| | Visualization of congenital thoracic vascular anomalies using multi-detector row computed tomography and two- and three-dimensional post-processingReceived 4 August 2006; accepted 4 August 2006. Abstract Anomalies of the vascular system are caused by false embryogenesis and are therefore present from birth. Single-detector row spiral computed tomography angiography (CTA) and multi-detector row computed tomography angiography (MDCTA) have gained increasing importance in the non-invasive assessment of vascular pathologies and replace conventional angiography in many cases. High-resolution volumetric datasets that are acquired during a single breath-hold give the possibility of two- (2D) and three-dimensional (3D)-post-processing. Due to post-processing, even complex vascular malformations are visualized in an understandable way. Furthermore, CTA, in contrast to conventional angiography, depicts not only the vascular structures but also allows assessment of the surrounding anatomical structures. We present cases of rare congenital anomalies of the thoracic vessels using MDCT with special respect to 2D- and 3D-post-processing. 1. Introduction  Until recently the incidence of congenital thoracic vascular anomalies has been increasing steadily (approximately 12–14 per 1000 live births) [1]. The reason for the mounting occurrence is probably not due to a real increase in anatomical variants and malformations but to a rising number of patient referrals to specialized centers for further assessment and an increasing availability of better diagnostic tools. Anomalies of the heart and the great vessels are mostly present from birth. The majority of such disorders arise from faulty embryogenesis during gestational weeks 3–8, when major cardiovascular structures develop. The most severe anomalies may be incompatible with intrauterine survival. Many other anomalies are associated with live birth and are now amenable to surgical repair with good results. Immense strides have been made in the diagnosis and therapy of congenital anomalies of the heart and great vessels, allowing extended survival for many children [2]. Conventional catheter-based angiography has been the “gold standard” for the evaluation of vascular pathologies for many years. Numerous authors have illustrated the utility of single-row spiral computed tomography angiography (CTA) or multi-detector row computed tomography angiography (MDCTA) for the non-invasive assessment of vascular pathologies [3], [4], [5], [6], [7]. The fast data acquisition of the spiral CT allows acquisition of volumetric data sets during a single breath-hold. Furthermore, MDCT provides nearly isotropic (4–8-channel scanners) or isotropic (16-channel scanners) spatial resolution [8]. Based on these technical improvements, MDCT has been found to be useful for the non-invasive diagnostic assessment of the thoracic vessels [4], [5], [7]. Axial image presentation is often not suitable for demonstration purposes. The high spatial resolution of modern MDCT scanners, however, encourages the application of alternative image presentation techniques based on two-dimensional (2D) image reconstruction (e.g. multi-planar reformation (MPR)) or three-dimensional (3D) image reconstruction (e.g. minimum intensity projection (MinIP), shaded surface display (SSD) and volume rendering technique (VRT)). In this pictorial review, we will focus on the assessment of congenital anomalies of the aorta, the supra-aortic arteries, the pulmonary arteries, and the vena cava using four-channel MDCT in combination with 2D- and 3D-image post-processing. MDCT image acquisition was performed without electrocardiogram (ECG) gating, because actual equipment (i.e. 4-channel as well as 16-channel scanners) does not support ECG-gated data acquisition techniques with high-resolution datasets of the entire chest (e.g. 1 mm or sub-millimeter collimation) [9]. Anomalies of the heart and the coronary arteries were not included in this study because of these limitations. 2. MDCT data acquisition and post-processing technique 2.1. MDCT acquisition technique All patients were examined using a four-channel MDCT scanner (Siemens Somatom VolumeZoom, Siemens Medical Systems, Forchheim, Germany). Optimal CT protocols were mandatory for each anatomic area and intravenous contrast media injection had to be tailored for the examination of the different vascular regions. In most of the cases we used a CTA protocol with 4mm×1mm collimation, 1.25mm slice width, and 0.5mm reconstruction increment. In several cases the vascular malformation was detected incidentally during a CT performed for another reason. Our routine chest CT protocol was used with 4×2.5mm collimation, 3mm slice width, and 2mm reconstruction increment in these cases. For both