Cigarette smoke is an aerosol that contains >4,000 chemicals, including nicotine, carbon monoxide, acrolein, and oxidant compounds. Exposure to cigarette smoke induces multiple pathological effects in the endothelium, several of which are the result of oxidative stress initiated by reactive oxygen species, reactive nitrogen species, and other oxidant constituents of cigarette smoke. Cigarette-smoke exposure interferes adversely with the control of all stages of plaque formation and development and pathological thrombus formation. The reactive oxygen species in cigarette smoke contribute to oxidative stress, upregulation of inflammatory cytokines, and endothelial dysfunction, by reducing the bioavailability of nitric oxide. Plaque formation and the development of vulnerable plaques also result from exposure to cigarette smoke via the enhancement of inflammatory processes and the activation of matrix metalloproteases. Moreover, exposure to cigarette smoke results in platelet activation, stimulation of the coagulation cascade, and impairment of anticoagulative fibrinolysis. Many cigarette-smoke-mediated prothrombotic changes are quickly reversible upon smoking cessation. Public health efforts should urgently promote our understanding of current cigarette-smoke-induced cardiovascular pathology to encourage individuals to reduce their exposure to cigarette smoke and, therefore, the detrimental consequences of associated atherothrombotic disease.
A large body of literature strongly suggests that cigarette smoke unfavourably influences all major stages of atherosclerosis as well as pathological atherothrombus formation
Cigarette smoke contains oxidant compounds that cause oxidative stress in the endothelium, leading to endothelial dysfunction and injury, initiation of the atherosclerotic process, and subsequent formation of atherosclerotic plaques
Cigarette smoke promotes the development of vulnerable plaques and plaque rupture by enhancing inflammation and activating matrix metalloproteinases
Cigarette smoke causes platelet activation, and promotes platelet aggregation and platelet adhesion to sites of endothelial injury
Exposure to cigarette smoke shifts the balance of haemostasis towards thrombus formation by enhancing blood clotting and, at the same time, reducing the fibrinolytic capacity
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D. Bernhard is supported by the Austrian National Bank (Project 14745).
The authors declare no competing financial interests.
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Csordas, A., Bernhard, D. The biology behind the atherothrombotic effects of cigarette smoke. Nat Rev Cardiol 10, 219–230 (2013). https://doi.org/10.1038/nrcardio.2013.8
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