Effect of aspirin on spontaneous contrast in the brachial veins of normal subjects

Blood cell aggregates are thought to be the cause of spontaneous echo contrast (SEC), although there is disagreement as to whether red cell or platelet aggregates produce this effect. One way to differentiate between these 2 possibilities is to evaluate the effect of aspirin on SEC because aspirin would not be expected to affect red cell aggregates. To eliminate the need to perform repetitive transesophageal echocardiographic studies, and the possible effect of the underlying disease process on SEC, the effect of aspirin on SEC in the brachial vein was studied in normal volunteers using a single-blind, before-and-after study design. Other factors known to affect blood echogenicity including hematocrit, sedimentation rate, and the presence of platelet aggregates by microscopy were also studied. The amount of SEC was quantitated by image analysis and expressed as the aggregate score. The results in 10 volunteers showed that all had SEC in brachial veins before aspirin, but there was no significant day-to-day variation in the amount of SEC during the control period (mean ± SEM 104,248 ± 23,088, 153,722 ± 35,664, and 124,568 ± 22,827 for days 1, 3, and 5, respectively). A significant decrease in the aggregate score occurred after 7 days of aspirin, 650 mg twice a day (51,690 vs 127,513, p = 0.002); this was accompanied by a striking decrement in the size of the largest platelet aggregate found in venous blood. Aspirin caused no significant change in the hematocrit or sedimentation rate. These results indicate that there is a component of SEC that is aspirin-sensitive and is likely to represent platelet aggregates.