Hypercoagulability was first discovered by Dr. Rudolf Virchow, a German physician, in the mid-1800s. In 1965, the first descriptions of inherited thrombophilia were published by Dr. Roger O. Egeberg, an American physician.^[1][2][3] Later, in the 1990s, the more common mutations associated with primary hypercoagulable states were identified.^[4][5]

• 1821-1902: A German physician, Rudolf Virchow, began describing the pathophysiology of hemostasis at age 24.^[1]
• 1856: Rudolf Virchow proposed a hypothesis to explain the etiology of pulmonary emboli, which lead to the understanding of the three primary causes of venous and arterial thrombosis: stasis, injury to the vessel wall and abnormalities in the circulating blood. ^[6]
• 1906: Wasserman et al. described the antiphospholipid syndrome. ^[7]
• 1965: The first descriptions of inherited thrombophilias were Antithrombin deficiency by Egeberg et al. and dysfibrinogenemia by Beck et al.^[2][3]
• 1981-1984: Dr. John Griffin and Dr. Philip Comp described protein C deficiency and protein S deficiency respectively as a primary hypercoagulable state.^[8][9]
• 1993-1994: Dr. Rogier Bertina and his colleagues identified that activated protein C (APC) resistance was primarily due to a mutation in the factor V gene (guanine to adenine substitution at nucleotide 1691, G1691A) resulting in the Factor V Leiden molecule.^[4]
• 1996: Swibertus R Poort described a prothrombin gene mutation, specificaly the substitution of adenine to guanine at nucleotide 20210 (Prothrombin G20210A), and its association with inherited thrombophilia.^[5]