Echocardiographic image of a moderate ventricular septal defect in the mid-muscular part of the septum. The size and location is typical for a VSD in a new-born child.  The trace in the lower left shows the flow during one complete cardiac cycle and the red mark the time in the cardiac cycle that the image was captured. Colours are used to represent the velocity of the blood.  Flow is from the left ventricle (right on image) to the right ventricle (left on image).A nitinol device for closing muscular VSDs, 4 mm diameter in the centre. It is shown mounted on the catheter into which it will be withrawn during insertion.
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Ventricular septal defect

A ventricular septal defect (or VSD) is a defect in the ventricular septum (the wall dividing the left and right ventricles of the heart). more...

VACTERL association
Van der Woude syndrome
Van Goethem syndrome
Varicella Zoster
Variegate porphyria
Vasovagal syncope
VATER association
Velocardiofacial syndrome
Ventricular septal defect
Viral hemorrhagic fever
Vitamin B12 Deficiency
VLCAD deficiency
Von Gierke disease
Von Hippel-Lindau disease
Von Recklinghausen disease
Von Willebrand disease

The ventricular septum consists of a muscular (inferior) and membranous portion (superior). The membranous portion (which is close to the atrioventricular node) is most commonly affected.

Congential VSDs are collectively the most common congenital heart defect.


VSDs can be detected by cardiac auscultation, as they typically cause systolic murmurs. Confirmation of findings from cardiac auscultation can be obtained with a cardiac ultrasound (echocardiography) (less invasive) and cardiac catheterization (more invasive).

Auscultation is generally considered sufficient for ruling-out a significant VSD, if done by a pediatric cardiologist. This holds true as long as the pressures on the right side of the heart is low.


Large VSDs result in a significant left-to-right shunt and increase load on the right ventricle. If untreated, they result in hypertrophy of the right ventricle, which ultimately leads to right heart failure and death.


Treatment is either surgical (open or percutaneous endovascular) or conservative. Smaller congenital VSDs often close on their own (as the heart grows) and are thus treated conservatively. Open surgical procedures require a heart-lung machine and are done with a median sternotomy. Percutaneous endovascular procedures are less invasive and can be done on a beating heart, but are only suitable for certain patients. Repair of most VSDs is complicated by the fact that the conducting system of the heart is in the immediate vicinity.


VSDs are the most common congenital cardiac anomaly. It is found in 30% of all newborns with a congenital heart defect, or about 2-3 per 1000 births.

Congential VSDs are frequently associated with other congential conditions, such as Down syndrome.

A VSD can form a few days after a myocardial infarction (heart attack) due to mechanical tearing of the septal wall, before scar tissue forms, when macrophages start remodeling the dead (heart) tissue.


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Detection of aortopulmonary window with ventricular septal defect by Doppler color flow imaging - Selected Reports
From CHEST, 1/1/92 by Hiroyuki Horimi

Aortopulmonary window is a rare cardiac anomaly that results from incomplete division of the aortopulmonary septum between the ascending aorta and the main pulmonary artery. Noninvasive diagnosis of this lesion is sometimes difficult because of associated cardiac anomalies.

Although the two-dimensional echocardiographic features of aortopulmonary window are well-established,[1-3] Doppler color flow imaging of this anomaly has not been reported sufficiently.[4,5] We report the case of an infant who had an aortopulmonary window associated with a ventricular septal defect, in whom Doppler color flow imaging demonstrated blood flow through an echo dropout between the ascending aorta and the main pulmonary trunk.

Case Report

A two-year-old girl was admitted to the hospital for evaluation of a cardiac murmur. She was born at full term, and a systolic murmur was discovered when she was one month old. Digoxin and diuretics were then administered because of congestive heart failure.

At the age of two years, she was admitted to the hospital because of respiratory infection and congestive heart failure. Physical examination revealed a grade 3/6 pansystolic murmur along the left sternal border and a grade 2/6 diastolic murmur at the cardiac apex. Her liver was enlarged. At this time, the patient was referred to our hospital because of continuing congestive heart failure.

The chest roentgenogram showed cardiomegaly, with a cardiothoracic ratio of 0.58 and increased pulmonary vascularity. The electrocardiogram showed left axis deviation of the mean QRS axis as well as biatrial and biventricular hypertropy. Two-dimensional and Doppler echocardiography (A Toshiba model SSH-65A system with a 3.75 MHz transducer; Toshiba, Tokyo, Japan) showed a large ventricular septal defect, a dilated ascending aorta, and a dilated main pulmonary trunk with normally positioned bilateral pulmonary arteries.

