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J Am Coll Cardiol, 2004; 44:1712, doi:10.1016/j.jacc.2004.07.029
© 2004 by the American College of Cardiology Foundation
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LETTER TO THE EDITOR

Risk of thrombus formation on devices used to close transcatheter atrial septal defect and patent foramen ovale

Chessa Massimo, MD, PhD, Butera Gianfranco, MD, PhD and Carminati Mario, MD

Pediatric Cardiology Department and GUCH Unit, IPSD, Via Morandi, 30, 20097 San Donato Milanese, Milan, Italy

(Email: massimo.chessa{at}lycos.com).

In a recent issue of the Journal, Krumsdorf et al. (1) discussed the incidence of thrombus formation on atrial septal defect (ASD) and patent foramen ovale (PFO) closure devices in 1,000 consecutive patients. The investigators report a group of 593 patients with PFO but only 235 patients had an embolic event. Closure of a PFO is usually indicated if there is a spontaneous or provokable right-to-left shunt during contrast transesophageal echocardiography (TEE) in a patient with clinic and/or radiologic evidence of an ischemic stroke, a transient ischemic attack, or an extracranial peripheral thromboembolic episode.

Most of the thrombi (14 out of 20) were detected at the four-week TEE study, but it is not clear whether the investigators excluded the presence of them immediately after the procedure. Krumsdorf et al. (1) described different protocols of anticoagulation during the procedure.

Regarding our experience (751 ASDs; 170 PFOs) we believe that the two most sensitive points are: 1) monitoring of the anticoagulation of the patient during the procedure using the activated clotting time, and 2) duration of antiplatelet therapy after transcatheter ASD closure.

This last point is not yet clarified; endothelialization of an ASD device is supposed to occur within a few months after implantation; this information is supported by animal studies (2). It is accepted that six months of antiaggregation (with one or two drugs) is a long enough period to prevent thrombus formation on the device (3,4). The researchers found three thrombi at the six-month TEE; this might indicate that the endothelialization could not be completed at that time. Therefore, a longer period of antiplatelet therapy may be useful.


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 References
 

  1. Krumsdorf U, Ostermayer S, Billinger K, et al. Incidence and clinical course of thrombus formation on atrial septal defect and patent foramen ovale closure devices in 1,000 consecutive patients J Am Coll Cardiol 2004;43:302-309.[Abstract/Free Full Text]
  2. Sharafuddin MJA, Gu X, Titus JL, et al. Transvenous closure of secundum atrial septal defects. Preliminary results with a new self-expanding nitinol prosthesis in a swine model Circulation 1997;95:2162-2168.[Abstract/Free Full Text]
  3. Brandt RR, Neumann T, Neuzner J, et al. Transcatheter closure of atrial septal defect and patent foramen ovale in adult patients using the Amplatzer occlusion device: no evidence for thrombus deposition with antiplatelet agents J Am Soc Echocardiogr 2002;15:1094-1098.[CrossRef][Medline]
  4. Chessa M, Carminati M, Butera G, et al. Early and late complications associated with transcatheter occlusion of secundum atrial septal defect J Am Coll Cardiol 2002;39:1061-1065.[Abstract/Free Full Text]

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Ulrike Krumsdorf, Stefan Ostermayer, Kai Billinger, Thomas Trepels, Elisabeth Zadan, Kathrin Horvath, and Horst Sievert
J. Am. Coll. Cardiol. 2004 44: 1714-1716. [Full Text] [PDF]




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