Hostname: page-component-586b7cd67f-gb8f7 Total loading time: 0 Render date: 2024-11-24T14:01:33.389Z Has data issue: false hasContentIssue false

The distance from the Amplatzer septal occluder to the mitral valve in patients undergoing interventional closure of defects in the oval fossa increases with growth of the patient

Published online by Cambridge University Press:  21 January 2005

Robert F. English
Affiliation:
Division of Pediatric Cardiology, Department of Pediatrics, University of Florida, Jacksonville, FL, USA
Jose A. Ettedgui
Affiliation:
Division of Pediatric Cardiology, Department of Pediatrics, University of Florida, Jacksonville, FL, USA

Abstract

The Amplatzer septal occluder is an alternative to operative closure of atrial septal defects within the oval fossa. An issue when deploying the device is its distance from the mitral valve. The purpose of this study is to determine how this distance changes with growth of the patient. We identified, through a review of charts, all patients undergoing closure of defects within the oval fossa by insertion of an Amplatzer septal occluder. Data were obtained from the echocardiogram 24 hours after closure, and at most recent follow-up, including left ventricular end-diastolic diameter, left atrial diameter, degree of mitral valvar regurgitation, body surface area, and distance from the device to the mitral valve. We divided the patients into 2 groups based upon change in body surface area. The first group had an increase in body surface area of at least 10%. All others were in the second group.

We inserted 55 Amplatzer septal occluders in 54 patients. Of these we excluded 17 patients, 1 because quality of images was inadequate, 1 who underwent placement of 2 devices, 1 in whom the device embolised to the left ventricle the day after deployment, and 14 who have not yet had a follow-up echocardiogram.

The group which exhibited an increase in body surface area of greater than 10% demonstrated an increase in distance from the device to the mitral valve, left ventricular end-diastolic, and left atrial diameters. Those who did not undergo significant growth had no increase in distance from the device to the mitral valve, but did have an increase in left atrial and left ventricular end-diastolic diameters. No patient developed mitral regurgitation. We conclude that, when deploying an Amplatzer septal occluder close to the mitral valve in children, the distance from the device to the mitral valve can be expected to increase with growth of the patient.

Type
Original Article
Copyright
© 2004 Cambridge University Press

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Losay J, Petit J, Lambert V, et al. Percutaneous closure with Amplatzer device is a safe and efficient alternative to surgery in adults with large atrial septal defects. Am Heart J 2001; 142: 544548.Google Scholar
Du ZD, Hijazi ZM, Kleinman NH, Larntz K. Comparison between transcatheter and surgical closure of secundum atrial septal defect in children and adults: results of a multicenter nonrandomized trial. J Am Coll Cardiol 2002; 39: 18361844.Google Scholar
Omeish A, Hijazi ZM. Transcatheter closure of atrial septal defects in children and adults using the Amplatzer septal occluder. J Interv Cardiol 2001; 14: 3744.Google Scholar
Cao QL, Du ZD, Joseph A, et al. Immediate and six-month results of the profile of the Amplatzer septal occluder as assessed by transesophageal echocardiography. Am J Cardiol 2001; 88: 754759.Google Scholar
Salaymeh KJ, Taeed R, Michelfelder EC, Beekman III RH, Shim D, Kimball TR. Unique echocardiographic features associated with deployment of the Amplatzer atrial septal defect device. J Am Soc Echocardiogr 2001; 14: 128137.Google Scholar
Kort HW, Balzer DT, Johnson MC. Resolution of right heart enlargement after closure of secundum atrial septal defect with transcatheter technique. J Am Coll Cardiol 2001; 38: 15281532.Google Scholar