protocols bolus tracking software (CareBolus, Siemens Medical Systems, Forchheim, Germany) was used for optimal synchronization of contrast media injection and image acquisition. A region of interest, which was located in the pulmonary artery or the aorta depending on the vascular anomaly under investigation, was defined. The threshold for starting the acquisition was set to 130HU. In all patients a 150ml non-ionic, iodinated, low-osmolar contrast agent (Visipaque 320; Amersham Health, Buckinghamshire, UK) was injected into a cubital vein at a flow rate of 3ml/s and subsequently flushed by 30ml saline fluid at the same flow rate using a power injector (Ulrich Medical, Ulm, Germany). Contrast media injection and the bolus tracking software were started at the same time. The bolus tracking software initiated the acquisition of serial images with automatic measurements of the HU values in the region of interest. After reaching the threshold value (130HU) a delay of 4s for table feed and breathing instruction was applied. Data acquisition of the entire chest was performed in a cranio-caudal direction. 2.2. Post-processing technique 2D- and 3D-post-processing of the axial CT data was performed using a Siemens Somatom VolumeZoom Wizard (Siemens Medical Systems, Forchheim, Germany) and an Advantage Windows 4.0 workstation (General Electrics Medical Systems Europe, Buc Cedex, France) for MPR, MinIP, and VRT reconstructions. 3. Congenital thoracic vascular anomalies 3.1. Anomalies of the aortic arch Anomalies of the aortic arch are a complex group of malformations. The incidence of aortic arch malformation is difficult to determine because most of the anomalies are asymptomatic. Aortic arch anomalies are common, occurring in 0.5–3% of the population [10]. In certain cases the trachea, the esophagus, or both may be compressed due to the aberrant course of a vessel. The vascular malformation may, therefore, become symptomatic. In other cases vascular symptoms may occur, such as embolic disease caused by aneurysms or impairment of the peripheral blood supply as seen in aortic coarctation. Understanding of the development of aortic arch malformations requires basic knowledge of the embryogenesis of the aorta. 3.1.1. Embryology of the aorta The thoracic aorta and its great vessels develop from six paired embryologic aortic arches by a complex process of regression and preservation [11]. Most of these arches regress, but some remain and become arteries of the head, neck, and chest. The fourth and the sixth arches are the most important, because they build the aorta and the pulmonary arteries [12]. The right part of the fourth arch forms the right subclavian artery, and the left part of the fourth arch forms the aortic arch. The right part of the sixth arch forms the right pulmonary artery, and the left part of the arch forms the left pulmonary artery and ductus arteriosus [12]. The fifth arch normally disappears. Wrong-side dissolution, wrong-level obliteration, or wrong-end absorption account for different known anomalies of the aorta and other thoracic vessels. 3.1.2. Aberrant right subclavian artery (arteria lusoria) An arteria lusoria (named after lusus naturae, freak of nature) is an abnormal origin of the right subclavian artery from the aortic arch (Fig. 1, Fig. 2). It is the most common congenital aortic arch anomaly with a reported prevalence of 0.4–2% [13]. This anomaly is caused by the persistence of the posterior segment of the embryologic fourth aortic arch. The artery crosses the midline between the esophagus and vertebral column to reach the right side (Fig. 1, Fig. 2). This vessel anomaly is usually an incidental X-ray finding on a chest roentgenogram and is often misdiagnosed as a mediastinal tumor [14]. MDCT and conventional angiography, including direct catheterization of the aberrant right subclavian artery, confirm the diagnosis. Rarely does an arteria lusoria become symptomatic and cause dysphagia (i.e. the so-called dysphagia lusoria). 3.1.3. Right-sided aortic arch and aberrant left subclavian artery A right-sided aortic arch is a rare anatomic variant (0.1% of the population). Half of the cases have an aberrant left subclavian artery that crosses the midline to the left [15], [16], [17] (Fig. 3, Fig. 4). The right-sided aortic arch results from persistence of the embryologic right fourth aortic arch and involution of the left [18], [19], [20]. This anomaly may be isolated or in combination with other congenital heart diseases, such as Tetralogy of Fallot or patent ductus arteriosus [21]. The right arch passes the right main bronchus to the right of the trachea and esophagus. Persistence or disappearance of the embryologic left or right dorsal aorta determines the course, whether in the left or right hemithorax, of the descending thoracic aorta [22]. The typical radiographic appearances are the visible right aortic arch and a density posterior to the esophagus [12]. This density is caused sometimes by the aortic diverticulum and sometimes by the medial displacement of the proximal descending aorta. Right-sided aortic arch may be asymptomatic. However, in infancy symptoms due to compression of mediastinal structures, such as the trachea or esophagus, may occur. In adulthood symptoms are more often related to early atherosclerotic changes of the anomalous vessels, to dissection, or to aneurismal dilatation (Fig. 3), which may cause dysphagia or dyspnea [23]. 