lntraaortic

Debris as a Potential Source of Embolic Stroke

David C. Rubin,

MD,

Gary D. Plotnick,

MD,

and Mary W. Hawke,

MD

is estimated that 10 to 20% of strokes are due to phenomena.* Patients with embolic strokes Iaretembolic often referred for echocardiographic evaluation to

Between September 1989 and March 1991, we enrolled 64 consecutive stroke patients referred by the neurologic service for TEE. All 64 patients were thought by identify potential cardiac sourcesof emboli. Transthorac- a neurologist to have embolism as a mechanism of stroke ic echocardiography(TTE) is often unsuccessfulin iden- based on complete neurologic evaluation, including CT tifying an embolic source.Transesophagealechocardiog- scan or magnetic resonance imaging, or both. Carotid raphy (TEE) has beenshownto have a higher sensitivity ultrasound scanning for atherosclerotic disease was eifor identifying sourcesof emboli, but in almost 50% of ther negative or inconclusive, and all patients were rethese patients, no cardiac source of emboli is found.2 ferred for TEE to find potential cardiac sources of emHowever, the heart is only 1 possiblesource of emboli. boli. Prior TTE did not reveal the source of emboli in any For many years, atherosclerotic lesions in the carotids patient. The control group consisted of 50 consecutive and ascendingaorta have beenknown to generatedebris patients aged >40 years who were referred for TEE that embolize distally to produce cerebral ischemia.3T4 during the same time period for any indication other TEE offers the ability to visualize the intimal surfaceof than the source of emboli, or aortic dissection. Examinations were performed in all patients using a the thoracic aorta and allows detection of atherosclerotic lesions that may have the potential for embolization.5 5 MHz monoplane phased array transesophageal probe This study examines whether patients with embolic and the Hewlett Packard Sonos 500. All patients were strokesreferred to find the cardiac sourceof emboli have prepared according to standard protocol (no oral intake complex aortic atherosclerotic plaques more often than 6 to I2 hours before procedure, topical anesthesia to the oral pharynx with aerosolized lidocaine, and intravedo age-matchedcontrol subjects. nous sedation with midazolam and demerol). A comFrom the Division of Cardiology, Room S2C22, University of Maryplete 2-dimensional echocardiographic examination was land Hospital, 22 S. GreeneStreet, Baltimore, Maryland 21201.Manuscript received September 26, 1991; revised manuscript receivedNo- performed using standard views as described by the Mayo Clinic.6 The heart was evaluated for potential vember 25,1991, and acceptedNovember 30.

flGUREl.A,mildplaqm @llWOihruhca,lDO*dbn, md p#aNdhg 0.75 cm into the aortic lumen, (2) ulcerated plaque with ulcer cavity >0.5 cm in depth, and (3) plaque with adherent mobile thrombus. Less severe atherosclerotic lesions not meeting any of these criteria were considered with the mild to moderate plaque group. Statistical comparison between the 2 groups wasperformed using the Student t test, and significance was considered at the 0.05 level. Mean age of the 64 stroke patients (30 men and 34 women) was 60 f 1S (SEM) years (range 40 to 87), and that of the 50 control patients (22 men and 28 women) was 61 f 1.7 (range 40 to 89). There were no significant differences in age or sex between the 2 groups. Table Z demonstrates the atherosclerotic plaque assessment in the 2 groups. Of the 64 stroke patients, 11 had complex atherosclerotic debris within the thoracic aorta, whereas only 2 in the control group had similar findings (p

Intraaortic debris as a potential source of embolic stroke.

lntraaortic Debris as a Potential Source of Embolic Stroke David C. Rubin, MD, Gary D. Plotnick, MD, and Mary W. Hawke, MD is estimated that 1...
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