) Light cases: the flow rate from left to right is small, and the pulmonary artery pressure is normal.

(2) The defect is 0.5 to 1.0 cm in size: there is a moderate amount of left-to-right shunt, and the right ventricle and pulmonary artery pressure are increased to some extent.

(3) Defect >1.5cm: The left-to-right sub-flow is large, the pulmonary circulation resistance is increased, and the right ventricle and pulmonary artery pressure are significantly increased.

(4) Huge defect with significant pulmonary hypertension: pulmonary artery pressure is equal to or higher than systemic circulation pressure, bidirectional shunt or right-to-left shunt occurs, causing cyanosis and forming Eisenmenger syndrome.

According to the hemodynamic changes of ventricular septal defect, Keith is divided into:

1 low flow and low resistance;

2 high flow and low resistance;

3 high flow and mild high resistance;

4 high flow and high resistance;

5 low flow and high resistance;

6 high-resistance reverse flow, these classifications have a certain significance for considering surgery and estimating prognosis.

Pediatric septal defect prevention

1. Get rid of bad habits, including pregnant women and their spouses, such as smoking, alcohol and so on.

2. Actively treat diseases affecting fetal development before pregnancy, such as diabetes, lupus erythematosus, anemia, etc.

3. Actively do prenatal checkups to prevent colds. Try to avoid using drugs that have been proven to have teratogenic effects and avoid contact with toxic and harmful substances.

4. For elderly women, family history of congenital heart disease, and serious illness or defects in couples, it should be monitored.

Complications of ventricular septal defect Complications subacute infective endocarditis heart failure

A common complication of ventricular septal defect is subacute infective endocarditis.

Individual cases may be associated with congenital atrioventricular block, brain abscess, and cerebral embolism. Later in the course of the disease, more complicated heart failure. If you choose the right time for surgery, the prognosis is good.

Surgical complications include:

1, residual ventricular septal leakage: more often occurred in the repair of ventricular septal defect, poor exposure during surgery and leakage, and tissue tear. The key is that intraoperative prevention occurs. In the early stage after ventricular septal defect repair, if the patient has unstable circulation and auscultation has obvious murmur, it is necessary to perform bedside echocardiography in time to exclude residual shunt. Once the ultrasound confirms participation in the shunt, it should be repaired as soon as possible.

2, III degree atrioventricular block: Because the heart conduction system (His bundle) to the tricuspid valve and the anterior valve junction to enter the ventricular septum, so after the repair of the perimembranous ventricular septal defect, it is prone to atrioventricular conduction Blocking. For patients with non-sinus rhythm and heart rate slowing after surgery, cardiac pacing leads should be installed, the heart rate should be adjusted by temporary pacing, and drugs that increase heart rate and accelerate atrioventricular conduction should be added. If there is still no improvement after one month of surgery, electrophysiological examination should be performed and a permanent pacemaker should be installed if necessary.

3, aortic regurgitation: due to congenital aortic valve prolapse or intraoperative suture traction of the aortic annulus, even direct trauma or sutured aortic valve leaflet caused by postoperative aortic regurgitation, resulting in the end of surgery Difficulty in cardiac resuscitation, or postoperative cardiac enlargement, wide pulse pressure, diastolic murmur on the left sternal border, and cardiac dysfunction. Therefore, the aortic valve should be detected during surgery to confirm its anatomical relationship and avoid trauma. Once it happens, you should try to repair it as soon as possible. Patients with cardiopulmonary dysfunction and ventricular septal defect complicated with pulmonary hypertension, due to surgical trauma, poor myocardial protection or residual leakage, conduction block, aortic valve insufficiency, etc., postoperative cardiopulmonary insufficiency, manifested as low cardiac output Signs of right heart failure, pulmonary congestion, etc., seriously affect the recovery of patients.

