Vascular plasminogen activator and deep vein thrombosis

In attempts to determine the aetiology of deep vein thrombosis (DVT) it has been established that some patients with a history of lower limb DVT have a low level of vascular plasminogen activator (VPA) in their superficial hand veins and this combined with a poor VPA release is thought to predispose to thrombosis (1). Hand veins rarely develop thrombosis and so the level of VPA has been measured quantitatively in the more commonly at risk veins of the lower limb. In 6 limbs operated on for varicose veins, paired samples of vein from the groin and from the calf were examined. The median activity score for the groin veins (8138 cpm/μg) was significantly higher than the activity in the calf veins (2353 cpm/μg) (P = 0·01). In 9 limbs amputated for critical ischaemia, paired samples of calf long saphenous vein and soleal vein were examined. The VPA in the former was 1675 cpm/μg compared with 6796 cpm/μg in the soleal veins. This difference is significant at the 1 per cent level. A correlation has been shown between the VPA content of these two sets of veins (R = 0·87). The low level of VPA in the superficial calf veins may be an aetiological factor in superficial thrombophlebitis, but the commonest site for DVT, the soleal veins of the calf, have a high level of VPA.