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© Springer International Publishing 2016 M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease, DOI 10.1007/978-3-319-28219-0_23
Computed Tomographic Angiography in the Assessment of Congenital Heart Disease and Coronary Artery Anomalies
Priya Pillutla and Stephen C. Cook
Abstract
Advances in medical and surgical care have signifi cantly increased the numbers of children and adults living with congenital heart disease (CHD). This chapter will discuss anatomical and imaging considerations for the major CHD lesions. Additionally, the role of computed tomography in the planning of percutaneous and surgical repairs will be addressed, as well as the use of this modality to monitor for possible post-intervention complications. Finally, clinically signifi cant coronary anomalies will be reviewed.
Keywords
Congenital heart disease • Cardiac computed tomography • Coronary anomalies
Introduction
Congenital heart disease (CHD) is the most common con­genital disorder in newborns [ 1 – 3 ]. Approximately 6 per 1000 live births in the United States are affected by complex CHD and as many as 75 per 1000 live births have simple lesions such as ventricular septal defects [ 4 ]. Improved med- ical and surgical care in addition to evolving percutaneous methods of intervention have decreased early and late mor­tality. As a result, mortality in infants and children with CHD dropped 31 % between 1987 and 2005 [ 5 ] and the adult pop- ulation has undergone rapid growth. As of 2000, there were nearly equal numbers of adults and children with severe CHD [ 6 ]. Currently, it is estimated there are approximately 800,000 adults with CHD in the United States [ 7 ] with a prevalence in the adult population of 3000 per million [ 8 ].
Prior to the introduction of cardiovascular magnetic resonance (CMR) imaging and cardiovascular computed tomographic angiography (CCTA), transthoracic echocar­diography (TTE) and cardiac catheterization were the primary imaging modalities in the diagnosis and evaluation of the patient with complex CHD [ 9 ]. Advances in TTE imaging and its widespread availability have allowed it to largely replace cardiac catheterization as the predominant imaging modality for CHD in children in most centers and the use of diagnostic cardiac catheterization in CHD appears to have declined [ 10 ]. In the hands of a skilled technologist, TTE provides non-invasive information regarding complex CHD while avoiding radiation and intravenous contrast exposure associated with serial cardiac catheterizations. It also can be performed rapidly, provides important hemodynamic data and is relatively inexpensive.
Both TTE and catheterization have disadvantages with regards to imaging the adult with CHD. Anatomic windows for ultrasound may be limited by chest wall deformities (e.g., pectus deformities, spinal abnormalities) and post-surgical changes. Transesophageal echocardiography can circumvent some of these pitfalls but it requires an experienced operator and carries the risks of any invasive procedure including con­scious sedation. Additionally, it has limited use in the assess­ment of anterior structures such as conduits.
P. Pillutla , MD (*) Adult Congenital Heart Disease Program , Harbor-UCLA Medical Center , 1124 W. Carson Street, RB2 , Torrance , CA 90502 , USA e-mail: ppillutla@labiomed.org
S. C. Cook , MD, FACC Adult Congenital Heart Disease Center , Heart Institute, Children’s Hospital of Pittsburgh of UPMC , Pittsburgh , PA , USA
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CMR allows for three-dimensional structural and func­tional assessment of the heart as well as delineation of extra­cardiac structures without ionizing radiation. The benefi ts of CMR in the evaluation of the adult CHD patient are diverse including quantifi cation of both left and right ventricular size and systolic function, shunt quantifi cation, evaluation and quantifi cation of valvar disease, and assessment of myocar­dial perfusion and fi brosis [ 11 ]. Despite these numerous applications and advantages, CMR has several limitations including prolonged acquisition time, signal void artifact due to prior transcatheter interventions [ 12 ], claustrophobia, high acquisition costs and the inability to perform CMR in patients with implantable cardioverter defi brillators or pacemakers.
Concurrently, there have been numerous advances (e.g., reduced scan times; higher spatial/temporal resolution) in the fi eld of cardiovascular CT [ 13 ]. Consequently, CCTA provides a suitable alternative to CMR. It yields an accurate assessment of intra- and extra-cardiac anatomy for patients with both simple and complex CHD while overcoming the limitations of CMR. Furthermore, CCTA can provide accurate quantifi cation of volume and function comparable to CMR although such protocols typically require higher radiation doses [ 14 ]. In contrast to CMR, acquisition time is brief. Therefore, this technique should be strongly considered in patients with poor echocardiographic windows and contraindications to CMR.
