Paediatric cardiology is often experienced as a noisy environment. Outpatient clinics, echocardiography laboratories, ICUs, catheterisation suites, and operating theatres are filled with alarms, conversations, machines, movement, and continual clinical activity. Beneath this activity, however, another dimension of CHD care exists: silence. These pauses are not simply absences within clinical work, but moments through which patients, families, nurses, physiologists, and clinicians encounter uncertainty, adaptation, fear, relief, and continuity across time. Across fetal diagnosis, infancy, childhood, adolescence, transition to adult services, and survivorship, silence emerges repeatedly within care. Some silences wound. Others sustain. At times, they create space for reflection and presence; at others, they may leave questions unspoken or emotions unsupported. Over years of care, individuals may be shaped by these experiences in ways rarely acknowledged within clinical medicine. This reflective perspective explores the role of silence, listening, and presence across the longitudinal experience of children and families living with CHD and those who care for them.

Pulmonary arterial hypertension in children remains a progressive disease marked by right ventricular failure and early mortality despite advances in targeted therapy. In resource-limited settings, access to parenteral prostacyclin is often constrained by cost, infrastructure, and challenges related to chronic administration. The atrial flow regulator is a transcatheter device that creates a controlled interatrial shunt to provide right-heart decompression. We describe our single-center experience with atrial flow regulator implantation in children with severe pulmonary arterial hypertension. We retrospectively reviewed six children with World Health Organization Group 1 pulmonary arterial hypertension who underwent device implantation between 2021 and 2024. Baseline assessment included echocardiography, cardiac magnetic resonance imaging, right-heart catheterization, N-terminal pro-B-type natriuretic peptide (NT-proBNP), and 6-minute walk distance. All patients had advanced pulmonary vascular disease despite combination oral therapy. Median indexed pulmonary vascular resistance was 17.0 Wood units·m² (10.8–28.5), median right ventricular ejection fraction was 31% (22–39), and median 6-minute walk distance was 250 m (190–280). Device implantation was successful in all patients, with no periprocedural mortality. During follow-up, NT-proBNP levels decreased and 6-minute walk distance improved. Friedman testing demonstrated significant changes over time for NT-proBNP (p = 0.002) and 6-minute walk distance (p = 0.003). In this small cohort, atrial flow regulator implantation was technically feasible and associated with favorable longitudinal trends in biomarker and functional measures. In resource-constrained settings, it may serve as an adjunctive strategy for carefully selected high-risk patients. Larger multicenter studies are needed to refine patient selection and long-term outcomes.

Twenty-three patients with dilated cardiomyopathy were recruited and compared with 10 age-and sex-matched controls using 2D-speckle tracking images of the apex and base of the left ventricle. Follow-up was performed after a period of 6 years. Ten patients with dilated cardiomyopathy presented with diminished rotation and 13 patients presented with reverse apical rotation, which was associated with poorer outcomes.

Cor triatriatum sinister is an exceptionally rare congenital cardiac anomaly [1]. While restrictive forms are typically present in infancy or early childhood, survival into adolescence with a 2–3 mm fenestration is unusual [2, 3]. We report a 14-year-old male, misdiagnosed with refractory asthma for years, who presented with palpitations. Imaging and catheterisation revealed severe post-capillary pulmonary hypertension with echocardiographic evidence of right-sided chamber dilatation, D-shaped left ventricular configuration, moderate tricuspid regurgitation, and an estimated pulmonary artery pressure of 85 mmHg. Cardiac catheterisation showed PA pressure of 50/30 mmHg (mean 39 mmHg), PCWP of 28 mmHg, Qp/Qs of 1.14, and a favourable PVR/SVR ratio of 0.12, indicating reversibility. Successful surgical resection of a calcified membrane was performed via right anterolateral thoracotomy. This case underscores the importance of considering cor triatriatum sinister in adolescents with unexplained respiratory symptoms or wheezing and highlights the value of correlating echocardiographic evidence of obstruction with invasive haemodynamic assessment before surgery [4, 5].