3.1.4. Kommerell's diverticulum Because the persisting right aortic arch forms the root of the aberrant left subclavian artery, the origin of the artery is often broad-based. This is called Kommerell's diverticulum (Fig. 3, Fig. 4). Kommerell described a diverticulum of the descending aorta at the ligamentum arteriosum caused by the persistence of the posterior segment of the fourth aortic arch [24]. This diverticulum is a rare anomaly, occurring in less than 1% of the population [25]. Symptomatic Kommerell's diverticulum is even less common and is usually caused by an associated aneurysm. Incidentally, the diverticulum is usually identified by chest X-ray and misdiagnosed as a mediastinal tumor. The most common symptom is dysphagia due to a compression of the esophagus (Fig. 4). Dyspnea due to airway compression is rare [14]. 3.1.5. Double aortic arch The double aortic arch is the most frequent type of aortic-arch malformation (55% of all vascular ring malformations). It presents as a vascular ring due to persistence of the fetal double aortic arch built by the fourth arch. Associated cardiac anomalies are usually rare. However, the double aortic arch may occur with the Tetralogy of Fallot and the transposition of the great arteries [26]. One arch is mostly dominant, whereas the other may be of smaller caliber or presented by a fibrous band. The ascending aorta divides into two arches that pass to either side of the esophagus and trachea and reunite to form the descending aorta [27] (Fig. 5). Diagnostic features as seen using conventional imaging almost always include the larger and higher right aortic arch. A widening of the upper mediastinum in the postero-anterior view (Fig. 5A) and a mass-like density in the posterior mediastinum due to the retro-esophageal and retro-tracheal fusion of both arches (vascular ring) in the lateral X-ray (Fig. 5B) of the chest can be seen. The “four-artery sign” is a typical CT finding and means that each aortic arch gives rise to two vessels – a carotid and a subclavian artery – each artery of the pair lying one in front of he other [28] (Fig. 5D). Usually, the double aortic arch causes tracheal and esophageal compression in the first few months of life [29] (Fig. 5E). Dyspnea, stridor, and recurrent pulmonary infections are the leading symptoms. Typical symptoms in early childhood lead to prompt diagnosis and surgical treatment of the double aortic arch. Surgical resection of the smaller aortic arch should be performed in oligosymptomatic patients to prevent complications [30], [31]. 3.2. Anomalies of the descending aorta 3.2.1. Coarctation of the aorta Coarctation of the thoracic aorta is a common vascular anomaly (5–8% of all cases of congenital heart disease) [32] that may occur in isolation (2%), in association with cardiac anomalies such as bicuspid aortic valve (75–85%) [33], or as part of constellation of cardiac and non-cardiac birth defects. Usually, coarctation is characterized by a discrete narrowing or constriction of the lumen of the aorta distal to the origin of the left subclavian artery near the insertion of the ligamentum arteriosum (Fig. 6, Fig. 7). An enlarged heart because of left ventricular prominence and a prominent shadow in the left superior mediastinum due to the enlarged left subclavian artery are observed upon roentgenographic examination. Mostly there is an area of poststenotic dilatation of the descending aorta (“figure of three sign”). The classic clinical sign of coarctation of the aorta is disparity in pulsations and blood pressures of the arms and legs. The pulsations of the legs are weak and delayed or absent in contrast with the bounding pulses of the arms and carotid arteries. Patients with significant coarctation or re-coarctation, whether symptomatic or asymptomatic, should be treated surgically (Fig. 6) or interventionally (Fig. 7) to reduce or eliminate the gradient [34]. Surgery is based on end-to-end repair, interposed graft, or bypass graft (Fig. 6) [35]. Balloon dilatation with or without stent insertion has been performed with good results in children and adolescents. However long-term data are still lacking [36]. In 80% of patients the diagnosis is made during infancy or childhood and survival into adulthood is common [37]. 