RESUMO
Smoking is well established and important risk factor for cardiovascular disease. Cessation of smoking clearly decreases the risk of cardiovascular events. Nicotine is known to be the addicting component of tobacco products. Nicotine replacement therapy (NRT) increases the probability of quitting smoking. Studies have indicating no increase in cardiovascular events in smokers with known cardiovascular disease.
Assuntos
Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/prevenção & controle , Nicotina/administração & dosagem , Abandono do Hábito de Fumar/métodos , Prevenção do Hábito de Fumar , Fumar/epidemiologia , Doenças Cardiovasculares/etiologia , Comorbidade , Humanos , Fatores de Risco , Fumar/efeitos adversos , Abandono do Hábito de Fumar/estatística & dados numéricosRESUMO
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.