The Eighth World Congress of Pediatric Cardiology and Cardiac Surgery (WCPCCS) will be held in Washington DC, USA, from Saturday, 26 August, 2023 to Friday, 1 September, 2023, inclusive. The Eighth World Congress of Pediatric Cardiology and Cardiac Surgery will be the largest and most comprehensive scientific meeting dedicated to paediatric and congenital cardiac care ever held. At the time of the writing of this manuscript, The Eighth World Congress of Pediatric Cardiology and Cardiac Surgery has 5,037 registered attendees (and rising) from 117 countries, a truly diverse and international faculty of over 925 individuals from 89 countries, over 2,000 individual abstracts and poster presenters from 101 countries, and a Best Abstract Competition featuring 153 oral abstracts from 34 countries. For information about the Eighth World Congress of Pediatric Cardiology and Cardiac Surgery, please visit the following website: [www.WCPCCS2023.org]. The purpose of this manuscript is to review the activities related to global health and advocacy that will occur at the Eighth World Congress of Pediatric Cardiology and Cardiac Surgery.

Acknowledging the need for urgent change, we wanted to take the opportunity to bring a common voice to the global community and issue the Washington DC WCPCCS Call to Action on Addressing the Global Burden of Pediatric and Congenital Heart Diseases. A copy of this Washington DC WCPCCS Call to Action is provided in the Appendix of this manuscript. This Washington DC WCPCCS Call to Action is an initiative aimed at increasing awareness of the global burden, promoting the development of sustainable care systems, and improving access to high quality and equitable healthcare for children with heart disease as well as adults with congenital heart disease worldwide.

In an 11-year old boy with a large coronary arteriovenous fistula between the left coronary artery and the right atrium, we achieved successful closure using a 10–8 Amplatzer Duct Occluder introduced from the right internal jugular vein. Angiography 6 weeks later showed complete occlusion of the fistula, with normal opacification of the left coronary arterial system. This technique may be used as an alternative to coils and surgery in selected patients.

Follow-up cardiac catheterization and angiography was performed in 23 patients after complete, staged repair of pulmonary atresia with ventricular septal defect and multiple systemic-to-pulmonary collateral arteries. Time interval from repair varied from 0.2 to 89 months (mean 26 months). Major residual anomalies of arborization of the pulmonary arteries, with or without pulmonary vascular disease, were present in six patients, two of whom had die patch on the ventricular septal defect perforated because of systemic or suprasystemic right ventricular pressure in the early postoperative period after repair. Both of these children later died, while the other four patients were found to have moderately to severely elevated ventricular pressure ratios and pulmonary arterial pressure measurements, though they are all alive at follow-up intervals from 20 months to 6.8 years. The remaining 17 patients all had hemodynamically satisfactory or good results, with pulmonary arterial mean pressures ranging from 8 to 30 mm Hg (mean 22 mm Hg) and pressure ratios between the ventricles from 0.24 to 0.75 (mean 0.43)—the higher ratios generally reflecting gradients across the conduit valve. Angiography demonstrated that the hypoplastic pulmonary arteries increased in size to normal dimensions, during staging, in most patients, though abnormalities of arborization persisted in several. Analysis of the data from the entire cohort of 58 patients, who were accepted for staging towards repair, showed a significant association between early age at entry to the program and likelihood of complete repair being achievable.

Innocent murmurs are common in childhood. They require accurate diagnosis to avoid unnecessary anxiety and/or restrictions. With this in mind, we studied prospectively children diagnosed by a paediatric cardiologist as having innocent murmurs to review the necessity of investigations in excluding organic abnormalities. We included 63 children in the study. The majority had the so-called Still's, or musical/vibratory murmur. None had abnormal investigations, suggesting that such investigations are largely superfluous for the purpose of diagnosis in those patients with innocent murmurs seen by a paediatric cardiologist. They are often done, nonetheless, as part of the assessment and/or expectations of the parent or the referring physician.