Unfortunately, CCTA is not without disadvantages. This technique still requires exposure to ionizing radiation as well as nephrotoxic contrast. Importantly, patients with CHD have many potential sources of ongoing radiation exposure that often begin in infancy and continue throughout life. Serial chest radiography, nuclear scans, computed tomography scans and diagnostic/therapeutic catheterizations are frequently performed in the setting of prior corrective or palliative interventions [ 15 ]. Therefore, physicians who perform and/or refer patients for this procedure should be familiar with radiation exposure and techniques available to reduce radiation exposure at the time of CCTA examination. Fortunately, there are now a number of low-radiation protocols that can be employed to signifi cantly reduce the radiation exposure including reduction of tube voltage (for example to 80 kVp when feasible), adequate heart rate control, use of prospectively triggered scanning, iterative reconstruction and spectral detectors [ 16 – 25 ].
CT Imaging Protocol
Methodical pre-study planning is of critical importance in the patient with CHD. Repeating a study due to suboptimal technique exposes the patient to excessive contrast and radiation exposure. Furthermore, crucial structures may be missed on a “standard” study. Collaboration with a specialist
in adult CHD may avoid many potential pitfalls. Prior to commencing a study, the following should be described if possible: the diagnostic indication, the original anatomic defects, operative repairs if any and post-surgical anatomic and hemodynamic changes. Thus, the study can be tailored for the individual patient to provide the appropriate extent of anatomic coverage, proper timing of contrast administration, selection of the best image acquisition protocol and special attention to the structures of interest.
Cardiac Anatomy: A Sequential Approach
CHD is highly variable in its complexity and anatomic arrangements. Attempts to adequately describe complicated lesions have led to a nuanced taxonomy of eponyms, synonymous and near-synonymous terms. For instance, even the basic terms of “left” and “right” can lead to confusion. By convention, they refer to morphologic characteristics of a cardiac chamber rather than position within the chest.
To reduce clinical confusion and facilitate academic study, various systematic schemata have been developed. Van Praagh’s “segmental approach” [ 26 ] describes each of the three main segments of cardiac anatomy (the atria, ventricles and great arteries) in series. This is analogous to the construction of a home, where each segment builds off the prior with the atria serving as the foundation. The sequence is often abbreviated by a sequence of three letters (X, Y, Z) where the fi rst letter describes visceral-atrial situs, the second ventricular looping and the third the relationships of the great arteries. This analysis is often helpful, particularly for the evaluation of those with complex CHD, as it provides a systematic and standardized approach that can be applied to any patient.
Atrial Situs
Atrial situs most often follows the positioning of the unpaired abdominal viscera. For instance, the normal arrangement is situs solitus ( S , _, _), in which the morphologic right atrium, systemic venous return and liver are on the right side of the patient. The morphologic left atrium, pulmonary venous return, stomach and spleen are on the left side. The morphology of the atrial appendage provides important clues regarding right or left-sidedness (See Fig. 23.1 ).
The mirror image of this arrangement (with the morpho­logic right atrium and liver on the patient’s left and the mor­phologic left atrium, stomach and spleen on the patient’s right) is situs inversus ( I , _, _). Cases of both atria having characteristics of either the left or right atrium (atrial isomer­ism) are described as situs ambiguus ( A , _, _), also known as the heterotaxy syndrome.
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Bronchial morphology may further assist in determining atrial situs as the two frequently correlate with one another. Normally, the fi rst branch of the right mainstem bronchus courses above (eparterial) the right pulmonary artery whereas
the fi rst branch of the left mainstem bronchus courses below (hyparterial) the left pulmonary artery (See Fig. 23.2 ). This bronchial confi guration indirectly suggests atrial situs solitis.