Suprasternal, long-axis scanning of the aortic arch demonstrated a large communication (12mm) between the aortic arch and the main pulmonary trunk (Fig 1, top). Color flow imaging revealed a flow signal crossing the communication from the aorta to the pulmonary trunk during systole (Fig 1, bottom). High parasternal, short-axis scanning above the aortic and pulmonary valves confirmed the diagnosis. Diastolic flow reversal was observed proximal to the aortic isthmus by pulsed Doppler echocardiography, which indicated that the aortic runoff was located proximal to where the ductus arteriosus opened (Fig2).

Cardiac catheterization was performed to obtain hemodynamic information. There was a marked elevation of pulmonary arterial pressure (104/56 mm Hg; mean 77 mm Hg), with a large pulmonary flor (Qp/Qs=2.98) and an elevated pulmonary resistance ration (Rp/Rs=0.5). Right heart catheterization revealed left-to-right shunting at the ventricular and arterial levels. Aortography opacified the ascending aorta, the main pulmonary trunk, and the pulmonary arteries simultaneously, confirming the diagnosis of aortopulmonary window and ventricular septal defect.

Operation was undertaken with cardiopulmonary bypass, supplemented by circulatory arrest. The aorticopulmonary septal defect (10 x 12 mm) was closed with a prosthetic patch by the transpulmonary approach. The ventricular septal defect (20 x 10 mm) was closed with the same material via the transatrial approach. Postoperative pulmonary arterial pressure was 47/17 mm Hg (mean, 27 mm Hg) and the postoperative course was uneventful.


The present patient had an aortopulmonary window with a ventricular septal defect and the diagnosis was confirmed by echocardiography: Accurate diagnosis of aortopulmonary window is extremely difficult on clinical grounds when it coexists with a ventricular septal defect. The heart murmur of this anomaly is often mistaken for the murmur of a high ventricular septal defect, because although a continuous murmur may be present in patients with aortopulmonary window, more often there is only a systolic murmur that is generally heard along the upper left sternal border. In this case, there was no continuous murmur because there was little left-to-right diastolic flow through the aortopulmonary window, due both to the elevated pulmonay arterial diastolic pressure and to the large size of the communication.

The other cardiac anomaly that can mimic the findings in this case is a large ventricular septal defect associated with patent ductus arteriosus. Aortopulmonary window can be distinguished from patent ductus arteriosus by the detection of diastolic flow reversal proximal to the aortic isthmus using pulsed Doppler echocardiography.[6]

In recent years, two-dimensional echocardiography has been found to be extremely helpful in the noninvasive diagnosis of various conotruncal anomalies. In many normal individuals (especially infants), the contiguous proximal aortic and pulmonary arterial walls are thin and many appear as a false dropout on two-dimensional echocardiography. Therefore, this could potentially result in a false diagnosis of aortopulmonary window. However, Droppler color flow imaging can verify the presence of a defect by displaying evidence of flow across the echo-free space into the main pulmonary artery from the aorta.[4.5] In this case, two-dimensional echocardiography showed a large communication between the aortic arch and the main pulmonary trunk, and Droppler color flow imaging clearly indicated the flow between the aorta and the pulmonary artery. A large ventricular septal defect was also confirmed by both two-dimensional echocardiography and Doppler color flow imaging. Thus, the combination of two-dimensional echocardiography and Doppler color flow imaging as well as pulsed Doppler echocardiography can rule out other diseases that mimic or are associated with aortopulmonary window.


[1.] King DH, Huhta J, Gutgesell HP, Ott DA. Two-dimensional

echocardiographic diagnosis of anomalous origin of the pulmonary

artery from the aorta; differentiation from aortopulmonary window.

J Am Coll Cardiol 1984; 4:351-55 [2.] Satomi G, Nakamura K, Imai Y, Takao A. Two-dimensional;

echocardiographic diagnosis of aortopulmonary window. Br Heart

J 1980;43:351-56 [3.] Mendoza DA, Tadashi V, Nishioka K, Yokota T, Mikawa H,

Nomoto S, et al. Aortopulmonary window, aortic origin of the

right pulmonary artery, and interrupted aortic arch: detection

by two-dimensional and color Doppler echocardiography in an

infant. Pediatr Cardiol 1988; 7:49-52 [4.] Rice MJ, Seward JB, Hagler DJ, Mair DD, Tajik AJ. Visualization

of aortopulmonary window by two-dimensional echocardiography.

Mayo Clin Proc 1982; 57:482-87 [5.] Alboliras ET, Chin AJ, Barber G, Helton JG, Pigott JD. Detection

of aortopulmonary window by pulsed and color Doppler echocardiography.

Am Heart J 1988; 115:900-02 [6.] Daniels O, Hopman J, Deknecht A, Vanoort A, Busch H. Pulsed

Doppler echocardiography in patients with aorto-pulmonary

connection. Acta Paediatr Scand 1986; 329(suppl):44-52

COPYRIGHT 1992 American College of Chest Physicians
COPYRIGHT 2004 Gale Group

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