In vivo and in vitro studies on the mechanism and clinical significance of spontaneous echocardiographic contrast in patients with atrial dysrhythmias.

The pathogenesis of spontaneous echocardiographic contrast (SEC) is complex and multifactorial. Although originally described in low-flow state situations such as in the left atrium of patients with mitral stenosis or in the false lumen of patients with aortic dissection, its detection is highly dependent on technical factors such as the frequency of the transducer used. Multiple blood components have been implicated in SEC formation and erythrocyte aggregation currently appears to be the most likely mechanism. SEC is related to atrial fibrillation and is commonly found in patients with thrombus or prior history of thromboembolism. In addition, it may represent a prognostic marker for patients with atrial fibrillation because patients with SEC have a higher incidence of subsequent thromboembolic events. Therapeutic options include anticoagulation and, perhaps, antiplatelet therapy. Further prospective studies are necessary to better define SEC pathogenesis and treatment.