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Fig. 23.1 Oblique axial view ( a ) demonstrates the features of a morphologic left atrium ( LA ), including its fi nger-like appearance and pectinate muscles ( arrows ). In contrast, the oblique coronal view ( b )
demonstrates a broad-based triangular appendage ( arrowhead ) sugges- tive of a right atrial appendage. RA right atrium
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Fig. 23.2 Volume-rendered three-dimensional reconstructions ( a , b ) demonstrating pulmonary situs solitus. The pulmonary artery of the morphologic right lung travels anteriorly to the bronchus ( R ). The pul-
monary artery of the morphologic left lung ( L ) travels over its main bronchus and posterior to the upper lobe bronchus
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Atrial Isomerism
Atrial isomerism, commonly referred to as heterotaxy syn­drome, is the result of duplication of the structures typical of either the left or right side of the body. This syndrome is associated with intestinal abnormalities, poorly functioning or absent splenic tissue, and complex CHD [ 27 ]. In right atrial isomerism, both atria have the broad based triangular atrial appendages typical of the right atrium and receive systemic venous return (superior vena cava or SVC, infe­rior vena cava or IVC, and coronary sinus). This is typically associated with bilateral trilobed lungs, a large liver which spans the abdomen and asplenia. Left atrial isomerism is characterized by both atria having narrow based atrial appendages and receiving the ipsilateral pulmonary veins. This is associated with bilateral bilobed lungs, interruption of the IVC, a midline liver and polysplenia.
Ventricular Looping
The normal anatomic position of the morphologic right ven­tricle is to the right and anterior of the left ventricle. This arrangement is called “ D-loop ” (_, D , _) and results from rightward or dextro-looping of the primitive heart early in fetal development. If the primitive heart developed in a left­ward (levo-) fashion, it can result in the left ventricle anterior and rightward of the right ventricle or “ L-loop ” (_, L , _).
Features of the morphologic right ventricle include the presence of coarse trabeculae, a prominent moderator band,
tricuspid valve attachments to the septum and free wall, and absence of fi brous continuity between the tricuspid valve and semilunar valve. Additionally, the tricuspid valve is normally located more apically within the right ventricle when com­pared to the mitral valve. In contrast, the morphologic left ventricle has a smooth septal surface and fi brous continuity between the mitral and semilunar valves.
Semilunar Valve Relationships
Van Praagh described six potential relationships of the aortic and pulmonary valves. Each variant is defi ned by the position of the aortic valve relative to the pulmonary valve. In the normal rela­tionship, solitus (_, _ , S ) , the aortic valve is rightward and poste- rior of the pulmonary valve. If the aortic valve is leftward and posterior, it is termed inversus (_, _, I ). When the aortic valve is rightward and anterior, it is termed D-malposition ( _ , _, D ), and when the aortic valve is leftward and anterior, it is L-malposition (_, _, L ). Uncommonly, the aortic valve can lie directly anterior (_, _, A ) or directly posterior (_, _, P ) to the pulmonary valve.
Concordant/Discordant Relationships
Tynan and colleagues [ 28 ] proposed an alternate means of describing complicated CHD. Their approach places greater emphasis on the connections between the different segments. Segments can be concordant (normally related) or discor- dant (See Fig. 23.3 ). For instance, if the right atrium connects
ab
Fig. 23.3 Atrioventricular and ventriculoarterial concordance. The oblique coronal view ( a ) demonstrates atrioventricular concordance between the left atrium ( LA ) and left ventricle ( LV ). The oblique coro-
nal view ( b ) demonstrates ventriculoarterial concordance between the LV and the aorta ( Ao )
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normally via a tricuspid valve to the right ventricle, there is atrioventricular concordance . If the right ventricle then gives rise to the pulmonary artery, there is ventriculoarterial concordance . In d-transposition of the great arteries (d-TGA), in which the right ventricle gives rise to the aorta, there is ventriculoarterial discordance . Atrioventricular connections may also be absent (e.g., tricuspid atresia) or doubly- committed (connected to both ventricles, either equally or unequally).
Congenital Heart Defects of Simple and Moderate Complexity
Venous Abnormalities
Systemic Venous Abnormalities
Systemic venous anomalies include bilateral SVC (which may or may not be connected via a bridging innominate vein), a unilateral left SVC (which most frequently drains into an enlarged coronary sinus, less commonly draining directly to the left atrium) and interrupted IVC (often with continuation via the azygous or hemiazygous veins).
Pulmonary Venous Abnormalities
Abnormal pulmonary venous return is described as being total or partial. In total anomalous venous return (TAPVR), all four pulmonary veins drain anomalously. There are four variants of TAPVR: supracardiac, cardiac, infracardiac and mixed. Supracardiac -type is the most common with the pul- monary veins connecting to the systemic venous circulation via the SVC, innominate vein or azygos vein. Cardiac -type describes the pulmonary veins draining to the coronary sinus or a similar vein into the right atrium. In patients with the infracardiac -type, the pulmonary veins drain into the portal or hepatic veins. Mixed is any combination of the above venous abnormalities. If any of these lesions are associated with any degree of obstruction, which is particularly com­mon in the infracardiac-type, severe pulmonary congestion may result. In this setting, surgical palliation is usually required during the newborn period.