Symptoms of ventricular septal defect Common symptoms Increased sputum pulse rate Rapid stimuli Fatigue Hong systolic murmur systolic tremor dyspnea Difficulties in right ventricular outflow tract

1. Small defect: The child is asymptomatic. Usually, the heart murmur is unexpectedly found during the physical examination. The child has normal growth and development, the complexion is ruddy, the reaction is flexible, the chest wall is not deformed, the left ventricle is normal, and the peripheral vascular pulsation is normal. The main signs are : There is a loud systolic murmur at the lower left edge of the sternum, often accompanied by tremor. Most of the murmurs are full systolic; if the sub-arterial defect, murmur and tremor are limited to the upper left sternal border, for small muscle defects, the murmur is characterized by the sternum. The systolic murmur of the lower left margin is short, and the murmur is narrowed or sealed due to myocardial contraction. The murmur is terminated in the middle of the contraction. The intensity of the heart murmur is not directly related to the size of the ventricular septal defect.

2. Moderate to large defects: Children often have clinical manifestations when the pulmonary circulatory resistance decreases 1 to 2 months after birth. Pulmonary edema is caused by pulmonary circulatory flow, pulmonary venous pressure is increased, lung compliance is decreased, and breast dysfunction is difficult. Easy to fatigue, a lot of sweating, weight loss, and then gradually appear height development delay, shortness of breath, easy to repeat respiratory infections, further exacerbate the formation of heart failure, physical examination: children with ruddy complexion, poor response, pulse rate increased fast and weak normal, However, when there is severe heart failure or a large left-to-right shunt, the pulse is weakened, the child has difficulty breathing, and there is shortness of breath. The intercostal space is invaginated. Because the left ventricle is overcapacity, the anterior ventricular beat is obvious. Seeing obvious anterior bulge and Harrison ditch, palpation, apex pulsation, left ventricular lift, systolic tremor at the lower left edge of the sternum, auscultation 2nd heart sound, if there is pulmonary hypertension The left lower edge of the sternum can be scented with typical full systolic murmurs, such as the sub-arterial defect type. The murmur is usually the most obvious in the second rib space on the left sternal border. When there is a large When diverting from left to right, the third heart sound and the mid-diastolic rumbling noise can be heard at the apex of the heart. In contrast, when the child grows to 6 months to 2 years old, the proportion of heart failure can be reduced.

This may be due to the natural closure of the defect, the valve fiber tissue and the prolapsed valve leaf cover the gap, the right ventricular constriction or the increase of pulmonary circulation resistance reduces the left-to-right shunt, as the pulmonary vascular pressure increases, the flow rate decreases, the heart The pulsation of the anterior region is gradually weakened and only severe pulmonary hypertension appears: the second heart sound hyperthyroidism, single, systolic murmur is short and eventually disappears. If there is pulmonary regurgitation, the diastolic murmur can still be heard on the left sternal border; The flap is relatively closed, and there is severe tricuspid regurgitation. The systolic murmur is available in the lower left sternal border. In the teenage pediatrics, the cyanosis caused by the right-to-left shunt is more common. A few children, Post-natal pulmonary circulation pressure has not decreased, mainly manifested as pulmonary hypertension, and the symptoms of heart failure are not obvious. When the right ventricular conus is progressive hypertrophy, the signs of right ventricular enlargement can be more obvious than the left ventricle, such as right ventricular outflow obstruction. When the second heart sounds weaker, if the stenosis is further aggravated, the left and right ventricular systolic pressure is balanced, and the full systolic murmur is weakened or even disappeared, on the upper left edge of the sternum. And loud systolic jet murmur, aortic valve prolapse can cause aortic regurgitation, due to increased left ventricular end-diastolic volume, flood veins, apical beats and characteristic sternal left sorghum diastolic airflow The murmur, the third edge of the sternum, the loud and rough systolic murmur between the four intercostals, the left ventricular enlargement with X-ray and electrocardiogram examination, combined with the clinical manifestations such as no cyanosis, the first should be suspected of the disease, generally two Peacekeeping color Doppler ultrasound can confirm the diagnosis.

Pediatric ventricular septal defect examination

Under normal circumstances, routine examination is normal, such as pulmonary infection, endocarditis, infection, blood sedimentation, increased erythrocyte sedimentation rate, anemia, blood culture positive.

