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Aortic Regurgitation
Published in K. Gupta, P. Carmichael, A. Zumla, 100 Short Cases for the MRCP, 2020
K. Gupta, P. Carmichael, A. Zumla
Such a pulse is a reflection of a rapid aortic run-off and has the eponymous name of 'water hammer' or Corrigan's pulse. It may also be found in patients with: A large patent ductus arteriosus.An aortopulmonary window.A ruptured aneurysm of the aortic sinus.High fever, due to the marked peripheral vasodilatation.Widespread active Paget's disease.Pregnancy.Severe anaemia.
Combined bronchial and pulmonary artery sleeve resections
Published in Larry R. Kaiser, Sarah K. Thompson, Glyn G. Jamieson, Operative Thoracic Surgery, 2017
Abel GÓmez-caro, Laureano Molins
On either side, when the PA is involved, intrapericardial control of the main PA should be achieved. Lymph nodes of the aortopulmonary window may complicate the main artery and bronchus dissection. The superior pulmonary vein is encircled intraor extrapericardially and divided, allowing full exposure of the proximal PA and better exposing the artery to permit optimal clamp placement for proximal control. The left main PA is clamped as far proximally as possible, with distal control achieved by clamping the artery within the fissure.
Multiple endocrine neoplasia *
Published in Demetrius Pertsemlidis, William B. Inabnet III, Michel Gagner, Endocrine Surgery, 2017
If no significant neck disease is found and the PTH does not fall, there may be a need to explore the mediastinum. In general, this should only be contemplated during the same procedure if hypercalcemia is a major clinical problem, this eventuality was planned from the outset, and ideally, it was indicated by imaging or venous sampling, or both. A targeted approach via the neck is preferred for inferior parathyroid glands in the anterior superior mediastinum and descended superior parathyroid glands in the posterior mediastinum, and via thoracoscopy for most other locations. If imaging is negative, then a full mediastinal exploration by thoracoscopy or sternotomy may be necessary. In the search for a middle mediastinal lesion, the aortopulmonary window should be examined [45].
Berry syndrome diagnosed by three-dimensional computed tomographic angiography
Published in Acta Cardiologica, 2020
A 7-month-old Chinese boy from a remote village with a heart murmur was referred to our institution for minimally invasive transthoracic patent ductus arteriosus (PDA) closure. Physical examination revealed a different oxygen saturation level in the upper and lower extremity of 95% and 90%, respectively. Blood pressure in the arm was 117/55 mmHg and 78/51 mmHg in the leg. A grade 3/6 systolic murmur was audible at the third left intercostal space. An echocardiogram showed aortopulmonary window (APW) (Figure 1(A), arrow) and the intracardiac shunt direction (two-way shunt, left to right shunt dominates) (Figure 1(B), arrow), PDA and pulmonary hypertension (PH). Computed tomographic angiography (CTA) revealed and demonstrated APW (Figure 1(C and D)), an anomalous origin of the right pulmonary artery from the aorta (AORPA) (Figure 1C), interrupted aortic arch (IAA) (Figure 1(D and E)), PDA (Figure 1(D and E), arrow). Since there might not exist irreversible pulmonary hypertension, invasive hemodynamics was not assessed. This congenital cardiac anomaly requires early diagnosis and timely surgical repair in order to restore normal perfusion especially for the lower body and to prevent the pulmonary damage. The APW morphology was type III (complete absence of the aortopulmonary septum) and closed with auto-pericardium graft. Postoperative CTA revealed the left and right pulmonary arteries and aorta blood flow without interference (Figure 1(F)). One stage repair may be a safe and efficient option for treating Berry syndrome, providing fixed pulmonary hypertension is excluded.
Prenatal diagnosis of aortopulmonary window by foetal echocardiography: ‘U or reversed U sign’
Published in Journal of Obstetrics and Gynaecology, 2019
Başak Kaya, Ali Ekiz, Deniz Kanber Acar, Salim Sezer, Helen Bornaun, Gökhan Yildirim, Halil Aslan
An aortopulmonary window (APW) is a rare congenital cardiac malformation, which is characterised by a communication between the ascending aorta and the main pulmonary artery before the bifurcation just above the semilunar valves (Hayashi et al. 2010; Aslan et al. 2012). It accounts for 0.2–0.6% of all congenital cardiac defects (Kutsche et al. 1987). Prenatal diagnosis of APW enables the early closure of the defect with a low operative mortality and improves the postnatal outcome (van Son et al. 1993; Backer and Mavroudis 2002). Between January 2014 and May 2017, about 12,487 foetal echocardiographies were performed in our maternal and foetal medicine unit and two cases were diagnosed prenatally as an aortopulmonary window. The main purposes of this paper are to discuss the ultrasonographic diagnosis of this rare defect and to demonstrate the importance of the prenatal diagnosis.
Eisenmenger syndrome and other types of pulmonary arterial hypertension related to adult congenital heart disease
Published in Expert Review of Cardiovascular Therapy, 2019
Carla Favoccia, Andrew H Constantine, Stephen J Wort, Konstantinos Dimopoulos
Shunting associated with PAH may occur at different levels. The underlying congenital heart defects can be divided into pre-tricuspid, as in the case of an atrial septal defect (ASD), and post-tricuspid, i.e. VSD, PDA, aortopulmonary window and various forms of truncus arteriosus. Surgical systemic-to-pulmonary palliative shunts, such as the Waterston and Potts shunt, aimed at augmenting pulmonary blood flow, have often been associated with the development of PAH [2,5,6]. PAH in post-tricuspid shunts typically develops during childhood and is severe when the defect is large [6,7]. The rate of progression of PVD varies between individuals, with some patients developing severe PAH and reversal of the shunt early in life (especially patients with Down syndrome), while in others, the disease progresses more slowly, and severe PVD may only occur in the second or third decades of life. The timing of the development of PVD depends on the type of defect. For example, patients with transposition of the great arteries and a VSD develop pulmonary vascular disease sooner than patients with an isolated VSD, whilst patients with large ASD who develop PAH, do so much later. In patients with aortopulmonary window and truncus arteriosus, there is also an early and rapidly progressive rise in PVR [8,9].