RT Book, Section A1 Agarwal, Sunil K. A1 Maslov, Petra A1 Narula, Jagat A1 Fuster, Valentin A2 Fuster, Valentin A2 Harrington, Robert A. A2 Narula, Jagat A2 Eapen, Zubin J. SR Print(0) ID 1191187164 T1 EPIDEMIOLOGY OF SMOKING AND PATHOPHYSIOLOGY OF CARDIOVASCULAR DAMAGE T2 Hurst's The Heart, 14e YR 2017 FD 2017 PB McGraw-Hill Education PP New York, NY SN 9780071843249 LK accesscardiology.mhmedical.com/content.aspx?aid=1191187164 RD 2024/10/14 AB SummaryThis chapter discusses the epidemiology of cigarette smoking, particularly with regard to cardiovascular disease, and the pathophysiology of smoking-induced cardiovascular damage (see accompanying Hurst’s Central Illustration). The majority of smokers are male. Globally, cigarette smoking is the leading cause of preventable cardiovascular morbidity and mortality, with around one in ten cardiovascular deaths still attributed to smoking. Smoking has been associated with the development of multiple cardiovascular conditions, including atherosclerosis, myocardial infarction, stroke, peripheral arterial disease, and abdominal aortic aneurysms. Three constituents of cigarette smoke have been shown to have a role in the initiation and progression of cardiovascular disease: nicotine, carbon monoxide (CO), and reactive oxygen species (ROS). Nicotine is the main cause of the smoking-induced hemodynamic changes, although CO has also been implicated. Free radicals, ROS, and reactive aldehydes from cigarette smoke are involved in the development of endothelial dysfunction, through negative effects on endothelial nitric oxide (NO) production. Various components of cigarette smoke have been shown to induce processes involved in cardiac remodelling, and cigarette smoke is also known to induce a prothrombotic state, vascular inflammation, alterations of lipid profile, and changes to glucose metabolism.