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J Am Soc Echocardiogr. 2013 Feb;26(2):192-9. doi: 10.1016/j.echo.2012.10.019. Epub 2012 Dec 21.

Defects in the oval fossa: morphologic variations and impact on transcatheter closure.

Author information

1
University Hospital Southampton, Southampton, United Kingdom. joseph.vettukattil@uhs.nhs.uk

Abstract

BACKGROUND:

Incomplete formation of the partition between the two atrial chambers in the region of the oval fossa results in a range of defects, which extend from patent foramen ovale to large secundum atrial septal defects (ASDs). There is wide variation in the morphology of the latter lesions. The spatial orientation of the margins of ASDs relative to the persisting flap valve is not easily definable with standard echocardiographic imaging. Careful evaluation of the morphology is essential in optimizing successful transcatheter closure to minimize complications. The advent of three-dimensional transesophageal echocardiography has changed the understanding of the morphology of these defects and facilitated successful percutaneous closure.

METHODS:

Since 2007, over a 4-year period, transcatheter closure of ASDs was performed in 105 patients.

RESULTS:

During the study period, there were two instances of embolization of the device. The morphology of the defects in the patients with embolization was evaluated carefully, and an unusual spiral configuration of the flap valve relative to the rims of the oval fossa was noted. These findings were then found in four additional patients and serve as the focus of this report. To facilitate understanding of the unusual morphology, the clinical findings were compared with images showing the mechanism of development of the atrial septum in the mouse, revealing a striking similarity.

CONCLUSIONS:

Although uncommon, spiral spatial orientation of the margins of ASDs predisposes to embolization of devices used for percutaneous closure. Standard cross-sectional techniques have limited use in identifying this variation. Understanding of the development of the atrial septum in the mouse heart may help explain the morphogenesis of the defect and the mechanism predisposing to embolization.

PMID:
23265438
DOI:
10.1016/j.echo.2012.10.019
[Indexed for MEDLINE]

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