Spontaneous contrast in the form of smokey echos in the cardiac chambers is considered to be a risk factor for thromboembolism. The aggregation of red blood cells results in larger target which diffuse a measurable in vitro ultrasonic signal. The phenomenon of erythrocytic aggregation is dependent on the red cells themselves, the plasma fibrinogen and conditions of blood flow. The other constituents of the blood only reflect a small amount of ultrasound, usually undetectable. Transoesophageal echocardiography with high frequency transducers (5 MHz) positioned in close proximity to the cardiac chambers, has become the reference method for detecting spontaneous contrast. This phenomenon is almost exclusively observed in the left atrium and left auricle and rarely in the other cardiac chambers or descending aorta. In pathological situations, spontaneous contrast is essentially implicated in two conditions: mitral valve obstacles and non-valvular atrial fibrillation. Conversely, moderate to severe mitral regurgitation is a negative predictive factor of spontaneous contrast. However, a purely qualitative appreciation of spontaneous contrast which may be influenced by the gain setting and technical specifications of the echocardiograph, and the subjectivity of the operator, is an important limitation. Therefore, the identification of quantitative markers of spontaneous contrats and new therapeutic antithrombotic protocols remain essential.