The arterial switch operation is the treatment of choice for complete transposition, and for the Taussig-Bing anomaly, with good early and mid-term results. This retrospective study examined the findings obtained at routine follow-up cardiac catheterization after primary arterial switch repair. We catheterized 111 patients after a mean of 16.9 months after surgery. These included 67 patients with an intact ventricular septum, 33 with a ventricular septal defect, and 11 with the Taussig-Bing anomaly. Right ventricular pressures were mildly elevated (mean 33.9±10.2 mm Hg) in the overall group with a mean pressure ratio between right and left ventricles of 0.34±0.1. Of the patients 74% had gradients across the right ventricular outflow tract of under 20 mm Hg, while three (2.7%) had gradients over 30 mm Hg. A significant gradient across the left ventricular outflow tract occurred in one patient (0.9%), while significant neo-aortic stenosis was not seen. The neo-aortic root remained dilated, with mild aortic valvar incompetence being seen in 12%, with none having higher grades of regurgitation. Left ventricular ejection fraction was normal in all patients, while left ventricular end-diastolic pressure was elevated in 38%. Coronary arterial stenosis was not seen, but one patient (0.9%) had left ventricular apical dyskinesia. Overall, therefore, we conclude that cardiac hemodynamics and ventricular systolic function after primary arterial switch are good. Minor gradients to the pulmonary arteries, and mild neo-aortic valvar incompetence were commonly noted. Left ventricular end-diastolic pressure was elevated in over a third of the patients. These subclinical and subtle abnormalities warrant ongoing follow-up to determine their long-term significance.

A heart is described in which there was a solitary arterial trunk that exited from the heart astride a large perimembranous ventricular septal defect, with the pulmonary arterial supply originating entirely from collaterals from the descending aorta. There was no evidence of either hilar pulmonary arteries or an atretic pulmonary trunk. The morphology of the ventricular outlet component, with absence of the outlet septum supports the description of this heart as solitary arterial trunk, rather than tetralogy of Fallot with pulmonary atresia.

Device closure of oval fossa atrial scptal defects with the Amplatzer Septal Occluder was performed in 26 patients ranging in age from 0.89 to 60.44 years. In eight additional patients no device implant was performed because of the presence of multiple defects or because the defect was of a size unsuitable for closure with the devices currently available. The strectched diameter of the defects that were closed ranged from 4 to 23 mm (mean 14±5.4 mm) and device sizes ranged from 4 to 24 mm. Two devices were unstable, of which one embolized to the right atrium after release. Both devices were retrived at the same procedure. One of these parients subsequently underwent a successful device closure of his defect using a larger (24-mm) device. Three patients had multiple defects, which were successfully closed with a single device. At 1-month follow-up 23/26 (88%) and at 3-month follow-up 22/24 (92%) patients had complete closure of their defects, while two had residual shunts. One further patient who had complete closure of his defect at 1-month post-implant had his device removed and his atrial septal defect patched surgically 8 weeks after device closure. This was done as a result of the development of a vegetation affecting the device after an episode of septicaemia, which was not relate to the cardiac problems. There was no procedure-related morbidty or martality and all patients remain well at the present time.

Interventional catheterization procedures performed via the arterial route are well recognized therapies which are being employed with increasing frequency. This review summarizes our experience with local arterial complications of such procedures performed on 44 patients in our institution since 1985. A total of 51 balloon dilations were performed. All patients were heparinized during the procedure. Twenty-one procedures (41%) were followed by clinical evidence of reduced arterial circulation to the affected leg more than four hours after the procedure. Continuing infusion of heparin was used in 17 patients, with return of the pulse concerned in six, while two further patients developed evidence of arterial obstruction after an interval (having initially been found to have ‘satisfactory’ pulses at the end of the procedure). The final infant, whose femoral artery had been torn and could not be repaired, was observed without continuing heparinization. Streptokinase and/or tissue plasminogen activator was employed in eight patients, with resultant success in four. The remaining three, and three who failed thrombolytic therapy, underwent embolectomy. The incidence of arterial damage was related to the size of the catheter (assessed by the size of sheath required to introduce the collapsed balloon, indexed to body surface area) and to low weight or young age at the time of the procedure. No relationship could be established with other variables, including operator, type of catheter, or year or duration of procedure. At long-term follow-up, 11 (22%) patients still have absent or reduced pulses in the leg concerned. Arterial damage following interventional catheterization procedures remains a frequent occurrence despite increasing experience and technical improvements.

