Publications

The relation between left atrial dimension measured by M-mode echocardiography and systemic embolization after valve replacement was examined prospectively among 397 patients with a prosthetic valve enrolled in the Department of Veterans Affairs Cooperative Study on Valvular Heart Disease. Baseline characteristics including several measures of left atrial enlargement were compared for 31 patients who developed systemic embolism and 366 who did not develop embolism during a 5 year follow-up period. Variables that were significantly related to left atrial dimension or systemic embolization in univariate analyses were included with several others in a multiple logistic regression model. The incidence rate of systemic embolism was more than three times higher after mitral valve replacement than after aortic valve replacement (4.4 and 1.3 per 100 patient-years, respectively); this difference persisted after adjustment for other factors. Univariate analysis indicated a threefold higher incidence of systemic embolism in patients with a left atrial dimension greater than or equal to 4 cm compared with that in patients with a dimension less than 4 cm (3 versus 1 per 100 patient-years, respectively). However, when the effect of valve location (mitral versus aortic) was taken into account using either univariate or multivariate techniques, left atrial dimension was found not to be associated with systemic embolism. In multivariate analysis, atrial fibrillation, age, ejection fraction and location of the prosthetic valve were significantly associated with embolism. Results of this multicenter study suggest that left atrial dimension is not independently related to the development of systemic embolism in patients undergoing valve replacement.

Transcriptional induction of the gene encoding the alpha-subunit of IL-2R has been shown to be mediated by a sequence element (GGGGAATCTCCC) that is homologous to the NF-kappa B-binding site of the kappa Ig gene enhancer. In this report we demonstrate that the induced transcription of this gene by mitogen and by the tax gene product of the type-I human T cell leukemia virus is dependent upon an additional sequence motif (GGGCGTAGC) located approximately 10 bp downstream of the previously identified site. This newly identified motif binds a factor that is present in extracts derived from different cell types and does not appear to be required for basal promoter activity. We conclude that proteins binding at both sites act coordinately, leading to maximal induction of the receptor gene.