X-ray

Small room deficiencies in children with X-ray films are often completely normal. There are large defects, large flow, large left ventricular hypercapsule children, chest radiographs appear to enlarge the left eye, left atrial enlargement, lung field congestion; if there is pulmonary hypertension, pulmonary trunk dry, right ventricular hypertrophy, apical upturn. In the case of a double arterial inferior defect, the pulmonary artery trunk is also prominent due to a large amount of rapidly shunting blood flow directly hitting the pulmonary artery. Pulmonary vascular disease is characterized by a thick trunk of the pulmonary artery and its main branch, but the surrounding blood vessels are not thick or even thin. Because the lung circulation resistance is very high, the left-to-right flow is reduced, so the heart shadow can be normal.

2. ECG

The ECG of children with small defects is similar to normal. Left ventricular hypertrophy in children with large defects: II, III, avF, V5, V6 deep Q wave, R wave high, T wave high tip; left atrium large, P wave widened. In the case of inflow ventricular septal defect, the left axis of the electric axis may appear. When there is pulmonary hypertension and right ventricular enlargement, V1 is rsR. When the right ventricular pressure is increased, the right chest lead R wave is high voltage and the T wave is erect. When there is severe right ventricular outflow obstruction or pulmonary vascular disease, the electrocardiogram shows a dominant pattern of the right ventricle.

3. Echocardiography

Two-dimensional ultrasound directly shows the location of the defect. Inflow tract defects can be seen by the apex and the lower ribs of the ribs; moving slightly forward, the defect in the perimembrane can be seen in the plane taken. In these planes, "tumor processes" derived from the tricuspid valve leaflets can also be seen. With the parasternal short axis plane, if there is a perimembranous defect and a "tumor process", it is located at 10 o'clock; the funnel hypertrophy can also be seen at this time. In addition, the sub-arterial defect at 1 o'clock can be seen in the main pulmonary valve joint fibers. If there is aortic valve prolapse, it can be clearly seen through the long and short sides of the sternum. The anterior muscle defect can be detected through the long axis. Multiple holes in the apex can be observed from the apex, the xiphoid, and the short axis to the mitral valve, apex and other adjacent parts. Color flow imaging is more helpful in locating the above defects.

Pulmonary arterial pressure can be estimated by non-invasive Doppler ultrasound using the Bcrnoulli correction formula. The pressure gradient between the ventricles can be extrapolated from the velocity of the blood flow through the defect. The systolic pulmonary artery pressure was calculated by measuring the systolic systemic circulation pressure and the interventricular pressure gradient (assuming no right ventricular outflow tract obstruction). Similarly, the orientation of the left and left ventricles provides sufficient information for the size of the left-to-right shunt.

4. Cardiac catheter

Currently, diagnostic cardiac catheterization is rarely used because echocardiography provides sufficient anatomical and hemodynamic information. However, when there is a moderately sized left-to-right shunt, the size of the ventricular septal defect is still determined by cardiac catheterization to select a specific surgical plan. For children suspected of having pulmonary vascular disease, a cardiac catheterization can be performed to determine the reversibility of pulmonary vascular disease. If the measured superior oxygen saturation is higher than normal, it means that there is a left-to-right shunt at the ventricular level, and the split flow can be calculated by the Fick principle. When the defect is medium to large, the pulmonary artery pressure can be increased. For those patients with excessive pulmonary vascular resistance and inoperability, the degree of pulmonary vascular resistance can be estimated by cardiac catheterization by inhaling 100% oxygen and NO gas. However, it is not clear whether different patients can identify surgical indications through this route. Similarly, although lung biopsy can also understand the extent of pulmonary vascular disease, misdiagnosis can still be caused by improper sampling.

The left heart catheter can measure the number, size, and location of ventricular defects. Periventricular septum and muscle defects located in the middle and apex can be shown by the long axis or the four-cavity, while the sub-arterial defect and anterior chamber septal defect can be visualized by the right anterior oblique diameter. A clear angiographic location is especially important for patients requiring catheter closure. Ascending aortic angiography is used to estimate the extent of associated aortic valve prolapse and aortic regurgitation. Right ventricular angiography can show the degree of stenosis in the funnel of the pulmonary artery.

