Why the study?
Does interventional closure of ASDs increase cardiac troponin I levels compared to diagnostic catheterization?
Does interventional closure of ASDs increase cardiac troponin I levels compared to diagnostic catheterization?
Interventional closure of ASDs causes a transient increase in cardiac troponin I, but normal CK/CK-MB levels can help differentiate this from myocardial infarction.
Transient cTn-I rise after ASD closure may not signify MI if CK/CK-MB normal; leaves open prognostic implications in observational data.
This study was designed to assess possible myocardial injury caused by interventional closure of atrial septal defects (ASDs) compared to diagnostic catheterization by measuring cardiac troponin I (cTn-I). Forty patients were enrolled; in 33 ASDs were successfully closed, while in 7 a diagnostic balloon sizing of the defect was performed only. Total cTn-I increased significantly from 0.1 to 1.9 microg/l at the end of the intervention and 2.23 at 4 hr and decreased to 1.35 at 15 hr. No significant increase could be detected in patients with diagnostic balloon sizing only or of CK/CK-MB levels either. Following interventional closure of ASDs with Amplatzer septum/PFO occluders, increased cTn-I levels for several hours indicate some transient, reversible myocardial membrane instability due to the device. Discrimination of ventricular myocardial infarction might be possible by estimating less sensitive CK and CK-MB levels only.
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Pees et al. (2002) studied this question.
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