3.2.2. Ductus botalli persistens (patent ductus arteriosus) Patent ductus arteriosus (PDA) is the most common type of extracardiac shunt [38] and one of the most common congenital cardiovascular anomalies (9% of all congenital heart diseases) associated with maternal first-trimester rubella during early pregnancy. The ductus arteriosus is a vessel leading from the bifurcation of the pulmonary artery to the aorta just distal to the left subclavian artery (Fig. 8). Conventional chest X-ray findings mimic a ventricular septum defect due to the left-to-right shunt. Furthermore, the chest X-ray shows a prominent pulmonary artery with increased intrapulmonary vascular markings and enlarged right and left ventricles. Normally, the ductus arteriosus is patent in the fetus but closes within 2 or 3 days after birth. If the ductus remains open when pulmonary vascular resistance falls, aortic blood is shunted into the pulmonary artery as a result of the higher aortic pressure. The patent ductus should be ligated or closed by coils. 3.3. Anomalies of the vena cava 3.3.1. Double vena cava superior (persistent left vena cava superior) Symptomatic anomalies in the vena cava superior (VCS) are generally associated with congenital heart disease; otherwise, they are usually asymptomatic. Double VCS is a rare congenital vascular anomaly with an incidence of 0.3–11% in patients with congenital heart disease [39]. It may be associated with an atrial septal defect and an azygos continuation. This is due to the failure in development of the left brachiocephalic vein and to the persistence of the left anterior cardinal vein. The left VCS commonly drains into the right atrium via the coronary sinus and rarely into the left atrium, creating a right-to-left shunt (Fig. 9). The double VCS only has clinical implications when the left branch enters the left atrium [40]. When utilizing chest radiography or CT of the chest without application of contrast media intravenously, the persistent left VCS may mimic an anterior mediastinal and aorto-pulmonary lymph node enlargement or another tumor. Therefore, the use of contrast medium is mandatory for identifying this anomalous structure when using CT. 3.3.2. Azygos continuation of the vena cava inferior An interrupted vena cava inferior (VCI) with azygos continuation anomaly has a prevalence of 0.6% [41]. In this anomaly a failure fusion of the right subcardinal vein with the hepatic vein occurs, which results in drainage of the supra-renal VCI into the heart via the azygos vein (Fig. 2). Although asymptomatic, this malformation may be associated with different anomalies, such as polysplenia syndrome (i.e. situs ambiguous or inversus parietalis with bilateral ‘left-sideness’) or azygos continuation. 3.3.3. Partial anomalous pulmonary venous connection Partial anomalous pulmonary venous connection (PAPVC) of one or two but not of all pulmonary veins occurs in approximately 0.6% of the population [42]. There are many patterns of PAPVC, but the most common is a pulmonary vein originating from the right upper and/or middle lobe and running into the VCS, thus creating a left-to-right shunt [43]. This rare disorder is often associated with other congenital heart defects, usually an atrial septal defect [43]. About 15% of all atrial septal defects coexist with a PAPVC anomaly [44]. When this coincidence exists, the symptoms as well as the clinical manifestations are indistinguishable from those of an isolated atrial septal defect [44]. Depending on the shunt volume, symptoms include exercise intolerance, dyspnea, fatigue, palpitations, syncope, and congestive heart failure. Chest X-ray normally reveals a right ventricular enlargement and an increased pulmonary blood flow (Fig. 10). Asymptomatic patients with a small shunt volume require no treatment. Those with significant left-to-right shunt eventually develop symptoms and thus benefit from early corrective surgery [45]. 3.4. Congenital pulmonary venolobar syndrome Felson coined the term “congenital pulmonary venolobar syndrome” (CPVS) in order to include the main findings of CPVS [46]. This terminology was confusing. Therefore, Woodring extended the term to cover a range of congenital anomalies of the thorax that often occur together but each of which represents a distinctly different congenital anomaly, including Scimitar syndrome, pulmonary hypoplasia, and pulmonary sequestration [46], [47]. 