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ORIGINAL ARTICLE
Year : 2018  |  Volume : 1  |  Issue : 1  |  Page : 31-34

Prevalence and determinants of myocardial damage after occluder implantation in patients with atrial septal defect


1 Department of Cardiology, King George’s Medical University, Lucknow, Uttar Pradesh, India
2 Department of Cardiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala, India

Correspondence Address:
Dr. Mahim Saran
B10/18, Sector-K, Aliganj, Lucknow - 226 024, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IHJI.IHJI_5_17

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Objective: The objective was to study the prevalence and extent of myocardial damage in patients undergoing atrial septal defect device closure (ASDDC) and to examine its determinants. Background: Little is known about myocardial lesions after occluder implantation in children. The influence of defect size and anatomy, device size, and other baseline patient characteristics on the occurrence and extent of myocardial damage remains unclear. We evaluated the occurrence and extent of myocardial damage and its relationship to the various patient characteristics using cardiac troponin T (cTnT) as the marker of myocardial damage. Methods: In a retrospective analysis, case records of patients undergoing ASDDC from May 2015 to June 2016 were analyzed. Anthropometric data, atrial septal defect (ASD) characteristics, and device characteristics were compared between troponin-positive (Group 1; cTnT ≥0.05 µg/L) and troponin-negative (Group 2; cTnT <0.05 µg/L) groups. Results: Troponin T was significantly increased following occluder implantation in 32 out of 200 patients who underwent the procedure. Complex ASDs (particularly multiple defects [odds ratio [OR] = 13.23] and deficient posterior rim [OR = 13.23]) contributed significantly to myocardial damage following occluder implantation as evidenced by significant troponin T release of ≥0.05 µg/L (P = 0.004). Considering quantitative troponin T estimation as a measure of extent of myocardial damage, there was a weak correlation between device size and the extent of myocardial damage (r2 = 0.125; P = 0.047). Conclusions: Complex ASDs, particularly those with multiple defects or deficient posterior rim, contribute significantly to myocardial damage following ASDDC. Larger device size is associated with greater myocardial damage.


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