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BMJ Case Rep. 2009;2009. pii: bcr11.2008.1211. doi: 10.1136/bcr.11.2008.1211. Epub 2009 Jul 23.

Patent foramen ovale and hypercoagulable state in the pathogenesis of acute thrombotic myocardial infarction.

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1
Catholic University, Cardiology Institute, 1, L.go F. Vito, Rome, 00168, Italy.

Abstract

Patent foramen ovale (PFO) is a known cause of cryptogenic stroke and, when associated with a condition of thrombophilia, its closure has been shown to reduce the recurrence of cerebral embolic events. Here we present a case of a young man, with a history of previous recurrent cerebral ischaemic episodes, that developed an inferior acute myocardial infarction (AMI) with angiographic evidence of thrombotic occlusion of the right coronary artery (RCA). Thrombus aspiration followed by balloon angioplasty was performed and, after 24 h of glycoprotein IIb/IIIa inhibitor infusion, thrombus was no longer evident at coronary angiography. Screening for thrombophilia revealed heterozygosis for prothrombin G20210A polymorphism. At transoesophageal echocardiography (TOE), a large PFO with right-to-left atrial shunt was present. Given the history of multiple thrombotic clinical events and the associated state of thrombophilia, transcatheter PFO closure was successfully performed. At 12 months of follow-up the patient was completely asymptomatic.

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