We present the case of a 36-year-old male with the anomalous origin of the left coronary artery from the pulmonary artery surgically corrected in childhood who has suffered from sudden cardiac arrest twice later in life. Anomalous left coronary artery from the pulmonary artery is a rare congenital abnormality most commonly manifesting itself in early infancy, less frequently only becoming apparent in adulthood. Uncorrected defect is associated with a high mortality rate hence surgical treatment is advisable, both in children and few asymptomatic adults. Adequate management of adult patients with anomalous left coronary artery from the pulmonary artery remains a subject of discussion as complications secondary to even a congenital anomaly corrected in childhood, such as myocardial scarring, could ultimately lead to life-threatening ventricular arrhythmias and/or sudden cardiac death.

Arrhythmogenic cardiomyopathy is a rare genetic disorder linked to malignant arrhythmias and sudden cardiac death. We report a 15-year-old girl presenting with sudden cardiac arrest. Imaging suggested left-dominant arrhythmogenic cardiomyopathy, and genetic testing identified a novel DSP variant. Cardioverter-defibrillator implantation was performed. Family screening revealed affected relatives, highlighting the importance of early diagnosis and risk stratification.

Late-onset infective endocarditis after transcatheter atrial septal defect device closure is uncommon, and in selected patients, mechanical factors related to adverse device–tissue interaction may contribute to the development of late device-related infection. A 15-year-old boy presented with fever and systemic embolic manifestations eight years after transcatheter atrial septal defect closure. Echocardiography demonstrated a mobile mass on the left atrial surface of the occluder device, and computed tomography revealed splenic infarction and a mass-like lesion adjacent to the right lower pulmonary vein orifice. Emergent surgical intervention revealed extensive vegetation and fibrotic thickening predominantly along the right lower pulmonary vein orifice–adjacent left atrial wall, rather than on the device surface. The device was removed, the defect was closed using an autologous pericardial patch, and the patient completed six weeks of antibiotic therapy with an uneventful recovery. This case suggests that incomplete endothelialisation and chronic device-related mechanical interaction may create a vulnerable endocardial environment that facilitates bacterial adherence and subsequent infective endocarditis. Careful patient selection, prudent device sizing, and long-term echocardiographic surveillance may help identify patients in whom consideration of antibiotic prophylaxis during exposure to transient bacteremia could reduce the risk of subsequent infective endocarditis.

High-degree atrioventricular block in young patients often requires pacing, posing long-term risks. We present a 15-year-old athlete with sickle cell trait and high-degree atrioventricular block managed with cardioneuroablation. Post-cardioneuroablation, atrioventricular conduction normalised, and a nine-month follow-up showed no arrhythmias. This case underscores cardioneuroablation as a promising, less invasive alternative to pacing for young patients, requiring further research.

A neonate with common arterial trunk presented with severe cyanosis rather than pulmonary overcirculation. Echocardiography, cardiac CT, catheterisation, and surgery showed a pulmonary trunk arising from a truncal valvar sinus, with systolic obstruction by a dysplastic truncal cusp. Staged palliation restored antegrade pulmonary flow, allowed pulmonary arterial growth, and enabled successful complete repair.

Clinical experience during fellowship training and post-graduation depends on training length, resources, and time at specific institutions, contributing to knowledge deficits. Institutional collaboration overcomes such barriers wherein case discussions share knowledge and management strategy, enhancing patient outcomes. Our discussion of the management of Tetralogy of Fallot highlights key insights between programmes differing in geography and resources, hosted by Heart University.

Severe pulmonary valvar stenosis may remain silent into adolescence. A 17-year-old girl attended with vaginal bleeding; the diagnosis rested on a grade 6/6 murmur found on examination. Aminotransferases rose despite correction of anaemia and hypotension and fell only after balloon valvoplasty relieved the obstruction. The valve being dysplastic, valvoplasty was not curative, but it reversed the hepatic injury and allowed valve replacement to proceed safely.

A one-year-old boy with repaired tetralogy of Fallot presented with recurrent fever. Blood cultures grew Streptococcus mitis/oralis, but transthoracic echocardiography showed no infective endocarditis. Cardiac CT angiography revealed an occult right ventricular outflow tract pseudoaneurysm, which was surgically resected. This case highlights CT angiography as a critical diagnostic tool when echocardiography fails to identify infectious sources in CHD.