BACKGROUND: Smoking increases the risk of atherothrombotic events. To determine whether smoking influences plaque thrombogenicity, we examined the effect of cigarette smoking and aspirin use on tissue factor (TF) expression in atherosclerotic plaques. METHODS AND RESULTS: A total of 23 apoE-/- mice were exposed to cigarette smoke with (n=9) or without (n=14) aspirin treatment. Eleven mice who were exposed to filtered room air served as controls. Aortic root plaques of mice exposed to smoke had higher immunoreactivity for TF (14+/-4% versus 6.4+/-3%; P=0.0005), vascular cell adhesion molecule-1 (15+/-4% versus 5+/-2%; P=0.002), and macrophages (16+/-5% versus 6+/-2%; P=0.002) compared with nonsmoking controls. Aspirin treatment attenuated smoking-induced changes in plaque composition. In human plaques obtained by carotid endarterectomy, TF immunoreactivity (8+/-5% versus 2+/-2%; P=0.0002) and activity (P=0. 03) were higher in the plaques from smokers (n=28) than those from nonsmokers (n=28). Aspirin use was associated with reduced TF expression in smokers (9+/-8% versus 3+/-4%; P=0.0017). CONCLUSIONS: Our results suggest increased plaque TF expression and thrombogenicity as a novel mechanism for the increased risk of atherothrombotic events in smokers. Treatment with aspirin may reduce TF expression.
BACKGROUND: Smoking increases the risk of atherothrombotic events. To determine whether smoking influences plaque thrombogenicity, we examined the effect of cigarette smoking and aspirin use on tissue factor (TF) expression in atherosclerotic plaques. METHODS AND RESULTS: A total of 23 apoE-/- mice were exposed to cigarette smoke with (n=9) or without (n=14) aspirin treatment. Eleven mice who were exposed to filtered room air served as controls. Aortic root plaques of mice exposed to smoke had higher immunoreactivity for TF (14+/-4% versus 6.4+/-3%; P=0.0005), vascular cell adhesion molecule-1 (15+/-4% versus 5+/-2%; P=0.002), and macrophages (16+/-5% versus 6+/-2%; P=0.002) compared with nonsmoking controls. Aspirin treatment attenuated smoking-induced changes in plaque composition. In human plaques obtained by carotid endarterectomy, TF immunoreactivity (8+/-5% versus 2+/-2%; P=0.0002) and activity (P=0. 03) were higher in the plaques from smokers (n=28) than those from nonsmokers (n=28). Aspirin use was associated with reduced TF expression in smokers (9+/-8% versus 3+/-4%; P=0.0017). CONCLUSIONS: Our results suggest increased plaque TF expression and thrombogenicity as a novel mechanism for the increased risk of atherothrombotic events in smokers. Treatment with aspirin may reduce TF expression.
Authors: Daniel J Conklin; Suzaynn Schick; Michael J Blaha; Alex Carll; Andrew DeFilippis; Peter Ganz; Michael E Hall; Naomi Hamburg; Tim O'Toole; Lindsay Reynolds; Sanjay Srivastava; Aruni Bhatnagar Journal: Am J Physiol Heart Circ Physiol Date: 2019-02-01 Impact factor: 4.733
Authors: Dixon Yang; Sunil Iyer; Hannah Gardener; David Della-Morte; Milita Crisby; Chuanhui Dong; Ken Cheung; Consuelo Mora-McLaughlin; Clinton B Wright; Mitchell S Elkind; Ralph L Sacco; Tatjana Rundek Journal: Cerebrovasc Dis Date: 2015-07-25 Impact factor: 2.762
Authors: Geetha Raghuveer; David A White; Laura L Hayman; Jessica G Woo; Juan Villafane; David Celermajer; Kenneth D Ward; Sarah D de Ferranti; Justin Zachariah Journal: Circulation Date: 2016-09-12 Impact factor: 29.690