3.4.1. Scimitar syndrome Scimitar syndrome is a rare congenital disorder (1–3 per 100,000 live births) characterized by an anomalous connection of the pulmonary vein with the VCI, partial systemic arterial blood supply, and a hypoplasia of the right lung [48], [49]. Only very rare cases have been published in the left lung [50]. The anomalous vein runs along the right contour of the heart, turns to the right, and then approaches the VCI where it inserts. The radiographic appearance of this anomalous right pulmonary vein resembles a curved Turkish sword, or scimitar, for which this syndrome is called (Fig. 11). CT provides a non-invasive method of confirming the diagnosis of Scimitar syndrome [51]. The infantile form presents normally in the first few weeks of life and is associated variably in 25% with other cardiopulmonary abnormalities, most commonly with septal defects [51], [52]. The adult form usually presents incidentally. Hypoplasia of the right lung can be found in 25% of the adult form cases. Heart failure is a rare complication, and the patients may be completely asymptomatic, especially with the isolated form [53]. 3.4.2. Pulmonary sequestration Pulmonary sequestration is the presence of an abnormal mass of pulmonary tissue that does not communicate with the tracheobronchial tree through a normal bronchial connection. Sequestration is commonly divided into two types: the more common intralobar (75%) and the rare extralobar (25%). The intralobar type is located within the normal lung parenchyma and is covered by normal pleura. Intralobar pulmonary sequestrations are associated with congenital anomalies in 6–12% (diaphragmatic hernia (3%), Tetralogy of Fallot). Both intralobar and extralobar sequestration receive their blood supply via an anomalous systemic artery, most commonly from the descending thoracic aorta or from the abdominal aorta or one of its branches (Fig. 12E) [54]. Intralobar sequestrations may drain over the pulmonary venous system in the left atrium (left-to-left shunt). Typically, age of presentation is adulthood (50%, >20 years), and the most common clinical manifestation for intralobar sequestration is recurrent infection [54], haemoptysis, and congestive heart failure due to a severe shunt [55]. In contrast, the extralobar sequestration is separated from the normal lung and is covered by its own pleura [56]. The extralobar types are more often associated with congenital anomalies, namely in 15–65% (diaphragmatic hernia (25%), cardiac anomalies (8%)) [54]. Extralobar sequestrations drain to the systemic venous system (left-to-right shunt). Usually, the age of presentation of extralobar sequestration is within the first 6 months (in 61%) of life due to the associated congenital anomalies that are responsible for the early detection of extralobar sequestration. For extralobar sequestration itself, clinical manifestations are less common than intralobar sequestration, and spontaneous hemorrhages are described [57]. Therefore, extralobar sequestrations are often discovered incidentally on a chest X-ray or during surgical repair of a congenital diaphragmatic hernia [54]. The appearance of both types of sequestration observed using plain chest radiography are typically those of an opacity at one or other base, postero-medially (Fig. 12, Fig. 13). In contrast to the intralobar type (Fig. 12) extralobar sequestrations (Fig. 13) typically show well-defined outer margins on a chest X-ray and, aside from pulmonal manifestation, a greater variety in location, such as in the mediastinum or in the retroperitoneum. Recurrent infections require surgical resection of the intra- and the extralobar sequestration. Coil embolization is a new and less invasive technique for eliminating right-to-left shunting and left ventricular volume overload [58]. 3.5. Anomalies of the pulmonary arteries 3.5.1. Pulmonic stenosis Pulmonic stenosis (PS) is one of the more common congenital cardiac malformations that allows survival to adulthood [59]. Approximately 80% of all patients with right ventricular outflow tract obstruction occur at the valvular level. Valvular PS (95% of all PSs) is due to partial fusion of a tricuspid or, less commonly, a bicuspid pulmonic valve. Dilatation of the main and left pulmonary artery (PA) is common [60] (Fig. 14). In the plain chest radiography, a normal pulmonary vascularity and a normal-sized heart is typical. The clinical course of PS varies, depending on the severity of obstruction. It is generally agreed that symptomatic adults should undergo either surgical valvulotomy or percutaneous balloon valvuloplasty. Balloon dilatation of the pulmonary valve is the therapeutic procedure of choice with typical pulmonary valvular stenosis and moderate to severe degrees of obstruction [61], [62], [63]. 