If at least one of the veins drains inappropriately, it is described as partial (PAPVR). There is a wide spectrum of anatomic malformations in PAPVR and many different types of connections between the systemic venous and pulmonary venous circulations have been reported [ 29 – 32 ]. PAPVR is often associated with a sinus venosus atrial septal defect (ASD). When the right-sided pulmonary veins drain anoma­lously to the IVC (typically near the diaphragm) and in the presence of right lung hypoplasia, this constellation is termed “scimitar syndrome” (from the resemblance of the curvilin­ear anomalous connection to a curved sword).
Late complications following surgical correction of either TAPVR or PAPVR include stenosis of the SVC, the
anastomosis site or the pulmonary veins. CCTA, which is well characterized in the evaluation of the pulmonary veins prior to or following radiofrequency ablation [ 33 ] is ideally suited to evaluate the pulmonary venous anatomy in the adult CHD patient with native disease as well as the post-operative patient to determine the presence/absence of stenosis after prior palliative repair (See Fig. 23.4 ).
Cor Triatriatum
Cor triatriatum is caused when there is stenosis of the com­mon pulmonary vein [ 34 ]. Hence, the pulmonary veins enter a “pulmonary venous” chamber which drains into the left atrium (cor triatriatum sinistrum) via an opening. It may alternatively communicate with the right atrium. This orifi ce may be imperforate, restrictive, multiple, or large and nonre­strictive. Cor triatiatrum dextrum is caused by persistence of the right valve of the sinus venosus and divides the right atrium into three chambers; it is far less common. Commonly associated defects include atrial septal defect or patent fora­men ovale, PAPVR and persistent left SVC.
Without surgical correction, a highly restrictive commu­nication between the pulmonary venous confl uence and the left atrium is associated with high mortality during infancy. In contrast, the patient with mild or no obstruction may not present until later in adult life. CCTA provides excellent spa­tial resolution for defi ning pulmonary venous and pulmonary venous anatomy in this condition, both in the unrepaired and post-operative state.
Defects in Septation
Atrial Septal Defects
Atrial septal defects, or ASDs, are among the most com­mon congenital heart defects. They are classifi ed by their anatomic location. The two most common variants, secun­dum and primum, are true defects within the atrial septum. The sinus venous defect is not a true defect in the atrial septum but rather a defi ciency in the wall separating the pulmonary veins from the right atrium. This results in a left-to-right shunt similar to the primum and secundum ASDs. The coronary sinus ASD shares a similar aberration and physiologic outcome. Here, there is a defi ciency in the wall separating the coronary sinus from the left atrium (See Fig. 23.5 ).
Of these, ostium secundum defects or secundum ASDs, are the most common variant. Ostium primum defects or pri- mum ASDs are the next most common. As the primum por­tion of the atrial septum is contiguous with the atrioventricular valves and intraventricular septum, primum ASDs are typi­cally classifi ed within the spectrum of atrioventricular septal defects (AVSDs or atrioventricular canal defects).
Sinus venous ASDs are uncommon and account for approximately 5–10 % of all ASDs [ 35 ]. They most often
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occur at the junction of the SVC and the right atrium. A defect in this area creates a connection between the right upper pulmonary veins and the right atrium. Less commonly, they can involve the junction of the IVC and the right lower pulmonary veins. Coronary sinus defects are more rare and often described as an “unroofi ng” of the coronary sinus, allowing drainage from the coronary sinus into the left
atrium. While these defects do not involve the atrial septum, they are physiologically similar.
Because of increased right atrial compliance, shunt fl ow across the ASD is left to right (in the presence of normal pulmonary vascular resistance). Signifi cant shunts lead to volume overload and dilation of the right-sided cardiac chambers. Thus, closure of an ASD is indicated (either surgi­cally or percutaneously) if right atrial or right ventricular enlargement are present, with or without symptoms [ 36 ]. In the presence of severe pulmonary hypertension, the shunt may reverse direction and fl ow from right to left (Eisenmenger physiology). The etiology of pulmonary hypertension in such patients is not clear and may not be solely due to a large left to right shunt over many decades [ 35 ]. ASD closure may be considered in patients with pulmonary hypertension pro­vided there is a net left-to-right shunt and evidence of sub­systemic pulmonary arterial pressure or evidence of pulmonary arterial vasoreactivity [ 36 ].
