Cigarette smoking and cardiovascular disease

Abstract

Clinical and experimental studies indicate that either active or passive cigarette smoke exposure promotes vasomotor dysfunction, atherogenesis, and thrombosis in multiple vascular beds. Although the precise mechanisms responsible remain undetermined, free radical-mediated oxidative stress appears to play a central role in cigarette smoking mediated athero-thrombotic diseases. These free radicals could potentially arise directly from cigarette smoke and indirectly from endogenous sources as well. Furthermore, potentiated by multiple prothrombotic and antifibrynolytic effects, intravascular thrombosis is the predominant cause of acute cardiovascular events. Epidemiologic, clinical, and experimental data also suggest that the pathophysiologic effects of cigarette smoke exposure on cardiovascular function may be nonlinear.