3.5.2. Aplasia of left or right pulmonic artery Aplasia of left or right PA is the result of the disappearance of the proximal left or right sixth arch and can be seen in 0.39% of the cases of congenital heart diseases, such as Tetralogy of Fallot or right-sided aortic arch (Fig. 15) and may include septal defects as a complicating feature [64], [65], [66], [67]. In the setting of pulmonary atresia or stenosis the PAs are usually fed by collateral vessels, such as a intercostal arteries, patent ductus arteriosus, or aortopulmonary collateral arteries [68] (Fig. 15, Fig. 16). The plain chest X-ray shows a small hemithorax with a hypogenetic lung of normal radiodensity, a mediastinal shift to the affected side, and a reticular network of vessels on the affected side with rib notching due to the collateral circulation [69]. 3.5.3. Pulmonary arteriovenous malformation Pulmonary arteriovenous malformation (PAVM) has an incidence of about 2–3 per 100,000 people [70]. PAVMs may be of single or multiple occurrences. Most solitary PAVMs are seen in the lower lobes [71] (Fig. 17). All PAVMs have an afferent supply, usually from one or more branches of the pulmonary artery. Usually, the efferent limb of a PAVM drains into one or more branches of the pulmonary vein. Physiopathologically, a right-to-left shunt that is responsible for the clinical presentation is established. On occasion the patients have systemic abscesses or infarction, notably of the brain, because the blood bypasses the lung filter due to the right-to-left shunt [72]. The PAVM is seen as a well-defined nodule on plain chest radiographs (Fig. 17A). CT is more sensitive than pulmonary angiography in detecting PAVM [73]. Of the lesions, 81% are located either subpleurally or partially embedded in the lung parenchyma [74]. Despite limited information about the natural history of PAVM, available data suggest that treatment should be done to all symptomatic patients and asymptomatic patients with lesions less than 2cm in diameter as seen using chest radiography [71]. Currently, the preferred treatment of PAVM, which has widely replaced surgery, is percutaneous embolotherapy using coils or balloons [75]. We report a case with hereditary hemorrhagic teleangiectasia (Osler–Weber–Rendu disease), which is an autosomal dominant disorder and is characterized by teleangiectasis, aneurysms, and arteriovenous malformations. The blood vessels of the lung, liver, and central nervous system can be affected [76] (Fig. 17). 4. Discussion Conventional imaging of congenital thoracic vascular anomalies has been based on digital subtractive angiography and duplex Doppler ultrasound, which have the disadvantage of being invasive and operator-dependent, respectively. Recent years have seen exciting new developments in magnetic resonance angiography (MRA) and CTA, and these two techniques are increasingly utilised as the non-invasive imaging modality of choice in vascular anomaly visualisation as well as coronary and peripheral vascular disease. MRA offers several advantages for cardiovascular imaging. MRA does not use ionizing radiation and does not necessarily require the injection of a contrast agent. However, this review article stresses on the recent progress in MDCT-techniques by using representative cases. With its capacity for fast data acquisition in high resolution, MDCT has greatly increased the quality of thoracic vascular imaging. MDCT angiography is now the modality of choice for non-invasive assessment of vascular pathologies of the chest, because it allows for the evaluation of the vascular structures and the lung parenchyma as well. 2D- and 3D-imaging, such as MPR, MinIP, and VRT gain more and more importance, and these kinds of multidimensional post-processing often help to demonstrate complex vascular anatomical structures as seen in vascular congenital anomalies of the chest. Further technical developments, such as high-resolution (i.e. sub-millimeter) cardiac gated MDCT acquisition of the entire chest within a single breath-hold, may help to strengthen the role of MDCT, especially in cases of combined malformations of the heart and the great thoracic vessels. Acknowledgements This research has been supported by the NCCR CO-ME of the Swiss National Science Foundation. 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a Department of Medical Radiology, Institute of Diagnostic Radiology, University Hospital Zurich, Switzerland b Department of Medical Radiology, Institute of Diagnostic Radiology, Kantonsspital Chur, Switzerland c Division of Cardiovascular Surgery, University Hospital Zurich, Switzerland d Institute of Diagnostic Radiology, Kantonsspital St.Gallen, Switzerland  Corresponding author at: Institut für Radiologie, Kantonsspital St.Gallen, CH-9007 St. Gallen, Switzerland. Tel.: +41 71 494 2182; fax: +41 71 494 6479.
PII: S0720-048X(06)00335-4 doi:10.1016/j.ejrad.2006.08.015 © 2006 Elsevier Ireland Ltd. All rights reserved. | |
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