Prior to the advent of atrial septal occlusion devices per­formed in the cardiac catheterization laboratory [ 37 ], the treat- ment of choice had largely been surgical management. Currently, many secundum defects can now be managed percutaneously with fewer complications and shorter inpatient hospital stays when compared with conventional surgical management [ 38 ]. The success of percutaneous closure is determined by the pres­ence of adequate rims of atrial tissue to secure the device.
The spatial resolution of multi-detector CT provides an excellent modality for pre-procedural planning in ASD
Fig. 23.5 Atrial septal defects: A indicates the superior sinus venosus atrial septal defect ( ASD ); B secundum ASD, C inferior sinus venosus ASD, D ostium primum ASD or partial atrioventricular septal defect, E secundum ASD without posterior septal rim, and F coronary sinus ASD. SVC superior vena cava, IVC inferior vena cava (Reprinted from Webb et al. [ 35 ] with permission of Wolters Kluwer)
ab
Fig. 23.4 Volume rendered three dimensional reconstructions demon­strate anomalous return of the right superior pulmonary vein ( RSPV ) to the superior vena cava ( SVC ) and right inferior pulmonary vein ( RIPV )
to the inferior vena cava ( a ). Note the normal return of the left pulmonary veins to the left atrium ( b ). LA left atrium, LIPV left inferior pulmonary vein, LSPV left superior pulmonary vein, RA right atrium
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closure, particularly if a percutaneous approach is planned [ 39 ]. Complete CT assessment prior to percutaneous closure of a secundum ASD should include assessment of pulmo­nary venous anatomy and exclusion of anomalous pulmo­nary venous return, the dimensions of the defect, presence of any fenstrations and characterization of the superior, inferior and retroaortic rims (See Fig. 23.6 ). Rims may be defi cient or absent and are a key factor in choosing the appropriate closure strategy. Sinus venosus and primum ASDs should be specifi cally excluded. Additionally, depending upon the age of the patient, characterization of the coronary arteries may be necessary.
CCTA may be useful in the post-procedure patient, par­ticularly if a percutaneous closure was performed. The study should include characterization of device seating, assessment to exclude tissue erosion from the device, impingement on surrounding structures such as the atrioventricular or semilu­nar valves, pulmonary venous obstruction, and pericardial effusion [ 40 ]. A residual shunt should also be excluded.
Ventricular Septal Defects
As with ASDs, ventricular septal defects (VSDs) are among the most common CHD lesions. They too are described by their position within the septum. The ventricular septum is divided into four regions: inlet, membranous, outlet and muscular. The inlet septum separates the mitral and tricuspid valves. The muscular septum extends from the inlet towards the apex of the heart. The membranous septum itself is small
and extends from under the aortic valve towards the septal leafl et of the tricuspid valve; defects that cross into the mus­cular, inlet or outlet septum are termed perimembranous. Outlet or supracristal (other terms include infundibular, conal, subpulmonary or doubly committed subarterial) defects are in the smooth-walled septum, in continuity with the crista supraventricularis and the pulmonary valve.
The natural history and presentation of VSDs are vari­able. Small defects located in the muscular septum may undergo spontaneous closure. Occasionally, aneurysmal tis­sue from the tricuspid valve may result in spontaneous clo­sure of a perimembranous VSD. Small, restrictive defects may be of little hemodynamic consequence. However, large nonrestrictive defects expose the right ventricle and pulmonary artery bed to the systemic pressure of the left ventricle. Over time, due to increased pulmonary blood fl ow, pulmonary vascular resistance will rise and ultimately lead to a reversal of the shunt (right-to-left) consistent with Eisenmenger physiology. Thus early surgical intervention is indicated for defects causing a signifi cant left-to-right shunt and evidence of left-sided volume overload [ 36 ] in order to avoid progressive and irreversible changes of pulmonary vascular disease. Other considerations for surgical referral include secondary phenomena such as infective endocarditis or aortic regurgitation (often seen in the setting of a suprac­ristal VSD).
