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. 2010 Aug;6(3):162-74.
doi: 10.2174/157340310791658794.

Patent foramen ovale in cerebral infarction

Affiliations

Patent foramen ovale in cerebral infarction

J Serena et al. Curr Cardiol Rev. 2010 Aug.

Abstract

Recent studies support the hypothesis of a close aetiological and pathogenic association between the presence of patent foramen ovale (PFO) and cryptogenic stroke. The therapeutic options currently used in the treatment of these patients range from standard antiaggregation and standard-dose anticoagulation to the percutaneous occlusion of the PFO. The use or recommendation of treatment is based both on clinical risk factors associated with PFO, such as age, detection of states of hypercoagulability and previous history of stroke, and on the risks associated to right-to-left shunt (RLSh) and PFO, such as the size of PFO, magnitude of RLSh and the presence of atrial septal aneurysm (ASA). However, there is currently no consensus regarding the most suitable treatment and it is surprising to observe the widespread use of certain therapeutic approaches which are not supported by clinical evidence. In this revision, we analyse the relevance of PFO in cryptogenic stroke, consider the main evidence available for determining the best management of these patients and make diagnostic and therapeutic management recommendations.

Keywords: Patent foramen ovale; cryptogenic stroke; echocardiography.; right-to-left shunt; transcranial Doppler.

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Figures

Fig. (1)
Fig. (1)
Prevalence of PFO in autopsy studies in subjects without heart disease.
Fig. (2)
Fig. (2)
Summary of the RLSh detection methodology using TCD.
Fig. (3)
Fig. (3)
Massive RLSh by transcranial colour coded duplex sonography detected 3 seconds after contrast infusion (agitated saline solution, 9 mL of saline solution and 1 mL of air). Video can be downloaded at http://www.telefonica.net/web2/jserenal/pulmonaryshunt/fistula.htm
Fig. (4)
Fig. (4)
Contrast TCD detected RLSh of less than 10 signals (upper panel), “shower” (middle panel), and “curtain” (lower panel) patterns in MCA after Valsalva manoeuvre.
Fig. (5)
Fig. (5)
Frequency of massive RLSh during Valsalva manoeuvre by age group in cryptogenic stroke, stroke of known aetiology, and in healthy controls. Number of patients in each group are given along the horizontal axis. Probability values representing the differences between groups are shown at the top of the bars.
Fig. (6)
Fig. (6)
CODICIA Study. Stroke recurrence by RLSh magnitude at rest and during Valsalva manoeuvre in the younger population.
Fig. (7)
Fig. (7)
Stroke recurrence by RLSh magnitude during Valsalva manoeuvre and presence of ASA in the whole and younger populations in the CODICIA Study.
Fig. (8)
Fig. (8)
Functional outcome using the modified Rankin Scale (mRS) at discharge, 3 months and 1 year after cryptogenic stroke in patients with and without massive RLSh.

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