Fig. 3

Schematic illustration of cross section of blood vessel and hemostatic components. (Reproduced and modified with permission from Chang JC. Clin Appl Thromb Hemost 2019 Jan-Dec; 25:1076029619887437). The most important part in the understanding of hemostasis in vivo is cognizance of the histological structure of the blood vessel and its role of vascular physiology in vascular injury. The reason is thrombosis cannot occur without vascular injury as explained in Table 3 and shown in novel “two-path unifying theory” of hemostasis [3, 4]. In intravascular injury, the local damage of ECs causes localized exocytosis of ULVWF to activate ULVWF path and damage extending into SET causes localized release of sTF to activate TF path. Both paths together lead to macrothrombogenesis and produce macrothrombus (e.g., DVT; pulmonary embolism; acute ischemic stroke). Should intravascular trauma extend further into EVT with additional release of eTF and bleed beyond EVT as seen in thrombo-hemorrhagic stroke, it produces macrothrombosis and hemorrhage (i.e., thrombo-hemorrhagic syndrome). Abbreviations: EVT, extravascular tissue; eTF, extravascular tissue factor; SET, subendothelial tissue; sTF, subendothelial tissue factor; RBC, red blood cells; ULVWF, unusually large von Willebrand factor multimers