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Arterioscler Thromb Vasc Biol. 2014 Mar;34(3):509-15. doi: 10.1161/ATVBAHA.113.300156.

Smoking and cardiovascular disease: mechanisms of endothelial dysfunction and early atherogenesis.

Author information

1
From the Cardiac Surgery Research Laboratory, Department of Surgery, Medical University of Vienna, Vienna, Austria (B.M.); and Cardiac Surgery Research Laboratory Innsbruck, University Clinic for Cardiac Surgery, Innsbruck Medical University, Innsbruck, Austria (D.B.).

Abstract

Smoking represents one of the most important preventable risk factors for the development of atherosclerosis. The present review aims at providing a comprehensive summary of published data from clinical and animal studies, as well as results of basic research on the proatherogenic effect of smoking. Extensive search and review of literature revealed a vast amount of data on the influence of cigarette smoke and its constituents on early atherogenesis, particularly on endothelial cells. Vascular dysfunction induced by smoking is initiated by reduced nitric oxide (NO) bioavailability and further by the increased expression of adhesion molecules and subsequent endothelial dysfunction. Smoking-induced increased adherence of platelets and macrophages provokes the development of a procoagulant and inflammatory environment. After transendothelial migration and activation, macrophages take up oxidized lipoproteins arising from oxidative modifications and transdifferentiate into foam cells. In addition to direct physical damage to endothelial cells, smoking induces tissue remodeling, and prothrombotic processes together with activation of systemic inflammatory signals, all of which contribute to atherogenic vessel wall changes. There are still great gaps in our knowledge about the effects of smoking on cardiovascular disease. However, we know that smoking cessation is the most effective measure for reversing damage that has already occurred and preventing fatal cardiovascular outcomes.

KEYWORDS:

endothelial damage; flow-mediated dilatation; inflammation; lipid modification; nitric oxide; oxidative stress

PMID:
24554606
DOI:
10.1161/ATVBAHA.113.300156
[Indexed for MEDLINE]

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