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Risk of embolization after institution of antibiotic therapy for infective endocarditis.
OBJECTIVES: This study was designed to assess the risk of systemic embolization in patients with left-sided infective endocarditis, once adequate antibiotic treatment had been initiated, on the basis of prospective clinical follow-up.
BACKGROUND: As one of the complications of infective endocarditis, embolization has a great impact on prognosis. Prediction of an individual patient's risk of embolization is very difficult.
METHODS: We studied 217 episodes of left-sided endocarditis that were experienced among a cohort of 211 prospectively recruited patients. According to the Duke criteria, 91% of the episodes were definite infective endocarditis. Seventy-two episodes involved infections located on prosthetic valves. All patients were studied by transthoracic and transesophageal echocardiography. Clinical, echocardiographic and microbiologic data were entered in a data base. The mean follow-up interval was 151 days.
RESULTS: Twenty-eight episodes (12.9%; group I) of endocarditis had embolic events after the initiation of antibiotic therapy. The remaining 189 episodes did not embolize (group II). Most emboli (52%) affected the central nervous system, and 65% of the embolic events occurred during the first two weeks after initiation of antibiotic therapy. Previous embolism was associated with new embolism (relative risk [RR] 1.73, 95% confidence interval [CI] 1.02 to 2.93; p = 0.05). There was an increase in the risk of embolization with increasing vegetation size (RR 3.77, 95% CI 0.97 to 12.57; p = 0.07). Vegetation size had no impact on the risk of embolization in streptococcal endocarditis or aortic infection. By contrast, large (> or = 10 mm) vegetations had a higher incidence of embolism when the microorganism was staphylococcus (p = 0.04) and the mitral valve was infected (p = 0.03). The increase in vegetation size at follow-up showed a higher risk for embolization (RR 2.64, 95% CI 0.98 to 7.16; p = 0.02).
CONCLUSIONS: Embolism before antimicrobial therapy is a risk factor for new emboli. The risk of embolization seems to increase with increasing vegetation size, and this is particularly significant in mitral endocarditis and staphylococcal endocarditis. An increase in vegetation size, despite antimicrobial treatment, may predict later embolism.
BACKGROUND: As one of the complications of infective endocarditis, embolization has a great impact on prognosis. Prediction of an individual patient's risk of embolization is very difficult.
METHODS: We studied 217 episodes of left-sided endocarditis that were experienced among a cohort of 211 prospectively recruited patients. According to the Duke criteria, 91% of the episodes were definite infective endocarditis. Seventy-two episodes involved infections located on prosthetic valves. All patients were studied by transthoracic and transesophageal echocardiography. Clinical, echocardiographic and microbiologic data were entered in a data base. The mean follow-up interval was 151 days.
RESULTS: Twenty-eight episodes (12.9%; group I) of endocarditis had embolic events after the initiation of antibiotic therapy. The remaining 189 episodes did not embolize (group II). Most emboli (52%) affected the central nervous system, and 65% of the embolic events occurred during the first two weeks after initiation of antibiotic therapy. Previous embolism was associated with new embolism (relative risk [RR] 1.73, 95% confidence interval [CI] 1.02 to 2.93; p = 0.05). There was an increase in the risk of embolization with increasing vegetation size (RR 3.77, 95% CI 0.97 to 12.57; p = 0.07). Vegetation size had no impact on the risk of embolization in streptococcal endocarditis or aortic infection. By contrast, large (> or = 10 mm) vegetations had a higher incidence of embolism when the microorganism was staphylococcus (p = 0.04) and the mitral valve was infected (p = 0.03). The increase in vegetation size at follow-up showed a higher risk for embolization (RR 2.64, 95% CI 0.98 to 7.16; p = 0.02).
CONCLUSIONS: Embolism before antimicrobial therapy is a risk factor for new emboli. The risk of embolization seems to increase with increasing vegetation size, and this is particularly significant in mitral endocarditis and staphylococcal endocarditis. An increase in vegetation size, despite antimicrobial treatment, may predict later embolism.
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