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(Circulation. 2007;115:e386-e387.)
© 2007 American Heart Association, Inc.
Images in Cardiovascular Medicine |
From the Sussex Cardiac Centre, Brighton, United Kingdom.
Correspondence to Tim Lockie, BSc, MBChB, Flat 6, 32 Coin St, London SE1 8YG, UK. E-mail timlockie@doctors.org.uk
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
A 54-year-old Caucasian male transatlantic airline pilot with no cardiovascular risk factors presented to a neurology clinic after a transient episode of dysphasia. He reported no additional neurological symptoms. Eleven years previously, he had developed asymptomatic sinus node disease and had undergone implantation of a dual-chamber permanent pacemaker to retain his commercial pilots license. He was in sinus rhythm, was normotensive (120/70 mm Hg), and had no cardiac murmurs or carotid bruits. Neurological examination was normal.
A computerized tomography scan of his head showed a focal left cerebral infarct. Carotid ultrasonography, holter monitoring, and a thrombophilia screen were normal. A diagnosis of a left-hemisphere transient ischemic event was made. The patient was referred for a transoesophageal echo to exclude an intracardiac source of embolus. Structurally, the heart was normal, but on venous bubble contrast injection from the left arm, there was dense simultaneous opacification of both the left and right sides of the heart, without Valsalva maneuvers (Figure 1). Transthoracic images were subsequently repeated with bubble contrast from the right arm; on this occasion, there was no opacification of the left side of the heart, even with Valsalva maneuvers, effectively excluding a significant patent foramen ovale or intrapulmonary arteriovenous malformation (Movie I).
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The patient underwent a venogram from the left basilic vein (Figure 2). This demonstrated a proximal occlusion of the left subclavian vein
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