5.CT and MRI

Simple ventricular septal defects generally do not require CT and MRI. CT and MRI examination to determine the presence or absence of ventricular septal defect by observing whether the continuity of the interventricular septum is interrupted. In order to avoid false positives, the interruption of interventricular septal continuity is usually observed at two different scanning angles as the basis for the diagnosis of ventricular septal defect by MRI. Observing whether the defect is relatively round and blunt is also helpful to avoid false positives. Contrast agents must be injected for CT examination. MRI examination generally uses the spin echo T1W image as the main to observe whether the continuity of the interventricular septum is interrupted. If an abnormal shunt blood flow is found in the gradient echo movie sequence at the same time, it is a reliable basis for the diagnosis of ventricular septal defect, gradient back. The wave movie sequence can also be used to observe the presence or absence of concomitant aortic regurgitation. CT and MRI examinations are still sensitive to the discovery of small defects in the muscle, where the spatial resolution of multi-slice spiral CT is higher. Contrast-enhanced magnetic resonance angiography sequences have little to do with ventricular septal defect diagnosis. In addition to direct signs of interruption of ventricular septal continuity, CT and MRI examinations clearly showed indirect signs of left atrial enlargement, left ventricular enlargement, right ventricular enlargement, and pulmonary artery dilatation.

6. Cardioangiography

Cardiac angiography of ventricular septal defect often begins with long-axis oblique left ventricular angiography. The left-heart contrast catheter of the pig tail was selected. The position of the catheter tip was located at the apex of the left ventricle. The contrast agent was generally 1.5ml/kg, and the amount of contrast agent for the small-sized infant ventricular septal defect could be increased to 1.8-2.0ml/kg. When the long-axis oblique position is projected, the X-ray is tangent to the anterior chamber, which is the best for the most common ventricular septal defect, membrane defect, and trabecular muscle defect. Long-axis oblique left ventricular angiography can also show muscle defects in the inflow tract. However, the left ventricular angiography of the liver lock shows a direct sign of the infarction muscle defect, because the interventricular septum is curved, and the anterior chamber is tangent to the X-ray at a left oblique 60° to 70°, while the posterior compartment is at When the left oblique 40°45° is tangent to the X-ray, the inflowing muscle defect position is backward, so the liver lock is better, and the inflow muscle defect is generally not too small. Left ventricular to right atrial shunt is also best seen with left ventricular angiography of the liver, because the angle of the liver lock is larger toward the head, the right atrium is projected to the head, and there is less overlap with the right ventricle. It can be shown that the contrast agent enters the right atrium first and then enters the right ventricle, which also shows the coexisting membrane compartment septum. Multiple ventricular septal defect is also best seen with long-axis oblique left ventricular angiography, because the most common multiple ventricular septal defect is membrane defect plus muscle defect, and long-axis oblique projection can show these two parts. Defects, separated up and down, can show direct signs of two defects on the same image. The funnel defect cannot show its direct signs in the long-axis oblique left ventriculography. The pulmonary artery develops first and then the right ventricle develops, which is a typical manifestation of the funnel defect in the long-axis oblique left ventriculography. Left ventricular angiography right anterior oblique position 30 ° ~ 45 ° projection. The X-ray and the funnel compartment are tangent to each other, which is the best contrast position of the funnel defect, which can show the direct sign of the funnel defect. On the right anterior oblique left ventricle, the funnel defect is shown by a contrast agent beam ejected from under the aortic valve below the pulmonary valve. According to whether the upper edge of the contrast agent bundle is close to the pulmonary valve when entering the right ventricle, it is judged whether it is a subvalvular defect or a funnel defect. Left anterior oblique left ventricular angiography not only shows direct signs of the funnel defect, but also shows the degree of accompanying aortic valve prolapse and aortic valve prolapse. When the right anterior oblique position is projected, the right aortic valve of the aorta is located in front and the coronary valve is not located in the posterior aspect. During the systole of the ventricle, the contrast agent is ejected from the left ventricle to the right ventricle. The right aortic valve of the aorta is displaced forward and downward, into the ventricular septal defect, and forms a papillary projection. Lighter aortic valve prolapse. The leaflets that are prolapsed during diastole of the ventricle can be substantially restored. Severe aortic valve prolapse, prolapse, variability in the ventricular diastolic valve leaflets, can not be restored.

