Cardiac troponin I release after transcatheter closure of atrial septal defects is associated with supraventricular arrhythmias on early follow-up.

Introduction: Atrial septal defects (ASD) are prevalent congenital heart anomalies found in the adult population. Percutaneous ASD closure has become a routine clinical practice. Elevation of postprocedural transient cardiac biomarkers and exacerbation of supraventricular arrhythmias have been reported in the subject literature.

Aim: To explore the relationship between cardiac troponin I (cTnI) elevation and supraventricular ectopy (SVE) following percutaneous closure of secundum atrial septal defect (ASD) in adult patients.

Material and methods: 600 consecutive patients who underwent successful transcatheter ASD secundum closure were analyzed. Serum levels of cTnI were measured before and within 72 h of device implantation. 24-hour Holter monitoring was performed before the procedure, at 1 month, and at 6 months of follow-up.

Results: SVE burden increased 1 month after the procedure (median 1021.00; min.-max. 11.00-29 862.00) compared to baseline values (median 146.00; min.-max. 0-1865.00; p < 0.01). 61.7% of patients demonstrated a cTnI rise exceeding 50% of the upper reference limit within 24 h of the procedure. A statistically significant positive correlation between SVE burden 1 month after the procedure and periprocedural cTnI increase (p < 0.05, r = 0.41) was observed, while cTnI levels significantly correlated with procedure and fluoroscopy time (p < 0.001), device size (p < 0.001) and maximal ASD diameter (p < 0.001).

Conclusions: A significant increase of cTnI is noted frequently after transcatheter ASD closure and seems to predict exacerbation in SVE burden on short-term follow up. The independent risk factors of cTnI rise are prolonged procedure duration and larger device sizes.