Echocardiography Predicts Embolic Events in Infective Endocarditis

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 to the Duke criteria, including silent embolism. BACKGROUND The value of echocardiography in predicting embolism in patients with endocarditis remains controversial. Some studies reported an increased risk of embolism in patients with large and mobile vegetations, whereas other studies failed to demonstrate such a relationship. METHODS Multiplane transesophageal echocardiograms of 178 consecutive patients with definite infective endocarditis (IE) were analyzed. The incidence of embolism was compared with the echocardiographic characteristics (localization, size and mobility) of the vegetations. To detect silent embolism, cerebral and thoraco-abdominal scans were performed in 95% of patients. RESULTS Among 178 patients, 66 (37%) had one or more EEs. There was no difference between patients with and without embolism in terms of age, gender and left valve involved. On univariate analysis, Staphylococcus infection, right-side valve endocarditis and vegetation length and mobility were significantly related to EEs. A significant higher incidence of embolism was present in patients with vegetation length .10 mm (60%, p , 0.001) and in patients with mobile vegetations (62%, p , 0.001). Embolism was particularly frequent among 30 patients with both severely mobile and large vegetations (.15 mm) (83%, p , 0.001). On multivariate analysis, the only predictors of embolism were vegetation length (p 5 0.03) and mobility (p 5 0.01). CONCLUSIONS Our study shows that the presence of vegetations on TEE is predictive of embolism and that the morphologic characteristics of vegetations are helpful in predicting EEs in both mitral and aortic valve IE. It also suggests that early operation may be recommended in patients with vegetations .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) © 2001 by the American College of Cardiology