Abstract

It is well known that one of the determinants of the paradoxical embolism through a patent foramen ovale is the presence of deep venous thrombosis. Deep venous thrombosis was detected in nearly 10% of patients with PFO and paradoxical embolism as the sole identifiable cardiac risk factor. Deep vein thrombosis is often clinically silent [ 1 Lethen H. Flachskampf F.A. Schneider R. et al. Frequency of deep vein thrombosis in patients with patent foramen ovale and ischemic stroke or transient ischemic attack. Am J Cardiol. 1997; 80: 1066-1069 Abstract Full Text PDF PubMed Scopus (176) Google Scholar , 2 Stollberger C. Slany J. Schuster I. Leitner H. Winkler W.B. Karnik R. The prevalence of deep venous thrombosis in patients with suspected paradoxical embolism. Ann Intern Med. 1993; 119: 461-465 Crossref PubMed Scopus (194) Google Scholar ]. Unfortunately, in this era in which the transcatheter closure of patent foramen ovale is gaining a worldwide acceptance and the technical procedural point of view seems to be the most attractive, the loss of attention for the main pathophysiological mechanism of paradoxical embolism may create some difficulties.

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