Factor VIIa increases platelet surface thrombin generation. With normal levels of the coagulation proteins (•), the pattern of thrombin generation shows a short lag phase, during which platelets are activated and the coagulation complexes assemble on the activated platelets. This is followed by a burst of thrombin generation that reaches a substantial peak value. The thrombin is ultimately inhibited by antithrombin. In hemophilia (♦), the lag is extended due to slow formation of the factor Xa/Va complex on the platelet surface. There is a weak burst of thrombin generation with a low peak value. Factor VIIa (▾) enhances factor X activation so that factor Xa/Va complexes form more rapidly on the platelet surface. This leads to a shorter lag with an enhanced burst of thrombin leading to a higher peak. Increasing the factor VIIa concentration (▪) further shortens the lag, enhances the burst, and leads to an even higher peak of thrombin generation.