“…8 The types of thermal affliction to endothelial cells that are known to trigger thrombosis, including hyperthermic activation, 26,27 necrotic cell death, 13 and denudation (i.e., exposure of the internal elastic lamina, a highly thrombogenic surface), 7 span a broad temperature range (41-100 C, Figure 1) that is easily achieved during ELT. 4,9,34 The biochemical response to this particular endovascular damage profile, which mainly entails secondary hemostasis (activation of coagulation), 31 is therefore believed to be responsible for the initial thrombotic closure of the vein, as shown in exemplary micrographs of histological preparations of veins that had been subjected to ELT (for example, Figure 3A and C in Proebstle et al, 35 Figures 2, 7, 9, and 11 in Vuylsteke et al, 36 and Figures 5 and 7 in Vuylsteke et al 37 ). Coagulation-mediated thrombus formation requires blood flow in the treated vein for the supply of coagulation factors that are responsible for producing fibrin, the main component of venous thrombi.…”