BUERGER originally described thromboangiitis obliterans as primarily a thrombotic process occurring in arteries and veins1 ; later he postulated that the thrombosis arose from an angiitis2. Impressed with the thrombotic aspects of the disease, our laboratory undertook an investigation of clot formation and dissolution in Buerger's disease. Clots obtained from patients diagnosed as suffering from Buerger's disease were exposed to varying concentrations of streptokinase (‘Varidase’; Lederle Laboratories) as were clots obtained from normal patients. While the blood clots obtained from normal patients were found to be resistant to high concentrations of streptokinase, similar concentrations of streptokinase completely dissolved the clots obtained from cases with thromboangiitis obliterans