HEMATOLOGIC CORRELATES OF SPONTANEOUS ECHO CONTRAST IN PATIENTS WITH ATRIAL-FIBRILLATION AND IMPLICATIONS FOR THROMBOEMBOLIC RISK

Spontaneous echo contrast has been observed in conditions of low blood Wow velocity, such as rheumatic mitral stenosis and atrial fibrillation (AF). The phenomenon has been attributed to increased echogenicity due to aggregation of blood cells at low shear rates. The aim of this study was to determine whether abnormalities of blood composition also might contribute to spontaneous echo contrast formation by promoting cellular aggregation. Transesophageal echocardiography was performed in 185 patients with AF (31 with valvular and 154 with nonvalvular AF). The left atrium was examined for thrombus and spontaneous echo contrast, which was graded from 0 (nil) to 4+ (severe) by 2 independent observers. Forty milliliters of venous blood was obtained from each patient for hematologic analysis. Spontaneous echo contrast was observed in 46% of patients (74% with valvular and 41% with nonvalvular AF). In linear regression analysis, positive correlations were found between tirade of spontaneous echo contrast and erythrocyte sedimentation rate (p < 0.001), lowshear blood viscosity (p <0.001) and anticardiolipin antibody (p = 0.02) in the total study population, and in patients with nonvalvular AF. Spontaneous echo contrast correlated with mitral valve area (p <0.01) and gradient (p = 0.03), but not with hematologic parameters in patients with valvular AF. Left atrial thrombus was present in 6 patients, all of whom had spontaneous echo contrast. Age (<0.01), spontaneous echo contrast (0 = 0.03) and the fibrinogen concentration (0 = 0.03) correlated with previous embolic events. These results suggest that, in addition to now disturbance associated with structural cardiac abnormalities and AF, blood composition may also be important in spontaneous echo contrast formation, particularly in patients with nonvalvular AF. The association between spontaneous echo contrast and both the erythrocyte sedimentation rate and low-shear blood viscosity supports a role for red cell aggregation in the pathogenesis of this phenomenon.