Abstract
Transcatheter closure of atrial septal defects has been employed increasingly in the past decade. This technique is now regarded as the treatment of choice for patients with appropriate atrial septal defects. Transcatheter closure of ventricular septal defects (VSDs) has undergone fewer clinical trials, even though VSDs are more common than atrial septal defects. The implanted device does not seem to embolize and complications are few. Decreases in left ventricular and diastolic pressure and improvement of ventricular function have been reported early following device closure, and the left-to-right shunt has been either eliminated or dramatically reduced. In small infants who are in heart failure at a young age and who weigh less than 8 kg, which is below the recommended threshold for device closure, technological advancements in device size and catheter manipulation are needed before VSDs can be closed. A large number of VSDs, particularly if small to medium in size, will become smaller or close spontaneously, making intervention unnecessary. Muscular VSDs have been closed with transcatheter devices for the past 15 years. Although perimembranous defects are more common than muscular defects, they have not become more amenable to closure since the introduction of the Amplatzer® VSD occluder device (AGA Medical Corporation, Golden Valley, MN). Previous devices, such as the Rashkind and button devices, have been unsuccessful in attempts at closure of the VSDs because of the proximity of the defects to the aortic valve and potential aortic valve damage. Before the transition is made to routine therapy, large, multicenter trials are justified to test the feasibility, safety and efficacy of nonsurgical closure of VSDs. In this review, I discuss the current applications of transcatheter closure of membranous, perimembranous and muscular VSDs, in particular with Amplatzer® devices, and the implications for future development.
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Moodie, D. Technology Insight: transcatheter closure of ventricular septal defects. Nat Rev Cardiol 2, 592–596 (2005). https://doi.org/10.1038/ncpcardio0351
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DOI: https://doi.org/10.1038/ncpcardio0351