Cardiac angiography of ventricular septal defect is often performed after ascending aorta angiography after long-axis oblique left ventriculography. The catheter was selected from the left ventricle catheter of the pig tail. The tip of the catheter was located in the ascending aorta. The contrast agent was also used for the purpose of excluding or diagnosing associated aortic regurgitation or patent ductus arteriosus. Lateral projection can not only show the shape of the aortic valve well, but also display the patent ductus arteriosus well, so it is the preferred position for projection. At the time of angiography, the tip of the cardiac catheter should not be placed too low to avoid the illusion of insufficiency of the aortic valve. It is necessary to quickly inject a sufficient amount of contrast agent to ensure that the aortic valve can be clearly displayed. Ventricular septal defect with aortic valve prolapse and regurgitation, ascending aorta angiography showed a downward displacement of the aortic valve, deformation, poor mobility, irregular contours and papillary projections, aortic regurgitation The contrast agent flows downward into the left ventricle and can enter the right ventricle through the ventricular septal defect. According to the extent of left ventricular development and the degree of contrast of the contrast agent, the severity of aortic regurgitation can be determined.

Diagnosis and diagnosis of ventricular septal defect

diagnosis

Diagnosis can be based on the cause, symptoms and related tests.

Differential diagnosis

Ventricular septal defects should be differentiated from the following diseases:

Atrial septal defect

The location and nature of the murmur is different from the ventricular septal defect, as described previously.

2. Pulmonary stenosis

The most loud part of the murmur is in the pulmonary valve area, which is jetted, P2 weakens or disappears, the right ventricle increases, and the pulmonary vasculature becomes thinner.

3. Idiopathic subaortic stenosis

For jet systolic murmurs, Q-waves on the electrocardiogram, echocardiography and other tests can assist in diagnosis.

4. Other

Ventricular septal defect with aortic regurgitation needs to be differentiated from patent ductus arteriosus, primary and pulmonary artery septal defect and aortic sinus aneurysm rupture. The patent ductus arteriosus has a large pulse pressure difference, the aortic node is widened, and there is continuous murmur. The right heart catheterization is located at the pulmonary artery level to help diagnose. The main and pulmonary artery septal defect murmurs were continuous, but the position was low, there was a shunt at the pulmonary artery level, and retrograde aortic angiography could be distinguished. The rupture of aortic sinus aneurysm has a history of sudden onset, and the murmur is mainly in the diastolic phase, which is continuous, and angiography can confirm the diagnosis.

5. Ventricular septal defect combined with malformation

(1) ventricular septal defect combined with aortic regurgitation: the incidence of ventricular septal defect with aortic regurgitation accounted for 4.6% to 8.2% of ventricular septal defect cases. If the high ventricular septal defect is located directly under the aortic valve, the lower part of the valve lacks supporting tissue, and a leaf (posterior or right lobe) of the aortic valve can be pulled down, prolapsed with blood flow, and enters the ventricle. Aortic regurgitation.

(2) ventricular septal defect with patent ductus arteriosus: usually a large ventricular septal defect with patent ductus arteriosus. There is a left-to-right shunt in the ventricle and pulmonary artery levels, with a large flow rate, often accompanied by pulmonary hypertension.

(3) ventricular septal defect with pulmonary stenosis: mostly ventricular septal defect with secondary funnel stenosis, common in children; if the pulmonary stenosis is less severe, it should be differentiated from tetralogy of Fallot.

(4) left ventricular right atrial channel: mostly ventricular septal defect with tricuspid valve lobes, fissure edge connected with the defect, a small number of interventricular septum formation aneurysm rupture to the tricuspid valve, resulting in left ventricle Right atrial traffic. In addition to the characteristics of ventricular septal defect, the clinical manifestations were increased in the right atrium and increased in the right atrium. Cardiovascular angiography can confirm the diagnosis.

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