“When the history of congenital heart disease comes to be written, Brown will be given a high and honourable place along with Farre, Peacock, Fallot, Théremin, Vierordt, and Maude Abbott, as one whose labours have contributed vitally to the subject.”1

Little is known about the implications of left ventricular noncompaction in children with additional congenital cardiac malformations. With this in mind, we conducted a retrospective review of every left ventricular angiogram performed in a single tertiary referral centre for paediatric cardiology, in Melbourne, Australia, between 1994 and 2000 in children with congenital heart disease, looking specifically for patients with angiographic evidence of noncompaction of the left ventricle. The outcome of patients identified as having noncompaction was compared with that of patients from the same population, stratified by their primary congenital cardiac malformation.

Of 1515 children undergoing left ventricular angiography, 31, with 13 being male, were found to have angiographic evidence of left ventricular noncompaction, giving a prevalence of 2% (95% CI: 1.3%–2.8%). Of 69 (22%) children with a functionally single left ventricle, 15 fulfilled the criterions for noncompaction, compared to 16 of 1446 (1.1%) children with a balanced ventricular arrangement (p is less than 0.0001). The presence of noncompaction and a functionally single left ventricle were each associated with a doubling of mortality, the effect being cumulative. Of surviving patients with left ventricular noncompaction, 19% (4%–34%) have left ventricular dysfunction at their latest follow-up. We suggest that the important late sequels of noncompaction justify careful scrutiny for this entity in children with congenital cardiac disease.

Congenitally corrected transposition is a complex cardiac lesion that is often associated with ventricular septal defect, obstruction of the outflow tract of the morphologically left ventricle, and abnormalities of the morphologically tricuspid valve.1,2 Nomenclature for this lesion has been variable and confusing.1 In this review, we define, and hopefully clarify this terminology. The lesion is a combination of discordant union of the atrial chambers with the ventricles, and the ventricles with the arterial trunks.1,2 In rare circumstances, discordant atrioventricular connections can be associated with concordant ventriculo-arterial connections. This malformation has been called “isolated ventricular inversion”. The term is less than precise, and the descriptive approach using the phrase “discordant atrioventricular connections with concordant ventriculo-arterial connections” is preferred, as discussed below.

Congenital cardiac malformations which include isomerism of the atrial appendages are amongst the most challenging of problems for diagnosis and also for medical and surgical management. The nomenclature for pathological description is controversial, but difficulties can be overcome by the use of a segmental approach. Such an approach sets out the morphology and the topology of the chambers of the heart, together with the types and modes of the atrioventricular, ventriculo-arterial, and venous connections. We have applied this method to a study of 35 hearts known to have isomerism of the atrial appendages. We have already published accounts of 27 of these cases, but these were reviewed for this study in the light of our increased awareness of the implications of isomerism, and 8 new cases were added. After examining, or re-examining, the morphology of every heart in detail, we grouped them together according to their ventricular topology and modes of atrioventricular connection. Then we studied the course of the specialised conduction system, by the use of the light microscope, first in each individual case, and then together in their groups. We conclude that the pathways for atrioventricular conduction in hearts with isomerism of the atrial appendages are conditioned both by ventricular topology, and by the atrioventricular connections. Based on our experience, we have been able to establish guidelines that direct the clinician to the likely location of the conduction tissues.