Inhibition of clot formation attenuates intravascular arrest of breast cancer cells. (A) Experimental design to study TC arrest and clot formation in control (ctr) mice vs 3 treatment groups during the first 24 hours after TC injection. (B) Quantification of arrested TCs after 24 hours with associated clot in control mice vs mice anticoagulated with tinzaparin (tinza) or ASAC (more than 100 cells in at least 3 mice per group; Student t test P < .0001). (C) Representative images for prolonged cell arrest quantification 0 and 24 hours after intracardial TC injection. The definition of 0 hours was determined by imaging <30 minutes after intracardial injection. Breast cancer cells in control mice show persistent arrest in the first 24 hours (circles). In treated mice, few TCs were visible 24 hours after intracardial TC injection (area, 600 × 600 µm2; scale bars: 150 µm). (D) Quantification of persistent intravascular TC arrest in all 3 cell lines upon antithrombotic treatment compared with control mice. For Jimt1: top, 383 metastases in 3 ctr mice vs 411 metastases in 3 tinzaparin-treated mice; middle, 425 metastases in 3 iso-ctr mice vs 281 metastases in 3 aVWF-treated mice; bottom, 383 metastases in 3 ctr mice vs 266 metastases in 3 ASAC-treated mice (P < .0001 for the entire column). For A2058: top, 451 metastases in 3 ctr mice vs 366 metastases in 3 tinzaparin-treated mice (P = .849); middle, 303 metastases in 3 iso-ctr mice vs 571 metastases in 3 aVWF-treated mice (P = .341). For H1: top, 249 metastases in 3 ctr mice vs 299 metastases in 3 tinzaparin-treated mice (P = .725); middle, 139 metastases in 3 iso-ctr mice vs 243 metastases in 3 aVWF-treated mice (P = .033). All P values from Student t test; *P < .05. Error bars: 95% CI.