Ongoing advances in transcatheter techniques now pro­vide an alternative method to address defects located in the
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Fig. 23.6 Oblique axial ( a ) and sagittal ( b ) views demonstrate the anatomy of the atrial septal defect (*) as well as anatomic information regarding surrounding rims that are often helpful in the pre-
interventional assessment to determine suitability for transcatheter clo­sure. ( I ) inferior rim, LA left atrium, ( R ) retroaortic rim, ( S ) superior rim, SVC superior vena cava
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perimembranous and muscular portions of the interventricu­lar septum in select cases [ 41 , 42 ]. This technique has been demonstrated to be safe and effective when performed in experienced centers. The most signifi cant late-onset compli­cation in the perimembranous closure group is complete atrioventricular block, which requires careful serial follow-up.
Following either surgical or percutaneous device closure, CCTA has utility in assessing the adequacy of closure via the detection of residual defects (See Fig. 23.7 ). It is also useful in the pre-catheterization assessment to evaluate defect size as well as relationship of the defect to surrounding anatomic structures to determine suitability for percutaneous closure.
Atrioventricular Septal Defects
Atrioventricular septal defects (AVSD) include a range of anomalies which share defects within the atrioventricular (AV) septum and, often, defects of the AV valves [ 43 ]. Up to 45 % of patients with Down syndrome have CHD and, of these, approximately 45 % have an AVSD [ 44 ].
A number of terms are used to further classify the various anatomic features and “balance” of the ventricles associated with the AVSD. A complete AVSD has a single defect with a primum ASD and inlet VSD along with a common AV valve. A partial AVSD always includes a primum ASD and there are two distinct AV valves. A transitional AVSD is a partial AVSD accompanied by a small inlet VSD; there are often anomalous chordal attachments to the ventricular septum. A balanced AVSD occurs when the left and right ventricles are
of equal size. Here, the common AV valve is symmetrically located over both ventricles. An unbalanced AVSD occurs when one of the ventricles is signifi cantly smaller than the other. AVSDs are characterized by anterior displacement of the left ventricular outfl ow tract (LVOT), causing it to elongate and narrow. This “gooseneck” deformity can cause signifi cant LVOT obstruction and may be worsened by abnormal attachments from the AV valves.
Thus, notable morphological features of AVSDs which may be seen on CT include the following: insertion of the AV valve leafl ets at the same level at the crux of the heart (rather than the normal apical displacement of the tricuspid valve); any defi ciency in the AV septum; anterior displacement and elongation of the LVOT and abnormal AV valves. The left AV valve is often cleft.
Most adult patients with this diagnosis will have undergone prior surgical palliation in infancy. Late complications associated with AVSDs include left or right AV valve regurgitation associated with a cleft or otherwise structurally abnormal valve, residual atrial or ventricular level shunt and LVOT obstruction.
Aortic Abnormalities
Patent Ductus Arteriosus
The ductus arteriosus is a fetal vascular channel connecting the main pulmonary trunk to the descending aorta and which is essential for fetal circulation. Before birth, the ductus arteriosus allows much of the oxygenated blood from the placenta to bypass the pulmonary vascular bed and supply the systemic circulation via the descending aorta. It typically closes spontaneously within a week following birth. Beyond this time, if the vessel remains patent, a shunt (patent ductus arteriosus or PDA) now exists between the systemic and pulmonary vascular beds.
This may be benefi cial in certain congenital heart condi­tions such as pulmonary atresia or hypoplastic left heart syn­drome, for which the PDA can provide a stable source of blood fl ow to either the pulmonary or systemic circulation. In an otherwise normal circulation, a PDA may have serious sequelae that are mainly determined by the size of the size of the ductus. As pulmonary vascular resistance falls following birth, the left-to-right shunt increases. Though a small PDA is often of little hemodynamic consequence, a large PDA can expose the pulmonary vascular bed to excess pulmonary blood fl ow, eventually causing increased pulmonary vascular resistance and pulmonary hypertension. Pulmonary hyperten­sion may persist even after the duct is closed.
While surgical ligation of a ductus is a straightforward surgical procedure, catheter-based techniques have now become the procedure of choice for the majority of PDAs [ 45 ]. Pre-intervention CCTA is useful to characterize the
Fig. 23.7 An oblique axial image demonstrates a restrictive, muscular ventricular septal defect (VSD; *)
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