Studies in Intravascular Coagulation

Abstract

ALTHOUGH much is known of the sequential biochemistry of blood coagulation, the mechanisms that may initiate the thrombotic process have not been significantly clarified since Virchow's day. Virchow postulated that thrombosis was caused by vascular injury, circulatory stasis and hypercoagulability of the blood. In animals experimental evidence has been obtained that thrombosis may be induced by a state of hypercoagulability combined with stasis in vessels free of intimal damage.¹ It has been postulated in man that hypercoagulability (defined as an increased tendency of circulating blood to clot) may, in some patients, be attributable to an alteration, as yet unrecognized, in . . .