Cardiac troponin I is increased after interventional closure of atrial septal defects

Area of Science:

• Cardiology
• Interventional Cardiology
• Biomarkers

Background:

• Atrial septal defects (ASDs) are congenital heart conditions often requiring intervention.
• Interventional closure of ASDs is a common alternative to surgical repair.
• Assessing potential myocardial injury post-intervention is crucial for patient safety.

Purpose of the Study:

• To evaluate myocardial injury following interventional ASD closure using cardiac troponin I (cTn-I).
• To compare cTn-I levels after interventional ASD closure versus diagnostic catheterization.
• To investigate the role of CK/CK-MB levels in detecting myocardial damage.

Main Methods:

• Study enrolled 40 patients undergoing procedures for ASDs.
• 33 patients underwent successful interventional closure with Amplatzer devices.
• 7 patients underwent diagnostic balloon sizing only.
• Cardiac troponin I (cTn-I) levels were measured serially post-procedure.

Main Results:

• A significant increase in cTn-I was observed post-interventional ASD closure, peaking at 4 hours.
• No significant cTn-I increase was detected in patients undergoing diagnostic balloon sizing only.
• Creatine kinase (CK) and CK-MB levels did not show significant changes.

Conclusions:

• Interventional ASD closure with Amplatzer devices causes transient myocardial membrane instability, evidenced by elevated cTn-I.
• The observed myocardial injury is likely reversible.
• CK and CK-MB may be less sensitive for detecting myocardial infarction in this context.