Abstract

BackgroundLimited data are available on the increase in cardiac troponin after transcatheter closure of interatrial septal defects, and the mechanism is not fully understood. The aim with the study was to examine retrospectively whether transcatheter closure of the interatrial septum leads to myocardial injury, and to determine the mechanism.MethodsTroponin T (TnT) serum concentrations were determined before and 1 day after transcatheter closure of an atrial septal defect (ASD) or patent foramen ovale (PFO) in a retrospective study in adults. Fifty-one patients were included, 36 ASD and 15 PFO (female/male 35/16), mean age 52 ± 16 y (range 17–80 y).ResultsAn increase in TnT was observed 1 day after the procedure (p = 0.000) in 44 patients (92%). The increase in TnT was significantly correlated to the size of the ASD (r = 0.424, p = 0.010), as well as to the size of the implanted ASD device (r = 0.542, p = 0.001), and the duration of the ASD intervention (r = 0.348, p = 0.035). In cases of PFO, the increase in TnT was not correlated with the size of the PFO or the PFO device, or the duration of the intervention. No correlations were found between the increase in TnT and the patient’s age, body weight or body surface area.ConclusionsTranscatheter closure of the interatrial septum causes an increase in TnT indicating a minor and clinically insignificant myocardial injury. The findings indicate that mechanical trauma caused by inserting the ASD device may play an important role in this elevation. The impact of the size of the device on the degree of TnT elevation reflects the amount of myocardium affected by the device.Trial registrationNCT03099967. Registered 4 April 2017, retrospectively registered.

Highlights

  • Limited data are available on the increase in cardiac troponin after transcatheter closure of interatrial septal defects, and the mechanism is not fully understood

  • The level of troponin T (TnT) was ≥15 ng/L at baseline in three patients (6%, one atrial septal defect (ASD) closure, one ASD balloon sizing only, and one patent foramen ovale (PFO) closure), and an increase in TnT was found in 47 patients (92%) 1 day after the procedure (Table 1)

  • The age, body surface area (BSA), TnT elevation and cardiovascular risk factors did not differ between the ASD and the PFO groups (Table 1)

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Summary

Introduction

Limited data are available on the increase in cardiac troponin after transcatheter closure of interatrial septal defects, and the mechanism is not fully understood. The aim with the study was to examine retrospectively whether transcatheter closure of the interatrial septum leads to myocardial injury, and to determine the mechanism. Limited data are available on the increase in TnT after transcatheter closure of interatrial septal defects, and the specific mechanism of myocardial damage is not yet fully understood [3,4,5,6]. The aim of this study was to investigate whether transcatheter closure of interatrial septal communications leads to myocardial injury, by measuring the serum concentration of TnT before and after catheter closure in adults, and to try to determine the cause of such an elevation

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