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Re: Response to Dr Guntheroth

Dear Editor

We appreciated the comments of Dr Guntheroth et al. We specifically chose to eliminate patent foramen ovale from our study, hence patients with a defect <3mm were excluded from inclusion. Dr Gunteroth raises an interesting point that some of the small ASDs which we described as undergoing spontaneous closure (particularly those measuring approximately 3-4mm) may have in fact represented stretched patent foramen ovale particularly if the infant was young and had a recent patent arterial duct with left atrial enlargement. The cases which were 3-4mm which underwent spontaneous closure were diagnosed in all cases in children greater than 1 year of age, and in no case was there a prominent septal flap to raise suspicion of a PFO.

Likewise, all these children had a left-to-right shunt via the defect which given such considerations resulted in our calling them small ASDs. Whether some of these represented stretched PFO is however quite difficult to refute emphatically. The question does however raise the interesting point of where the cut-off point is between a stretched PFO and a small ASD when solely using echocardiography to make this judgement? Irrespective of this point however our study set out to determine how many ASDs outgrew the potential for transcatheter closure using the specific device we had available at our institution at the time.

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Re: Secundum atrial septal defects and transcatheter closure

Dear Editor

In the March issue of Heart, McMahon and colleagues presented an excellent review of this subject.[1] I have one question for the authors. You describe four patients with small ASDs that had spontaneous closure of the defect. Since the method for spontaneous closure for ventricular septal defects, by consensus, is roughening of the endocardium of the rim of the defect by the high velocity of the jet, but the velocity across most ASDs is less than 1 m/s, it is difficult to think that an ASD would ever close from that means. Isn't it likely that these were simply foramen ovale that were stretched by enlargement of the left atrium due to ductal flow as an infant that has closed, leaving the incompetent foramen ovale to gradually regress as the enlargement disappeared. We found that this was a frequent occurrence in the premature infant population (Zhou and Guntheroth).[2]

References

(1) C J McMahon, T F Feltes, J K Fraley, J T Bricker, R G Grifka, T A Tortoriello, R Blake, and L I Bezold. Natural history of growth of secundum atrial septal defects and implications for transcatheter closure. Heart 2002; 87:256-259.

(2) Zhou TF, Guntheroth WG. Valve-incompetent foramen ovale in premature infants with ductus arteriosus. JACC 1987;10:193-9