Discussion

Neonatal left atrial appendage thrombosis is exceedingly rare, with only a few cases reported to date. Previously described cases have suggested that left atrial appendage thrombus in neonates may originate from prenatal or perinatal events, particularly when calcification or an organised thrombus is identified histologically.^{Reference Fujiwara, Yoshizawa and Sakazaki1} Surgical excision has been reported in cases with increasing thrombus mobility, highlighting the risk of systemic embolisation.

The clinical presentation of neonatal left atrial appendage thrombosis is often nonspecific. While arrhythmia or incidental imaging findings have been reported in prior cases, the present case illustrates that subtle signs of heart failure, such as poor feeding and a gallop rhythm, may be the primary manifestations in the absence of arrhythmic or embolic events.^{Reference Sheen, De Oliveira and Kim2–Reference Russo, Trappan and Benettoni4} The ventricular dysfunction observed in this patient was most likely multifactorial, with patent ductus arteriosus-related volume overload and perinatal haemodynamic stress representing the principal contributors. The left atrial appendage thrombus was unlikely to be the primary cause of ventricular dysfunction; however, it may have subtly influenced atrial mechanics and intracardiac flow.^{Reference Beigel, Wunderlich, Ho, Arsanjani and Siegel5} In neonates, high heart rates and limited diastolic filling time increase dependence of ventricular preload on atrial compliance, and a left atrial appendage mass may therefore interfere with ventricular filling.^{Reference Al-Saady, Obel and Camm6} Importantly, postoperative recovery of ventricular function was most likely driven by relief of volume overload following patent ductus arteriosus ligation, with removal of the left atrial appendage thrombus providing a complementary benefit. A direct causal relationship cannot be established.

Histopathological findings were consistent with a chronic or subacute organised thrombus rather than an acute thrombotic event, supporting a non-acute disease process in the absence of identifiable infection or perinatal inflammatory insult. Management of intracardiac thrombus in neonates should be individualised, considering thrombus size, mobility, location, and associated haemodynamic compromise.^{Reference Bendaly, Batra and Ebenroth7} Although anticoagulation is often the first-line therapy, surgical intervention may be appropriate in selected cases.^{Reference Monagle8} In the present case, the thrombus was large and mobile, located on the systemic side of the circulation, and persisted despite anticoagulation; in conjunction with a patent foramen ovale and ventricular dysfunction, this raised concern for systemic embolisation and ongoing haemodynamic impact. Surgical excision allowed definitive thrombus removal with simultaneous correction of associated shunt lesions.^{Reference De Rose, Mecarini and Campanale9}

Although intracardiac thrombus is extremely rare in neonates, this case underscores that careful attention to subtle clinical signs may prompt timely evaluation and facilitate detection of uncommon intracardiac pathology, enabling appropriate management even in such rare circumstances.