During tetralogy of Fallot repair, leaving or even create an interatrial communication may facilitate post-operative course particularly with right ventricle restrictive physiology. The aim of our study is to assess the influence of atrial communication on post-operative course of tetralogy of Fallot repair.

Retrospectively, we studied all children who had tetralogy of Fallot repair (2003–2018). We divided them into two groups: tetralogy of Fallot repair with interatrial communication (TOFASD) group and tetralogy of Fallot repair with intact atrial septum (TOFIAS) group. We performed propensity match score for specific pre- or intra-operative variables and compared groups for post-operative outcome variables. Secondarily, we looked for right ventricle restrictive physiology incidence and influence of early repair performed before 3 months of age on post-operative course.

One hundred and sixty children underwent tetralogy of Fallot repair including (93) cases of TOFIAS (58%) and (67) cases of TOFASD (42%). With propensity matching score, 52 patients from each group were compared. Post-operative course was indifferent in term of positive pressure ventilation time, vasoactive inotropic score, creatinine and lactic acid levels, duration and amount of chest drainage and length of intensive care unit and hospital stay. Right ventricle restrictive physiology occurred in 38% of patients with no effects on outcome. 12/104 patients (12%) with early repair needed longer pressure ventilation time (p = 0.003) and intensive care unit stay (p = 0.02).

Leaving interatrial communication in tetralogy of Fallot repair did not affect post-operative course. As well, right ventricle restrictive physiology did not affect post-operative course. Infants undergoing early tetralogy of Fallot repair may require longer duration of positive pressure ventilation time and intensive care unit stay.

Differentiation of the so-called sinus venosus defect from other defects permitting shunting between the atrial chambers remains problematic. The lesion is not a true septal defect, and current theories to explain the existence of the sinus venosus defect fall short. The presence of persistent systemic to pulmonary venous connections has been proposed to explain the existence of the sinus venosus defect.

Clinical histories and radiological findings of six patients are reviewed. Three patients have veno-venous bridges, two have partial anomalous pulmonary venous connections, and one patient has a sinus venosus defect. The clinical information is reviewed, along with current developmental and morphological considerations.

We provide radiographic, developmental, and morphological evidence to support the theory that a so-called sinus venosus defect is the consequence of persistence of foetal systemic to pulmonary veno-venous bridges, rather than of deficiencies in atrial septation.

To determine the frequency and factors associated with increase in microembolic signals during transcatheter closure of atrial septal defect using the Amplatzer septal occluder.

During the procedure in 16 patients, we measured microembolic signals using transcranial Doppler. Procedure time was divided into five periods: right cardiac catheterisation; left cardiac catheterisation; left cardiac angiocardiography; sizing and long sheath placement; device placement and release. We compared numbers of microembolic signals among the five periods and identified factors associated with them.

Mean size of septal occluder was 16 millimetres in diameter. Total number of microembolic signals was a median of 31.5, ranging from 3 to 113. Microembolic signals in three periods, left cardiac catheterisation; sizing, and long sheath placement; and device placement and release, were not significantly different from one another, but were significantly higher than those in the remaining two periods, right cardiac catheterisation and left cardiac angiocardiography (median was 9 in left cardiac catheterisation; 6 in sizing and long sheath placement; 6.5 in device placement and release, versus 0 in right cardiac catheterisation and 1 in left cardiac angiocardiography, p less than 0.05, respectively). Importantly, the time for device manipulation positively correlated with total number of microembolic signals (r equals 0.77, p less than 0.001), although fluoroscopic time, age, or size of septal occluder did not.

Transcatheter closure of atrial septal defect using the Amplatzer septal occluder produces microemboli, especially during device placement. To minimise the risk of systemic embolism, we must decrease the time for device manipulation.