Pathophysiologic Mechanisms of Tobacco Smoke Producing Atherosclerosis

Abstract

Introduction: Despite the convincing epidemiologic association between smoking and vascular disease, the pathophysiologic mechanisms by which smoking initiates and contributes to the progression of atherosclerosis remain incompletely understood. A precise dose-dependent correlation has never been demonstrated, suggesting that the biological relationship is complex and influenced by individual genetic and possibly environmental factors. Although endothelial dysfunction and intimal damage appear to be central to atherogenesis, how tobacco products cause this effect has not been established. The purpose of this review is to describe the current state of knowledge of the main pathophysiologic pathways of how tobacco smoking abets atherosclerosis Constituents of Tobacco Smoke: Tobacco combustion produces a mixture of organic substances derived from burning organic materials. The predominant gaseous phase constituents include carbon monoxide, acetaldehyde, formaldehyde, acrolein, and other carbonyls, as well as nicotine and tobacco-specific nitrosamines. Potential Pathophysiologic Mechanisms: Smoking-induced changes in coronary vasomotor tone, platelet activation, and endothelial integrity are major components of both the development of atherosclerosis and its clinical presentation. Smoking may initiate and accelerate the progression of atherosclerosis by injuring the vascular intima. Other potential mechanisms include intimal damage and endothelial dysfunction, oxidative stress and injury, thrombosis, lipid abnormalities, and inflammation. Conclusion: Smoking tobacco products contributes measurably to the incidence of acute vascular events and chronic disease. The causative compound, the exact mechanism of injury, and whether the atherogenic effect is modifiable are not known.