OBJECTIVES The aim of our study was to assess the value of transesophageal
echocardiography (TEE) in predicting embolic events (EEs) in a large group
of patients with definite endocarditis according tu the Duke criteria, incl
uding silent embolism.
BACKGROUND The value of echocardiography in predicting embolism in patients
with endocarditis remains controversial. Some studies reported an increase
d risk of embolism in patients with large and mobile vegetations, whereas o
ther studies failed to demonstrate such a relationship.
METHODS Multiplane transesophageal echocardiograms of 178 consecutive patie
nts with definite infective endocarditis (IE) were analyzed. The incidence
of embolism was compared with the echocardiographic characteristics (locali
zation, size and mobility) of the vegetations. To detect silent embolism, c
erebral and thoraco-abdominal scans were performed in 95% of patients.
RESULTS Among 178 patients, 66 (37%) had one or more EEs. There was no diff
erence between patients with and without embolism in terms of age, gender a
nd left valve involved. On univariate analysis, Staphylococcus infection, r
ight-side valve endocarditis and vegetation length and mobility were signif
icantly related tu EEs. A significant higher incidence of embolism was pres
ent in patients with vegetation length >10 mm (60%, p < 0.001) and in patie
nts with mobile vegetations (62%, p < 0.001). Embolism was particularly fre
quent among 30 patients with both severely mobile and large vegetations (>1
5 mm) (83%, p < 0.001). On multivariate analysis, the only predictors of em
bolism were vegetation length (p = 0.03) and mobility (p = 0.01).
CONCLUSIONS Our study shows that the presence of vegetations on TEE is pred
ictive of embolism and that the morphologic characteristics of vegetations
are helpful in predicting EEs in both mitral and aortic Valve IE. it also s
uggests that early operation may be recommended in patients with Vegetation
s >15 mm and high mobility, irrespective of the degree of valve destruction
, heart failure and response to antibiotic therapy. (J Am Coll Cardiol 2001
;37:1069-76) (C) 2001 by the American College of Cardiology.